A high proportion of individuals with Achilles tendinopathy continue to demonstrate long-term symptoms and functional impairments after exercise treatment. Thus, there is a need to delineate patient presentations that may require alternative treatment. The objective of this study was to evaluate if the presence of metabolic risk factors relates to tendon symptoms, psychological factors, triceps surae structure, and lower limb function in individuals with Achilles tendinopathy. One hundred and fifty-eight individuals (88 female) with diagnosed midportion Achilles tendinopathy were divided into three groups based on the number of metabolic risk factors linked to cardiovascular disease present at baseline: two or more factors, one factor, no factors. Metabolic risk factors were determined by clinical evaluation and past medical history. Achilles tendinopathy symptoms (Victorian Institute of Sport Assessment-Achilles, Patient Reported Outcome Measurement Information System, movement-evoked pain ratings), psychological factors (Tampa Scale for Kinesiophobia), triceps surae structure (B-mode ultrasound of tendon and muscle morphology, continuous shear wave elastography of tendon mechanical properties), and lower limb function (test battery) were compared among groups. Individuals with two or more metabolic risk factors had worse symptoms with loading (p = 0.011), smaller Achilles tendon size relative to body mass (p = 0.002), and worse lower limb function compared to individuals without metabolic risk factors (p < 0.02). No differences were observed between individuals with one metabolic risk factor and those without metabolic risk factors. Future consideration of multiple metabolic risk factors for individuals with Achilles tendinopathy could facilitate understanding the underlying impairments of tendon pathology and recovery that may be addressed with treatment.

This systematic review and meta-analysis evaluated the association between pain intensity and different body composition measures in adults suffering from chronic non-specific low back pain (CNLBP).

A systematic literature search across five databases-PubMed, Embase, CINAHL, Web of Science, and the Cochrane Library-was conducted. It identified observational studies published until January 2024. A meta-analysis was conducted incorporating a random-effects approach with Fisher's Z transformation. A critical appraisal of the included studies' quality was conducted.

Twenty-two studies were included. Of those, 20 were meta-analyzed, revealing positive, very weak correlations between pain intensity and body mass index (r = 0.11; 95% CI: 0.04 to 0.18), waist-hip ratio (r = 0.10; 95% CI: -0.14 to 0.34) and waist circumference (r = 0.09; 95% CI: -0.28 to 0.44). Not pooled study findings (e.g., hip circumference and body fat percentage) were narratively summarized, revealing 13 positive and four negative associations between pain intensity and body composition measures. Studies showed a substantial risk of bias due to unadjusted confounding factors and limited transferability of findings.

This systematic review and meta-analysis provided very low-quality evidence for a positive, very weak association between pain intensity and body composition measures in adults with overweight and obesity suffering from CNLBP. The included studies had a substantial risk of bias due to their observational and cross-sectional study designs, which prevents recommendations for clinical practice. Randomized controlled trials are needed to investigate the causal effect of interventions on body composition measures and pain intensity.

Mobility disability is a common condition affecting older adults, making walking and the performance of activities of daily living difficult. Frailty, cachexia and sarcopenia are related conditions that occur with advancing age and are characterized by a decline in muscle mass, strength, and functionality that negatively impacts health. Chronic low-grade inflammation is a significant factor in the onset and progression of these conditions. The toll-like receptors (TLRs) and the NLRP3 inflammasome are the pathways of signaling that regulate inflammation. These pathways can potentially be targeted therapeutically for frailty, cachexia and sarcopenia as research has shown that dysregulation of the TLR/NLRP3 inflammasome signaling pathways is linked to these conditions. Activation of TLRs with pathogen-associated molecular patterns (PAMPs or DAMPs) results in chronic inflammation and tissue damage by releasing pro-inflammatory cytokines. Additionally, NLRP3 inflammasome activation enhances the inflammatory response by promoting the production and release of interleukins (ILs), thus exacerbating the underlying inflammatory mechanisms. These pathways are activated in the advancement of disease in frail and sarcopenic individuals. Targeting these pathways may offer therapeutic options to reduce frailty, improve musculoskeletal resilience and prevent or reverse cachexia-associated muscle wasting. Modulating TLR/NLRP3 inflammasome pathways may also hold promise in slowing down the progression of sarcopenia, preserving muscle mass and enhancing overall functional ability in elderly people. The aim of this review is to investigate the signaling pathways of the TLR/NLRP3 inflammasome as a main target in frailty, cachexia and sarcopenia.

Pneumococcal infections pose a significant health problem in individuals with comorbid conditions such as Type 2 diabetes mellitus. Although pneumococcal vaccines are recommended in individuals with type 2 diabetes, there is a lack of data on the immunogenicity of pneumococcal vaccines in the type 2 diabetes population. This pilot study was therefore developed to determine if the humoral immune response to the 10-valent pneumococcal conjugate vaccine (PCV10) in those with and without type 2 diabetes is comparable.

A total of 40 (24 with type 2 diabetes and 16 without type 2 diabetes) adults were immunized with PCV10. WHO reference ELISA and multiplexed opsonophagocytic killing assay (MOPA) were used to measure the concentration and functionality of serotype-specific IgG at baseline and 14 days, 1 month, and 8 months post-vaccination.

The geometric mean IgG concentrations and opsonic titers increased significantly in post-immunization (T1-14 days, T2-1 month, and T3-8 month) serum samples compared to baseline (T0) in individuals with and without type 2 diabetes. In both groups, the highest post-immunization IgG concentrations were measured for serotype 19F at T2. Individuals with type 2 diabetes showed significantly lower IgG concentrations and opsonic titers for serotype 19F and 9V post-immunization compared to age and sex-matched non-diabetes individuals. Serotype-specific IgG concentrations declined rapidly in those with type 2 diabetes at 8 months post-immunization. Obese diabetes individuals had lower IgG concentrations compared to non-Obese individuals with type 2 diabetes.

Individuals with type 2 diabetes demonstrated a significant protective humoral immune response to the 10-valent pneumococcal conjugate vaccine (PCV10); however, the response was comparatively less robust and declined faster in those with type 2 diabetes compared to age and sex-matched non-diabetes controls.

Despite persisting health disparities between Black and White individuals, racial differences in inflammation have yet to be comprehensively examined.

To determine if significant differences in circulating levels of inflammatory markers between Black and White populations exist.

Studies were identified through systematic searches of four electronic databases in January 2022. Additional studies were identified via reference lists and e-mail contact.

Eligible studies included full-text empirical articles that consisted of Black and White individuals and reported statistics for inflammatory markers for each racial group. Of the 1368 potentially eligible studies, 84 (6.6 %) representing more than one million participants met study selection criteria.

Risk of bias was assessed via meta regressions that considered relevant covariates. Data heterogeneity was tested using both the Cochrane Q-statistic and the standard I2 index. Random effects models were used to calculate estimates of effect size from standardized mean differences.

Outcome measures included 12 inflammatory markers, including C-reactive protein (CRP), Fibrinogen, Interleukin-6 (IL-6), Tumor necrosis factor-alpha (TNF-α), and soluble intercellular adhesion molecule 1 (sICAM-1).

Several markers had robust sample sizes for analysis, including CRP (White N = 934,594; Black N = 55,234), Fibrinogen (White N = 80,880; Black N = 18,001), and IL-6 (White N = 20,269; Black N = 14,675). Initial results indicated significant effects on CRP (k = 56, pooled Hedges' g = 0.24), IL-6 (k = 33, g = 0.15), and Fibrinogen (k = 19, g = 0.49), with Black individuals showing higher levels. Results also indicated significant effects on sICAM-1 (k = 6, g = -0.46), and Interleukin-10 (k = 4, g = -0.18), with White individuals showing higher levels. Sensitivity analyses confirmed robust effects for CRP, IL-6, Fibrinogen, and sICAM-1 while also revealing significant effects on TNF-α (k = 18, g = -0.17) and Interleukin-8 (k = 5, g = -0.19), with White individuals showing higher levels of both.

Current meta-analytic results provide evidence for marked racial differences in common circulating inflammatory markers and illustrate the complexity of the inflammatory profile differences between Black and White individuals. Review Pre-Registration: PROSPERO Identifier - CRD42022312352.

This study aimed to investigate the effects of a 12-week high-intensity interval training on inflammatory cytokines, adipokines, and markers of bone turnover and examine whether high-intensity interval training-induced changes in inflammatory cytokines and adipokines were associated with changes in markers of bone turnover. Twenty-four women with obesity (mean [standard deviation]: age: 36.1 [3.38] years, height: 158.9 [11.9] cm, and body mass index: 31.9 [1.5] kg/m2) were randomly assigned to either control (n=10) or high-intensity interval training (n=14) groups. Body mass (- 2.7%), fat mass (- 15%), and percent body fat (- 6.2%) significantly decreased (p<0.05), while the predicted V̇O2max increased (29.6%; p<0.001) following the high-intensity interval training program. The training program resulted in increased adiponectin (7.6%) and osteocalcin (11.3%; p<0.05) and reduced tumor necrosis factor alpha (66.1%), interleukin-1α (18.6%), C-reactive protein (24.0%), leptin (21.5%), and carboxy-terminal telopeptide cross-linking type one collagen (14%; p<0.05). When high-intensity interval training and control groups were analyzed separately, training-induced changes in inflammatory cytokines and adipokines were not associated with changes in bone turnover markers (p>0.05), whereas significant associations were found when the data of the groups were analyzed together (p<0.05). In conclusion, a 12-week high-intensity interval exercise program improves the inflammatory state, adipokines, markers of bone turnover, cardiorespiratory fitness, and body composition in women with obesity.

The association of novel anthropometrics and novel atherogenicity indices with mortality remains uncertain.

To compare the association of novel anthropometrics and atherogenicity indices with all-cause, cardiovascular (CVD), and non-CVD mortality in Iranian adults.

Utilizing data from Isfahan Cohort Study, 5432 participants aged older than 35 years were enrolled. Three anthropometrics indices including a body shape index (ABSI), body roundness index (BRI) and abdominal volume index (AVI), and three atherogenicity indices including atherogenic index of plasma (AIP), Castelli risk index (CRI) and the cholesterol index (CI) were calculated. Cox proportional hazards regression models were used to explore the association between indices and mortality.

After a median follow-up of 11.25 years, the ABSI was independently associated with increased risk of all-cause mortality (HRQ4 vs. Q1 = 1.43, 95 % CI: 1.07, 1.92; P trend = 0.02). A positive, independent association was also observed between CRI-II (HRQ4 vs. Q1 = 1.49, 95 % CI: 0.99, 2.25; P trend = 0.04) and AIP (HRQ4 vs. Q1 = 1.81, 95 % CI: 1.92, 2.27; P trend = 0.01) and CVD mortality. For non-CVD mortality, despite a direct link for ABSI (HRQ4 vs. Q1 = 1.92, 95 % CI: 1.32, 2.80; P trend = 0.001), an inverse association was found for CI (HRQ4 vs. Q1 = 0.68, 95 % CI: 0.49, 0.95; P trend = 0.007).

Amongst various investigated anthropometric indices, ABSI was directly related to all-cause and non-CVD mortality. However, atherogenicity indices including CRI-II and AIP could predict the incidence risk of CVD mortality among Iranians. Further studies are warranted to confirm these findings.

Chronic diarrhea and constipation are known to be associated with obesity. Body roundness index (BRI), as a novel physical dimension assessment indicator, provides a more comprehensive evaluation of body and visceral fat than traditional methods. However, the relationship between BRI, chronic diarrhea, and constipation remains unclear. We aimed to investigate the relationship between BRI, chronic diarrhea, and constipation.

A cross-sectional study based on the National Health and Nutrition Examination Survey 2005-2010 was conducted. Weighted multivariable logistic regression was used to analyze the association between BRI, chronic diarrhea, and constipation. Restricted cubic spline curves were plotted to verify the linear associations.

7182 participants were included in this study, among whom 491 had chronic diarrhea and 441 had constipation. Significant positive correlations were discovered between BRI and chronic diarrhea, while no correlation was detected with constipation in the fully adjusted multivariable logistic regression analysis. Restricted cubic spline curves confirmed the linear relationship described above. Further treating BRI as categorical variables, compared with the lowest tertile, the highest BRI tertile showed a 79% increase in chronic diarrhea incidence and a 35% decrease in chronic constipation incidence. Consistent findings were observed across different subgroups, and sensitivity analyses generally confirmed the robustness of our results.

BRI is significantly and linearly associated with chronic diarrhea. Higher body and visceral fat increase the risk of chronic diarrhea while reducing the risk of chronic constipation.

Chronic metabolic inflammation is a common mechanism linked to the development of metabolic disorders such as obesity, diabetes, and cardiovascular disease (CVD). Chronic metabolic inflammation often related to alterations in gut homeostasis, and pathological processes involve the activation of endotoxin receptors, metabolic reprogramming, mitochondrial dysfunction, and disruption of intestinal nuclear receptor activity. Recent investigations into homeostasis and chronic metabolic inflammation have revealed a novel mechanism which is characterized by a timing interaction involving multiple components and targets. This article explores the positive impact of tea consumption on metabolic health of populations, with a special focus on the improvement of inflammatory indicators and the regulation of gut microbiota. Studies showed that tea consumption is related to the enrichment of gut microbiota. The relative proportion of Firmicutes/Bacteroidetes (F/B) is altered, while the abundance of Lactobacillus, Bifidobacterium, and A. muciniphila increased significantly in most of the studies. Thus, tea consumption could provide potential protection from the development of chronic diseases by improving gut homeostasis and reducing chronic metabolic inflammation. The direct impact of tea on intestinal homeostasis primarily targets lipopolysaccharide (LPS)-related pathways. This includes reducing the synthesis of intestinal LPS, inhibiting LPS translocation, and preventing the binding of LPS to TLR4 receptors to block downstream inflammatory pathways. The TLR4/MyD88/NF-κB p65 pathway is crucial for anti-metaflammatory responses. The antioxidant properties of tea are linked to enhancing mitochondrial function and mitigating mitochondria-related inflammation by eliminating free radicals, inhibiting NLRP3 inflammasomes, and modulating Nrf2/ARE activity. Tea also contributes to safeguarding the intestinal barrier through various mechanisms, such as promoting the synthesis of short-chain fatty acids in the intestine, activating intestinal aryl hydrocarbon receptor (AhR) and farnesoid X receptor (FXR), and improving enteritis. Functional components that improve chronic metabolic inflammation include tea polyphenols, tea pigments, TPS, etc. Tea metabolites such as 4-Hydroxyphenylacetic acid and 3,4-Dihydroxyflavan derivatives, etc., also contribute to anti-chronic metabolic inflammation effects of tea consumption. The raw materials and processing technologies affect the functional component compositions of tea; therefore, consuming different types of tea may result in varying action characteristics and mechanisms. However, there is currently limited elaboration on this aspect. Future research should conduct in-depth studies on the mechanism of tea and its functional components in improving chronic metabolic inflammation. Researchers should pay attention to whether there are interactions between tea and other foods or drugs, explore safe and effective usage and dosage, and investigate whether there are individual differences in the tea-drinking population leading to different effects of tea intervention. Ultimately, the application of tea drinking could be a universal therapy for regulating intestinal homeostasis, anti-chronic metabolic inflammatory responses, and promoting metabolic health.

The use of drains in reduction mammoplasty is highly variable among plastic surgeons. However, there is limited evidence to guide surgeons on the optimal timing and conditions for using drains to reduce the risk of seroma formation. The objective of this study was to identify factors that predict the possibility of developing postoperative seroma formation.

Retrospective review of patients who underwent bilateral reduction mammoplasty without intraoperative drain placement at our institution between January 2016 and July 2021 was performed. Demographics, clinical characteristics, and the rate of seroma that required aspiration or drainage were recorded. Univariate time-to-event analyses using Cox regression were performed to identify the predictors of seroma.

A total of 234 patients (468 breasts) were included. The mean age, body mass index, and resection weight were 40.9±17.6 months; 30.7±5.5 kg/m2, and 717.2±388 g, respectively. The superomedial pedicle was used in 268 (57.3%) breast reductions while the inferior pedicle was used in 200 (42.7%) cases. Median follow-up time was 3.2 months (IQR: 2.8 months). Seromas occurred in 17 breasts (3.6%). Patients who were of World Health Organization Obesity Class I (hazards ratio, HR = 15.5, p = 0.01), Class II (HR = 13.9, p = 0.016), and Class III (HR = 27.4, p = 0.004) had increased risk for developing seroma when compared to non-obese patients.

The rate of seroma formation was 3.6% in this cohort. Obesity significantly increased the risk of postoperative seroma formation that required aspiration or surgical drainage; therefore, surgeons who aim to further reduce the risk of seroma should consider using drains for these patients.

Obesity is closely associated with lipid metabolism, and the accumulation of lipids leads to low-level inflammation in the body, which can trigger cardiovascular disease. This study aimed to explore the association between a novel marker of lipid accumulation, the abdominal volume index (AVI), inflammatory parameters, and mortality.

This study enrolled 2,109 older adult senior citizens (aged over 60 years) with hypertension from the National Health and Nutrition Examination Survey. The primary endpoints included all-cause mortality and cardiovascular mortality, which were assessed by linking the data to the National Death Index records. Cox regression model and subgroup analysis were constructed to investigate the associations between AVI and both all-cause and cardiovascular mortality. Restricted cubic splines were employed to further explore the relationships among AVI, inflammatory parameters, and mortality. By considering inflammatory factors as mediators, we investigate the mediating effects of AVI on mortality.

After a median follow-up of 69 months, there were 1,260 deaths, with 337 attributed to cardiovascular causes within the older adult population studied. In the multivariable-adjusted model, AVI was positively associated with both all-cause and cardiovascular mortality [Hazard Ratio (HR) = 1.09, 95% CI = 1.06-1.11 for all-cause mortality; HR = 1.07, 95% CI = 1.03-1.12 for cardiovascular mortality]. Kaplan-Meier survival plots indicated an overall median survival time of 144 months. Mediation analysis revealed that Systemic Inflammatory Response Index (SIRI), Monocyte-to-HDL ratio (MHR), and Neutrophil-to-Lymphocyte ratio (NLR) mediated 27.15%, 35.15%, and 16.55%, respectively, of the association between AVI and all-cause mortality.

AVI is positively associated with all-cause mortality in older adults with hypertension, and this association appears to be partially mediated by inflammatory parameters.

Visceral obesity (VATob) increases the risk for many diseases. Central obesity has been associated with an augmented prescription use; however, there is a paucity of research focused on VATob. Here, the aim was to evaluate the association between VATob and prescription use.

Data was collected from the NHANES dataset (2011-2018). Visceral adipose tissue was measured using dual x-ray absorptiometry, and VATob was defined as ≥100 cm2. Prescription use was collected from the RXQ_RX files and classified according to Vademecum. Association between VATob and prescription use was determined with logistic regression and reported as odds ratios (ORs) with 95% confidence intervals (95%CIs).

10,952 participants (weighted: 121,090,702) were included, in which 41.8% were VATob and 52.0% of them had ≥1 prescription. Overall, VATob demonstrated an augmented rate of prescription use when compared to non-VATob (52.0% versus 36.7%, p<0.001), specifically with metabolic (4.5-fold increase), cardiovascular (3.9-fold increase), gastrointestinal (2.5-fold increase), and hematopoietic agents (2.3-fold increase). This was associated with increased the risk for overall prescription use (ORoverall = 1.9, 95%CI: 1.7-2.1, p<0.001). Similar results were observed with metabolic and cardiovascular agents. However, when stratified by BMI, normal weight participants (ORmetabolic = 10.4; 95%CI: 6.5-16.6 & ORcardiovascular = 7.0; 95%CI: 4.4-11.1, p<0.001) had a greater risk than the overweight (ORmetabolic = 4.1; 95%CI: 3.0-5.6 & ORcardiovascular = 3.4; 95%CI: 2.5-4.7, p<0.001) or obese participants (ORmetabolic = 3.5; 95%CI: 2.3-5.3 & ORcardiovascular = 3.5; 95%CI: 2.5-4.9, p<0.001).

VATob is associated with augmented prescription use, particularly with cardiovascular and metabolic agents. This association was higher for normal weight participants.

Obesity and underweight pose significant threats to human health as non-communicable diseases. In addition, body shape (like obesity or emaciation) is an important investigative clue in forensic practice. Body mass index (BMI) is a common indicator to reflect body shape of an individual. However, there is a lack of rapid, simple, and effective methods for identifying different BMI individuals. This research aimed to delve into the correlations between salivary proteins and BMI. A total of 418 differential expression proteins (DEPs) were identified through four-dimensional data independent acquisition quantitative proteomics analysis. The Kyoto Encyclopedia of Genes and Genomes analysis revealed that DEPs were primarily involved in oxidative phosphorylation, protein processing in the endoplasmic reticulum, and cholesterol metabolism pathways. Finally, we identified 17 protein markers that were correlated with BMI. Two machine-learning models (random forest and support vector machine) were also built based on these 17 markers. Obtained results demonstrated the efficacy of these 17 protein markers in accurately distinguishing different BMI individuals. In conclusion, our study not only provides potential salivary protein markers for identifying obesity and underweight individuals, it could also present a novel method for inferring BMI of saliva-related samples in forensic case investigation.

There is conflicting evidence regarding whether excess adiposity without metabolic abnormalities reflects a truly benign phenotype. This study evaluated the independent and joint associations of the presence of excess adiposity and metabolic abnormalities on arterial stiffness.

Participants in UK Biobank with body mass index (BMI) and arterial stiffness index (ASI) recorded between 2006 and 2010, free from cardiovascular diseases and not underweight (BMI <18.5 kg/m2) were included. The primary outcome was severity of ASI analysed using multivariate-adjusted linear regression.

Of 162 590 participants, 42.5% were overweight and 24.4% were obese. Within the normal BMI strata, 50.7% had ≥1 metabolic abnormality. Compared to individuals with normal BMI and no metabolic abnormality (reference group), increased BMI or metabolic abnormalities were similarly associated with higher ASI: normal BMI with metabolic abnormalities (adjusted β-coefficient and 95% CI, 0.35; 0.30-0.40); overweight without metabolic abnormalities (0.32; 0.26-0.37). Individuals with obesity and no metabolic abnormality had higher ASI (0.65; 0.57-0.74) but was lower than individuals with overweight and metabolic abnormalities (0.80; 0.75-0.84). Individuals with obesity and metabolic abnormalities had the highest ASI (1.07; 1.02-1.12) among all six metabolic combinations, p < 0.001 for each versus reference group. Sensitivity analysis suggested higher ASI with increasing number of metabolic abnormalities within BMI categories and higher ASI in the presence of abdominal obesity within metabolic categories.

Excess adiposity and metabolic abnormalities are independently associated with increased arterial stiffness to a similar degree, suggesting that metabolically healthy individuals with overweight and obesity are not benign groups. This reinforces the need to prevent excess adiposity and consider primary prevention strategies even before metabolic abnormalities emerge.

Cardiometabolic index (CMI), visceral adiposity index (VAI), and lipid accumulation product (LAP) are lipid-related parameters that reflect central obesity, which is closely associated with the development of non-alcoholic fatty liver disease (NAFLD). The aim of this study is to investigate the effectiveness of these lipid-related parameters in diagnosing NAFLD and to compare their predictive abilities.

This population-based study extracted datasets from the National Health and Nutrition Examination Survey (NHANES) 2017-2020. CMI, VAI, and LAP were included in the multivariate logistic model as both continuous and categorical variables to assess the relationship between different lipid-related parameters and NAFLD. To further elucidate this connection, we utilized restricted cubic splines and conducted subgroup analysis. Additionally, the receiver operating characteristics (ROC) curve was employed to evaluate the predictive effectiveness of CMI, VAI, and LAP for NAFLD.

The study included 2,878 adults as the study population, of whom 1,263 participants were diagnosed with NAFLD. When lipid-related parameters were analyzed as continuous variables, they showed a positive correlation with NAFLD. The OR(95%CI) were 2.29(1.81,2.89) for CMI (per 1-unit), 1.40(1.28,1.52) for VAI (per 1-unit) and 1.15(1.11,1.20) for LAP (per 10-units). This correlation remains statistically significant when the lipid-related parameters are analyzed as categorical variables. In descending order of diagnostic capability for NAFLD, the AUC values are as follows: LAP (0.794), CMI (0.752), and VAI (0.719).

CMI, VAI, and LAP may be important clinical indicators for identifying NAFLD, with LAP demonstrating the best predictive ability among them.

Probiotics play an important role in the control and treatment of non-alcoholic fatty liver disease (NAFLD). Kefir drink is a fermented beverage and has indicated some beneficial health effects. The aim of this study was to evaluate the effects of kefir drink on liver aminotransferases, anthropometric indices, glycemic index, lipid profile, blood pressure (BP), high sensitivity C-reactive protein, and malondialdehyde in patients with NAFLD.

In an 8-week randomized clinical trial, 80 patients with NAFLD were randomized into two groups of 40. After a 2-week run-in period, the groups received a dietary plan and dietary plan plus a cup of kefir drink twice a day (500 cc/d), respectively. Also, demographic, anthropometric, laboratory, BP, dietary intake, and physical activity assessments were analyzed before and after the intervention.

At last, seventy-two participants completed the study. No significant difference in changes in BP, anthropometric indices, and laboratory data (P > 0.05) except HDL-C (P = 0.02) and fat-free mass (P < 0.001) was observed between the two study groups.

Based on the results, Drinking 500 cc/d kefir beverage had no significant effect on liver aminotransferases and metabolic indicators, except for HDL-C and fat-free mass in patients with NAFLD.

IRCT20170916036204N6 (2018/08/03).

There are limited population-based studies examining the correlation between body roundness index (BRI) and mortality in diabetes and prediabetes patients.

Our final analysis encompassed 15,848 patients with diabetes and prediabetes sourced from the National Health and Nutrition Examination Survey(NHANES) spanning from 2003 to 2018. Cox proportional hazards model and restricted cubic splines (RCS) were utilized to assess the correlation between BRI and both all-cause mortality and cardiovascular mortality.

During an average follow-up period of 92.9 months, 2655 participants (12.73 %) died, including 730 (3.44 %) from cardiovascular diseases. RCS demonstrated a U-shaped nonlinear association between BRI with all-cause mortality and cardiovascular mortality, with threshold values of 5.54 and 5.21, respectively. When BRI was below the threshold, a negative correlation was observed between BRI and all-cause mortality (HR 0.87, 95 % CI 0.81-0.93).The correlation with cardiovascular mortality is not significant. Conversely, when BRI was above the threshold, a positive correlation was observed between BRI with all-cause mortality (HR 1.10, 95 % CI 1.06-1.14) and cardiovascular mortality (HR 1.13, 95 % CI 1.07-1.20).

Our research indicates that among US adults with diabetes or prediabetes, BRI exhibits a U-shaped relationship with all-cause and cardiovascular mortality, with threshold values of 5.54 and 5.21, respectively.

Osteoarthritis (OA) is a progressive degenerative disease affected by many factors, and there is currently no effective treatment. In recent years, the latest progress in metabolomics in OA research has revealed several metabolic pathways and new specific metabolites involved in OA. Metabolites play significant roles in the identification and management of OA. This review looks back on the development history of metabolomics and the progress of this technology in OA as well as its potential clinical applications. It summarizes the applications of metabolites in the field of OA and future research directions. This understanding will advance the identification of metabolic treatment goals for OA.

The development of metabolomics offers possibilities for the treatment of OA. This article reviews the relationship between metabolites associated with chondrocytes and OA. Selectively altering these three metabolic pathways and their associated metabolites may hold great potential as new focal points for OA treatment.

In elderly women, hormonal changes lead to elevated body fat content, which results in elevated levels of vascular inflammatory factors, thereby increasing the risk of cardiovascular diseases (CVDs) associated with endothelial dysfunction. Regular physical exercises tend to keep these in check and are protective to the body. Aerobic exercise has been reported to improve CVD in obese elderly women; in this regard, aquatic exercises have been demonstrated to be more efficient in energy metabolism than land-based exercise. This study aimed to examine the effect of aquatic walking exercises on the levels of inflammatory factors, nitric oxide (NO), and brachial-ankle pulse wave velocity (baPWV) in obese elderly women. We measured these in 26 obese elderly women who were randomly assigned to control (n = 12) and aquatic walking exercise (n = 14) groups. After subjecting them to aquatic walking exercises thrice a week for 12 weeks, we specifically found a significant reduction in IL-6 levels and an increase in NO levels in these obese elderly women. This was paralleled with a reduction in the right baPWV (baPWV-R). Together, these results indicate that aquatic walking exercises can help improve vascular inflammatory factors, NO levels, and arterial stiffness.

Obesity is a global public health issue, with limited epidemiologic studies on the relationship and mechanisms between organophosphate flame retardants (OPFRs) and metabolic obesity phenotypes (MOPs). We aimed to explore the link between OPFRs metabolite (m-OPFRs) and MOPs using a combined epidemiologic and bioinformatic approach. We used cross-sectional survey data from the U.S. National Health and Nutrition Examination Survey (2011-2018) to analyze the relationship between m-OPFRs and metabolic health obesity (MHO), as well as metabolic unhealthy obesity (MUO). The dataset encompasses eligible adults to assess the impact of individual, mixed, and mediated effects on the outcome variables through multivariate logistic regression, Bayesian kernel machine regression (BKMR), and mediation analysis. Multiple logistic regression models, stratified by tertiles of exposure showed that bis(1,3-dichloro-2-propyl) phosphate (BDCIPP) levels in the body significantly increased the risk of MHO, with OR and 95%CI of 1.454 (1.082, 1.953) for the second tertile (T2) and 1.598 (1.126, 2.268) for the third tertile (T3), compared to the first tertile (T1). Increased levels of BDCIPP in T3 (1.452(1.013, 2.081)) are associated with MUO, compared to T1. Mixed m-OPFRs and MHO risk in BMKR were positively correlated, with BDCIPP being the primary contributor. We found that the serum uric acid (SUA) and white blood cell count (WBC) indicators significantly mediated the association between BDCIPP and MHO (P < 0.05). Our study suggests that OPFRs, either individual or mixed, are associated with two distinct MOPs, with oxidative stress playing an important role. In addition, in silico analysis was used to screen for shared genes, and eight shared genes and eleven biological pathways identified during the screening process were used to construct the adverse outcome pathway, which suggests that exposure to OPFRs may activate the peroxisome proliferator-activated receptor (PPAR) pathway, thereby increasing the risk of obesity. Further studies are needed to validate our findings.

Individuals with metabolic syndrome have a high risk of developing cardiovascular disorders that is closely tied to visceral adipose tissue dysfunction, as well as an altered interaction between adipose tissue and the cardiovascular system. In metabolic syndrome, adipose tissue dysfunction is associated with increased hypertrophy, reduced vascularization, and hypoxia of adipocytes, leading to a pro-oxidative and pro-inflammatory environment. Among the pathways regulating adipose tissue homeostasis is the wingless-type mammary tumor virus integration site family (Wnt) signaling pathway, with both its canonical and non-canonical arms. Various modulators of the Wnt signaling have been identified to contribute to the development of metabolic diseases and their cardiovascular complications, with a particularly significant role played by Glycogen Synthase Kinase-3β (GSK-3β). GSK-3β levels and activities have various and often contrasting roles in obesity and related metabolic disorders, as well as their cardiovascular sequelae. Here, we explore the possibility that altered Wnt signaling and GSK-3β activities could serve as a connection between adipose tissue dysfunction and the development of cardiovascular disease in individuals with metabolic syndrome. We attempt to define a context-specific approach for intervention, which could possibly serve as a novel disease modifying therapy for the mitigation of such complications.

Data on the C-reactive protein (CRP) flare response in patients with metastatic and unresectable urothelial carcinoma (mUC) are limited. The present study aimed to clarify the clinical significance of the CRP flare response in patients with mUC who received pembrolizumab. Between March 2018 and December 2022, patients with mUC who received pembrolizumab following chemotherapy were retrospectively reviewed. Patients were categorized into three groups based on the early kinetics of CRP: i) Flare-responders, in which CRP levels increased >2-fold from baseline (BL) within 1 month after pembrolizumab administration (CRP flare) and decreased to below-BL levels within 3 months; ii) responders, in which CRP levels decreased ≥30% from baseline within 3 months without CRP flare; and iii) non-responders, which included the remaining patients. Tumor response, survival and incidence of immune-related adverse events (AEs) were compared between the groups. Of the 108 eligible patients, 17 (16%), 27 (25%) and 64 (59%) were classified as CRP flare-responders, CRP responders and CRP non-responders, respectively. Objective response rate was higher in CRP flare-responders and CRP responders than in CRP non-responders. Progression-free survival and overall survival were longer in CRP flare-responders and CRP responders than in CRP non-responders. Among CRP flare-responders, patients with low BL CRP levels had a better tumor response and survival than patients with high BL CRP levels. Notably, there was no difference in the incidence of immune-related AEs. In patients with mUC who received pembrolizumab, CRP flare-responders showed favorable oncological outcomes; therefore, BL CRP levels could predict oncological outcomes in CRP flare-responders.

Necrotizing fasciitis is a rare but severe soft tissue infection, and its diagnosis is difficult and often delayed. Immediate treatment comprising extensive debridement, highly dosed broad-spectrum antibiotic therapy and intensive care is necessary to prevent fatal outcomes. Considering the global rise in overweight patients and the known negative effects of obesity on the immune system, the aim of this study was to analyze whether overweight results in a more severe course of necrotizing fasciitis, worse outcomes and an increased mortality rate among overweight patients compared than in normal weight patients.

The present study involved a retrospective analysis of 29 patients who were treated for necrotizing fasciitis in our level one trauma center during the eight-year period between 2013 and 2020. Based on their BMIs, the patients were assigned to either the overweight group (BMI > 25) or the normal weight group.

In the study population, being overweight appeared to be a predictor for a more severe course of necrotizing fasciitis. Overweight patients suffered from sepsis significantly more often than normal weight patients (13 vs. 5; p = 0.027). Furthermore, they were dependent on invasive ventilation (26.6 ± 33.8 vs. 5.9 ± 11.9 days; p = 0.046) as well as catecholamine support (18.4 ± 23.7 vs. 3.6 ± 5.7 days; p = 0.039) for significantly longer.

Necrotizing fasciitis remains a challenging and potentially fatal disease. Within the patient collective, the severity of the disease and treatment effort were increased among overweight patients.

Exposure to artificial light during the night is known to promote disruption to the biological clock, which can lead to impaired mood and metabolism. Metabolic hormone secretion is modulated by the circadian pacemaker and recent research has shown that hormones such as insulin and leptin can also directly affect behavioral outcomes and the circadian clock. In turn, obesity itself is known to modulate the circadian rhythm and alter emotionality. This study investigated the behavioral and metabolic effects of constant light exposure in two models of obesity - a leptin null mutant (OB) and diet-induced obesity via high-fat diet. For both experiments, mice were placed into either a standard Light:Dark cycle (LD) or constant light (LL) and their circadian locomotor rhythms were continuously monitored. After 10 weeks of exposure to their respective lighting conditions, all mice were subjected to an open field assay to assess their explorative behaviors. Their metabolic hormone levels and inflammation levels were also measured. Behaviorally, exposure to constant light led to increased period lengthening and open field activity in the lean mice compared to both obesity models. Metabolically, LL led to increased cytokine levels and poorer metabolic outcomes in both lean and obese mice, sometimes exacerbating the metabolic issues in the obese mice, independent of weight gain. This study illustrates that LL can produce altered behavioral and physiological outcomes, even in lean mice. These results also indicate that obesity induced by different reasons can lead to shortened circadian rhythmicity and exploratory activity when exposed to chronic light.

Metabolic alterations, a hallmark of cancer, enable tumor cells to adapt to their environment by modulating glucose, lipid, and amino acid metabolism, which fuels rapid growth and contributes to treatment resistance. In primary breast cancer, metabolic shifts such as the Warburg effect and enhanced lipid synthesis are closely linked to chemotherapy failure. Similarly, metastatic lesions often display distinct metabolic profiles that not only sustain tumor growth but also confer resistance to targeted therapies and immunotherapies. The review emphasizes two major aspects: the mechanisms driving metabolic resistance in both primary and metastatic breast cancer, and how the unique metabolic environments in metastatic sites further complicate treatment. By targeting distinct metabolic vulnerabilities at both the primary and metastatic stages, new strategies could improve the efficacy of existing therapies and provide better outcomes for breast cancer patients.

Irritable bowel syndrome (IBS) is a common yet debilitating disorder of gut-brain interaction, characterized by gut-brain axis dysregulation, visceral hypersensitivity, and other comorbidities. Obesity has been hypothesized to be a risk factor linked to IBS, albeit evidence remains conflicting. Given the growing global prevalence of obesity and IBS, we performed a meta-analysis examining their purported association.

Embase, MEDLINE, and the Cochrane Library were searched to identify studies reporting the prevalence and odds ratios (ORs) of IBS according to BMI categories. Random effects meta-analyses were used for the primary analysis.

From 1713 articles, 27 studies were included. Our findings showed that using study-defined categories for overweight, obese, and normal BMI, the odds of the diagnosis of IBS were not associated with overweight (OR 1.02; 95% CI 0.89 to 1.17; p = 0.772) or obese BMI (OR 1.11; 95% CI 0.91 to 1.37; p = 0.309). The meta-analysis of study-reported adjusted odds ratios of IBS among individuals living with overweight or obesity also did not yield significant results. Further sensitivity analysis by the Rome criteria demonstrated a statistically significant association between obese BMI and IBS in studies using the Rome IV criteria (OR 1.59; 95% CI 1.13 to 2.23; p < 0.01), with significant subgroup difference between studies using the Rome II, Rome III, and Rome IV criteria. Further sensitivity analysis using the different cut-off values and subgroup analysis by geographical territory did not yield significant associations.

In summary, excess body weight may not be a primary driver of IBS risk. Future research should focus on longitudinal studies that account for changes in weight and other lifestyle factors, as well as detailed mechanistic investigations.

Obesity is a significant risk factor for obstructive sleep apnea (OSA). The weight-adjusted-waist index (WWI) reflects weight-independent centripetal obesity. Our study aims to evaluate the relationship between WWI and OSA.

The data used in the current cross-sectional investigation are from the National Health and Nutrition Examination Survey (NHANES), which was carried out between 2017 and 2020. We utilized weighted multivariable-adjusted logistic regression to evaluate the relationship between WWI and the risk of OSA. In addition, we applied various analytical methods, including subgroup analysis, smoothing curve fitting, threshold effect analysis and the receiver operating characteristic (ROC) curve. To further explore the relationship, we conducted a MR study using genome-wide association study (GWAS) summary statistics. We performed the main inverse variance weighting (IVW) method along with other supplementary MR methods. In addition, a meta-analysis was conducted to provide an overall evaluation.

WWI was positively related to OSA with the full adjustment [odds ratio (OR)=1.14, 95% confidence interval (95% CI): 1.06-1.23, P<0.001]. After converting WWI to a categorical variable by quartiles (Q1-Q4), compared to Q1 the highest WWI quartile was linked to an obviously increased likelihood of OSA (OR=1.26, 95% CI: 1.06-1.50. P=0.01). Subgroup analysis revealed the stability of the independent positive relationship between WWI and OSA. Smoothing curve fitting identified a saturation effect of WWI and OSA, with an inflection point of 11.62. In addition, WWI had the strongest prediction for OSA (AUC=0.745). Sensitivity analysis was performed to verify the significantly positive connection between WWI and stricter OSA (OR=1.18, 95% CI: 1.05-1.32, P=0.005). MR meta-analysis further supported our results (OR=2.11, 95% CI: 1.94-2.30, P<0.001). Sensitivity analysis confirmed the robustness and reliability of these findings.

WWI was significantly associated with the risk of OSA, suggesting that WWI could potentially serve as a predictor for OSA.

There is limited research on the relationship between Life Essentials 8 (LE8) score and metabolic syndrome (MetS). Our aim is to examine the association between LE8 cardiovascular health metrics and risk of MetS in a nationally representative sample.

We conducted a cross-sectional study using data from 23,253 adults aged ≥20 years from the National Health and Nutrition Examination Survey (2005-2018). LE8 score (range 0-100) was calculated based on the American Heart Association's definitions of ideal cardiovascular health behaviors (physical activity, diet, smoking, and body mass index) and factors (total cholesterol, blood pressure, fasting plasma glucose, and fasting triglycerides). Metabolic syndrome comprises a cluster of metabolic disorders, including obesity, hypertension, hyperglycemia, and dyslipidemia. Multivariable logistic regression and restricted cubic spline models, mediation analysis, subgroup analysis and weighted quantile sum (WQS) regression were used to assess the relationship between LE8 score and MetS risk.

A total of 23,253 participants were included, of whom 7,932 had MetS and 15,321 did not. The average age of the participants was 50.7 years (standard deviation (SD) 12.3), with 49.24% being male. Participants with high LE8 category (80-100 points) had 98% lower odds of having MetS compared to those with low LE8 category (0-49 points) after adjusting for potential confounders (adjusted odds ratio [OR]: 0.02; 95% confidence interval [CI]: 0.02-0.03; P < 0.001). There was a monotonic decreasing dose-response relationship between LE8 score and predicted probability of MetS (P-overall <0.001; P-nonlinear <0.001). Several biomarkers including serum albumin, uric acid and neutrophil count emerged as potential mediators.

While our studies suggest a potential association between cardiovascular health factors and reduced MetS risk, the cross-sectional nature of our study limits causal inferences. The LE8 score could still serve as a useful screening tool to identify individuals at high risk for MetS, facilitating targeted prevention and treatment strategies.

Leucine-rich alpha-2 glycoprotein (LRG) is a useful serum biomarker for monitoring disease activity during remission in ulcerative colitis (UC). Because LRG levels differ among patients, it is necessary to assess them after profiling patients, especially in patients with refractory UC undergoing treatment with molecular-targeted drugs. This study aimed to analyze LRG levels that indicate mucosal healing according to clinical characteristics and molecular-targeted drugs.

Among 214 patients with UC treated with biologics or Janus kinase (JAK) inhibitors, this study evaluated 111 patients (174 measurements) who achieved mucosal healing based on colonoscopy performed within 2 months before and after LRG measurement and experienced no changes in disease status or treatment during the same period. We analyzed the relationship of LRG with clinical characteristics (including sex, age, body mass index, and disease type and duration) and molecular-targeted drugs.

Compared with men, women had significantly higher LRG levels (9.5 μg/mL vs. 11.3 μg/mL, p < 0.001). In addition, LRG levels were significantly higher in older patients (12.0 μg/mL vs. 9.8 μg/mL, p < 0.01). LRG levels were the highest in patients treated with vedolizumab and lower in patients treated with JAK inhibitors (vedolizumab: 12.7 μg/mL; tofacitinib: 8.9 μg/mL; upadacitinib: 8.5 μg/mL; and filgotinib: 9.1 μg/mL; p < 0.0001).

Among the patients who achieved mucosal healing, LRG levels were significantly higher in women and older patients. LRG levels differed according to the molecular-targeted drug used and were higher with vedolizumab and lower with JAK inhibitors.

Transcranial direct stimulation (tDCS) targeted to the dorsolateral prefrontal cortex (DLPFC) reduces food intake and hunger, but its effects on circulating factors are unclear. We assessed the effect of repeated administration of tDCS to the left DLPFC (L-DLPFC) on concentrations of pro/anti-inflammatory and appetitive hormone concentrations.

Twenty-nine healthy adults with obesity (12 M; 42±11 y; BMI=39±8 kg/m2) received 3 consecutive inpatient sessions of either anodal or sham tDCS targeted to the L-DLPFC during a period of ad libitum food intake. Fasting plasma concentrations of IL-6, orexin, cortisol, TNF-α, IL-1β, ghrelin, PYY, and GLP-1 were measured before the initial and after the final tDCS sessions.

IL-6 (β=-0.92 pg/ml p=0.03) decreased in the anodal group compared with sham, even after adjusting for kcal intake; there were no changes in other hormones. Mean kcal intake was associated with higher IL-1β and ghrelin concentrations after the ad libitum period (β=0.00018 pg/ml/kcal, p=0.03; β=0.00011 pg/ml/kcal, p=0.02; respectively), but not differ by intervention groups.

IL-6 concentrations were reduced following anodal tDCS to the L-DLPFC independent of ad libitum intake. IL-6 concentrations reflect the inflammatory state of adiposity and may affect eating behavior and weight gain. These findings provide evidence of therapeutic benefit of tDCS.

Immune stressors, such as lipopolysaccharides (LPS), profoundly affect microbiota balance, leading to gut dysbiosis. This imbalance disrupts the metabolic phenotype and structural integrity of the gut, increasing intestinal permeability. During puberty, a critical surge in estrogen levels is crucial for mammary gland development. However, inflammation originating from the gut in this period may interfere with this development, potentially heightening breast cancer risk later. The long-term effects of pubertal inflammation on mammary development and breast cancer risk are underexplored. Such episodes can dysregulate cytokine levels and microRNA expression, altering mammary cell gene expression, and predisposing them to tumorigenesis.

This study hypothesizes that prebiotics, specifically Lentinula edodes Cultured Extract (AHCC), can counteract LPS's adverse effects. Using BALB/c mice, an acute LPS dose was administered at puberty, and breast cancer predisposition was assessed at 13 weeks. Cytokine and tumor-related microRNA levels, tumor development, and cancer stem cells were explored through immunoassays and qRT-PCR.

Results show that LPS induces lasting effects on cytokine and microRNA expression in mammary glands and tumors. AHCC modulates cytokine expression, including IL-1β, IL-17A/F, and IL-23, and mitigates LPS-induced IL-6 in mammary glands. It also regulates microRNA expression linked to tumor progression and suppression, particularly counteracting the upregulation of oncogenic miR-21, miR-92, and miR-155. Although AHCC slightly alters some tumor-suppressive microRNAs, these changes are modest, highlighting a complex regulatory role that warrants further study.

These findings underscore the potential of dietary interventions like AHCC to mitigate pubertal LPS-induced inflammation on mammary gland development and tumor formation, suggesting a preventive strategy against breast cancer.

Precarious employment is a plausible stressor, which may adversely affect health. We investigated the association between multidimensional precarious employment and perceived and biological stress in the U.S.

We used data from waves 4 (2008-2009) and 5 (2016-2018) of the National Longitudinal Study of Adolescent to Adult Health. Eight indicators were mapped to five dimensions of precarious employment to create a continuous score (PES, range: 0-5): material rewards, working-time arrangements, stability, workers' rights, and interpersonal relationships. Perceived stress was constructed from the four-item Cohen's perceived stress score (PSS; range: 0-16; wave 4). We measured biological stress in waves 4 and 5 via C-reactive protein (CRP). Given variability in CRP collection between waves, we treated wave 4 and 5 as cross-sectional. We employed adjusted linear regression models to estimate whether the PES was associated with the PSS in wave 4 (n = 11,510) and CRP in waves 4 (n = 10,343) and 5 (n = 3452).

Individuals were aged 28 and 37 years on average in wave 4 and 5, respectively. Half were female and most identified as non-Hispanic (NH)-White (∼73 %), followed by NH-Black (∼14 %), Hispanic (∼9 %) and NH-other (∼4 %). Average PES was inversely related to education. The PSS averaged 8.1 (Interquartile Range [IQR] = 7.0,9.0). Average CRP was 4.4 mg/L (IQR = 0.8,5.0) in wave 4 and 3.6 mg/L (IQR = 0.8,4.2) in wave 5. The PES was associated with perceived stress (β=0.06; 95 % CI = 0.01,0.10) and CRP in wave 5 (β=0.34; 95 % CI = 0.07,0.62).

Given the deleterious effects of stress on health, policies to reduce precarious employment warrant consideration.

The role of P2X ionotropic receptors in the behavior of purinergic signaling on pathophysiological processes has been widely studied. In recent years, the important participation of P2X receptors in physiological and pathological processes, such as energy metabolism, characteristic inflammatory responses of the immune system, and nociceptive activity in response to pain stimuli, has been noted. Here, we explore the molecular characteristics of the P2X receptors and the use of the different agonist and antagonist agents recently described, focusing on their potential as new therapeutic targets in the treatment of diseases with emphasis on obesity, diabetes, and some of the complications derived from these pathologies.

Excess adiposity is associated with a higher risk of breast cancer metastasis and mortality. Evidence suggests that dietary vitamin D inhibits breast cancer metastasis. However, the mechanistic link between vitamin D's regulation of adipocyte metabolism and metastasis has not been previously investigated. Therefore, the purpose of these experiments was to examine the effect of the active form of vitamin D, 1α,25-dihydroxyvitamin D (1,25(OH)2D), on adipocyte release of bioactive compounds and whether the impact on adipocytes leads to inhibition of breast cancer cell migration, an important step of metastasis.

Differentiated 3T3-L1 adipocytes were treated with 1,25(OH)2D for two days, followed by either harvesting the adipocytes or collecting adipocyte-conditioned media without 1,25(OH)2D. A transwell migration assay was conducted with vehicle- or 1,25(OH)2D-conditioned media. In order to explore the mechanism underlying effects on breast cancer metastatic capability, the mRNA expression of leptin, adiponectin, insulin-like growth factor (IGF-1), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1) was measured in adipocytes following either vehicle or 1,25(OH)2D treatment.

Conditioned media from 1,25(OH)2D-treated adipocytes inhibited the migration of metastatic MDA-MB-231 breast cancer cells compared to conditioned media from vehicle-treated adipocytes. Treatment of adipocytes with 1,25(OH)2D decreased mRNA expression of leptin, adiponectin, IGF-1, IL-6, and MCP-1. Consistent with mRNA expression, concentrations of leptin, adiponectin, IGF-1, and IL-6 in adipocyte-conditioned media were decreased with 1,25(OH)2D treatment, although MCP-1 remained unchanged.

In summary, these results suggest that 1,25(OH)2D alters adipocyte secretions to prevent breast cancer metastasis.

Numerous reports indicate that both obesity and type 2 diabetes mellitus (T2DM) are factors associated with cognitive impairment (CI). The objective was to assess the relationship between abdominal obesity as measured by waist-to-hip ratio adjusted for body mass index (WHRadjBMI) and CI in middle-aged and elderly patients with T2DM.

A cross-sectional study was conducted, in which a total of 1154 patients with T2DM aged ≥ 40 years were included. WHRadjBMI was calculated based on anthropometric measurements and CI was assessed utilizing the Montreal Cognitive Assessment (MoCA). Participants were divided into CI group (n = 509) and normal cognition group (n = 645). Correlation analysis and binary logistic regression were used to explore the relationship between obesity-related indicators including WHRadjBMI, BMI as well as waist circumference (WC) and CI. Meanwhile, the predictive power of these indicators for CI was estimated by receiver operating characteristic (ROC) curves.

WHRadjBMI was positively correlated with MoCA scores, independent of sex. The Area Under the Curve (AUC) for WHRadjBMI, BMI and WC were 0.639, 0.521 and 0.533 respectively, and WHRadjBMI had the highest predictive power for CI. Whether or not covariates were adjusted, one-SD increase in WHRadjBMI was significantly related to an increased risk of CI with an adjusted OR of 1.451 (95% CI: 1.261-1.671). After multivariate adjustment, the risk of CI increased with rising WHRadjBMI quartiles (Q4 vs. Q1 OR: 2.980, 95%CI: 2.032-4.371, P for trend < 0.001).

Our study illustrated that higher WHRadjBMI is likely to be associated with an increased risk of CI among patients with T2DM. These findings support the detrimental effects of excess visceral fat accumulation on cognitive function in middle-aged and elderly T2DM patients.

The role of dietary fat quality in promotion of cardiovascular diseases is studies before. However, the results are inconsistent. Recently, cholesterol to saturated fatty acid index (CSI) is suggested as a novel indicator of the atherogenicity and thrombogenicity potential of a diet. However, due to limited number of studies, in the current cross-sectional study, we aimed to evaluate the role of CSI in metabolic and inflammatory response among obese individuals.

In the current cross-sectional study 488 obese individuals aged 18-50 years old were involved in volunteer based invitation from outpatient obesity clinics. Subjects underwent anthropometric assays including weight, height, waist circumference (WC) and body composition and their fasting blood sample were obtained for biochemical assessments including blood sugar, serum lipids, hs-CRP and IL-6 concentrations by commercial kits. Physical activity was also assessed by short form of international physical activity questionnaire (IPAQ).

According to our results, being at the top tetile of CSI was associated with higher anthropometric indices including weight, height, WC, FFM, and basal metabolic rate (BMR) compared with those at the lowest tertile (P < 0.05). Similarly, those at the highest category of CSI had significantly higher levels of serum glucose and hs-CRP both in crude and adjusted models in ANCOVA and in multinomial logistic regression models (P < 0.05).

In the current study, for the first time, we identified the possible triggering role of dietary cholesterol to saturated fat index in increasing serum glucose and hs-CRP levels. due to cross-sectional design of the current study, causal inference is impossible. Further studies will help for better scientific justification.

Sedentary behavior (SB) is an essential risk factor for obesity, cardiovascular disease, and type 2 diabetes. Though certain levels of physical activity (PA) may attenuate the detrimental effects of SB, the inflammatory and cardiometabolic responses involved are still not fully understood. The focus of this secondary outcome analysis was to describe how light-intensity PA snacks (LIPASs, alternate sitting and standing, walking or standing continuously) compared with uninterrupted prolonged sitting affect inflammatory and cardiometabolic risk markers. Seventeen young adults with overweight and obesity participated in this study (eight females, 23.4 ± 3.3 years, body mass index (BMI) 29.7 ± 3.8 kg/m2, glycated hemoglobin A1C (HbA1c) 5.4 ± 0.3%, body fat 31.8 ± 8.2%). Participants were randomly assigned to the following conditions which were tested during an 8 h simulated workday: uninterrupted prolonged sitting (SIT), alternate sitting and standing (SIT-STAND, 2.5 h total standing time), continuous standing (STAND), and continuous walking (1.6 km/h; WALK). Each condition also included a standardized non-relativized breakfast and lunch. Venous blood samples were obtained in a fasted state at baseline (T0), 1 h after lunch (T1) and 8 h after baseline (T2). Inflammatory and cardiometabolic risk markers included interleukin-6 (IL-6), c-reactive protein (CRP), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TGs), visceral fat area (VFA), triglyceride-glucose (TyG) index, two lipid ratio measures, TG/HDL-C and TC/HDL-C, albumin, amylase (pancreatic), total protein, uric acid, and urea. We found significant changes in a broad range of certain inflammatory and cardiometabolic risk markers during the intervention phase for IL-6 (p = 0.014), TG (p = 0.012), TC (p = 0.017), HDL-C (p = 0.020), LDL-C (p = 0.021), albumin (p = 0.003), total protein (p = 0.021), and uric acid (p = 0.040) in favor of light-intensity walking compared with uninterrupted prolonged sitting, alternate sitting and standing, and continuous standing. We found no significant changes in CRP (p = 0.529), creatinine (p = 0.199), TyG (p = 0.331), and the lipid ratios TG/HDL-C (p = 0.793) and TC/HDL-C (p = 0.221) in response to the PA snack. During a simulated 8 h work environment replacement and interruption of prolonged sitting with light-intensity walking, significant positive effects on certain inflammatory and cardiometabolic risk markers were found in young adults with overweight and obesity.

Aging is a prominent risk factor for numerous chronic diseases. Understanding the shared mechanisms of aging can aid in pinpointing therapeutic targets for age-related disorders. Chronic inflammation has emerged as a pivotal mediator of aging and a determinant in various age-related chronic conditions. Recent findings indicate that C-C motif chemokine ligand 2 and receptor 2 (CCL2-CCR2) signaling, an important physiological modulator in innate immune response and inflammatory defense, plays a crucial role in aging-related disorders and is increasingly recognized as a promising therapeutic target, highlighting its significance. This review summarizes recent advances in the investigation of CCL2-CCR2 signaling in cardiovascular and neural aging, as well as in various aging-related disorders. It also explores the underlying mechanisms and therapeutic potentials in these contexts. These insights aim to deepen our understanding of aging pathophysiology and the development of aging-related diseases.

Obesity is characterized by a chronic low-grade inflammatory condition. Two emerging inflammatory biomarkers, the systemic immune-inflammation index (SII) and the systemic inflammation response index (SIRI), have gained attention. However, the relationships between obesity and SII/SRI remain unclear.

In this study, we analyzed data from the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2018 among adults. SII-SIRI/SII/SIRI were categorized into three groups based on tertiles. The association between obesity and SII-SIRI/SII/SIRI was assessed by multivariable logistic regression models. Restricted cubic spline (RCS) plots were used to examine the nonlinear association between obesity and SII/SIRI. Finally, potential independent associations between obesity and SII/SIRI were further explored using subgroup analyses.

The study included 20,011 adults, of whom 7,890 (39.32%) were obesity. In model 1, participants in the high (Q3) level of SII-SIRI had a significantly association with obesity than those in the low (Q1) level group. The high level of SII and SIRI were positively associated with obesity as compared to low levels. Model 2 revealed a positive association between obesity and high levels of SII-SIRI/SII/SIRI. Model 3 demonstrated a similar trend. RCS curves revealed a nonlinear association linking obesity to SII/SIRI. Subgroup analysis showed an interaction between SII/SIRI and age.

Our research suggested that obesity was positively associated with SII-SIRI/SII/SIRI in U.S. adults. SII/SIRI may represent a cost-effective and direct approach to assessing obesity.