This study aimed to develop a nomogram model based on computed tomography (CT) assessed body composition parameters to predict recurrence-free survival (RFS) and stratify the risk of recurrence in advanced gastric cancer (GC) patients.

This retrospective study included 111 patients with locally advanced GC. Preoperative CT-assessed body composition and parenchymal fat parameters of all patients were collected. Univariate and multivariate Cox analyses were performed to determine independent predictors for RFS. A nomogram model was subsequently established on the basis of the independent risk factors. The performance of the nomogram was evaluated utilizing the concordance index (C-index), calibration curve, and receiver operating characteristic curve analysis.

The nomogram model integrating four independent predictors, including the skeletal muscle index, visceral adipose tissue radiation attenuation, the body of pancreatic density (PD), and PD (tail), was established for predicting RFS in advanced GCs and achieved a C-index of 0.743 (95% confidence interval: 0.678-0.808). The calibration curves showed good concordances. In addition, compared to the pathological tumor-node-metastasis classification, the nomogram model showed comparable performance for predicting 1-year RFS and better efficacy for predicting 3- and 5-year RFS. The Kaplan-Meier curves demonstrated the ability of the nomogram to stratify patients according to risk (p < 0.001).

The nomogram model exhibited favorable predictive performance and could stratify patients according to the risk of postoperative recurrence for advanced GCs, which might help enhance individualized surveillance in clinical practice.

The objective of this study is to quantify abdominal obesity markers from computed tomography (CT) scans at primary diagnosis and follow-up in a large endometrial cancer cohort, and to assess temporal change in obesity markers in relation to surgicopathological patient characteristics and outcome.

Total- (TAV), subcutaneous- (SAV), visceral (VAV) abdominal fat volumes, and visceral-to-total fat percentage (VAV%) were derived from CT scans acquired in an endometrial cancer patient cohort at primary diagnosis (nprimary=293). Temporal (delta, δ) changes in CT obesity markers from primary diagnosis to follow-up were assessed for all patients with a follow-up CT 13 (7, 19) [median (interquartile range)] months after diagnosis (nfollow-up=152/293 patients). The CT obesity markers were assessed in relation to clinicopathological features and progression-free survival (PFS) using Mann-Whitney U-test, and Cox hazard ratios (HRs), respectively.

At primary diagnosis, VAV% was the only marker significantly associated with high-risk histology (median of 33% for endometrioid endometrial carcinoma (EEC) grade 1-2, 36% for EEC grade 3 and 36% for non-endometrioid EC, p = 0.003), myometrial invasion (MI) (median of 34% for MI < 50% vs. 35% for MI ≥ 50%, p = 0.03) and lymphovascular space invasion (LVSI) (median of 34% for no LVSI vs. 36% for LVSI, p = 0.009). High VAV% (≥ 35%) also predicted poor PFS both in univariable analysis (HR = 1.8, p = 0.02), and when stratified for surgicopathological FIGO stage (HR = 3.1, p = 0.03). At follow-up, median TAV, VAV, SAV, and VAV% were significantly lower than at primary diagnosis (p < 0.001 for all). Furthermore, patients with progression had larger reductions in visceral fat compartments (δVAV=-24%, δVAV% =-3%), than patients with no progression (δVAV=-17%, δVAV%=-2%, p ≤ 0.006 for both).

Visceral abdominal obesity (high VAV%) is associated with high-risk histologic features, myometrial invasion, and poor prognosis. Furthermore, high visceral fat loss during/following therapy is associated with disease progression.

We assessed the associations of visceral adiposity indexes such as Chinese Visceral Adiposity Index (CVAI), Visceral Adiposity Index (VAI), Lipid Accumulation Product (LAP), waist circumference (WC), and waist-hip ratio (WHR) with overall and specific cancer incidence in a Chinese population.

332,297 individuals from the Taiwan MJ cohort (1996-2007) were included. We utilized multivariable Cox proportional hazards models to examine associations of baseline visceral adiposity indexes and cancer incidences. Sex-specific CVAI, VAI, and LAP were calculated, incorporating WC and triglycerides levels. CVAI and VAI also included body mass index and high-density lipoprotein, with CVAI further incorporating age.

Higher CVAI was consistently associated with higher overall cancer incidence, with HRs of 1.45 (95% CI: 1.2-1.76) and 2.03 (95% CI: 1.52-2.72) for males and females, respectively, comparing the fifth quintile to the first. The HRs for WC were 1.27 (95% CI: 1.08-1.49) and 1.19 (95% CI: 1.01-1.40) for males and females, WHR was significantly associated with cancer risk in males (HR:1.28; 95% CI: 1.13-1.45), and LAP was significantly associated with cancer risk in females (HR: 1.25; 95% CI: 1.04-1.5). VAI was not associated with overall cancer incidence.

CVAI is a superior clinical biomarker for predicting cancer incidence in the Chinese population compared to traditional visceral obesity indices.

To explore whether there is a relationship between perirenal fat area (PFA) and the pathological types of renal cell carcinoma (RCC).

Two hundred ninety-seven cases of RCC patients were included in our study, which is a retrospective analysis. Based on pathological type, we divided the 297 RCC patients into two groups: the clear cell renal cell carcinoma (ccRCC) group (236 cases) and the non-clear cell renal cell carcinoma (non-ccRCC) group (61 cases). Computed tomography (CT) images at the renal vein level were used to measure PFA. A multivariate logistic regression model was employed to examine the connection between various pathological types of RCC and PFA.

Significant differences were observed between ccRCC and non-ccRCC patients in PFA (P = 0.007), contralateral PFA (P = 0.011), weight (P = 0.002), BMI (P < 0.001), pathological stage 1 (P = 0.010), and pathological stage 2 (P = 0.002). To study the link between pathological subtypes and PFA, a multivariate logistic regression model was employed. Stratifying patients by tumor location in the kidney, the multivariate logistic regression analysis showed that when the tumor is located outside the polar lines of the kidney (OPLK), for every 1 cm2 increase in PFA, the probability of developing ccRCC increases by 5% [1.05 (1.01, 1.10) P = 0.0153]. Furthermore, after stratifying patients by tumor location and pathological stage, it was found that in T1 stage patients with tumors located OPLK, for every 1 cm2 increase in PFA, the probability of developing ccRCC increases by 6% [1.06 (1.01, 1.11) P = 0.0300].

When the tumor is located OPLK in T1 stage patients, PFA is positively correlated with ccRCC. Perirenal adipose tissue may be a risk factor for ccRCC.

Obesity is a risk factor for both Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). However, it is unclear whether obesity drives the malignant progression of BE. We aimed to assess whether obesity is associated with high-grade dysplasia (HGD) or cancer in patients with BE.

We searched MEDLINE and EMBASE from inception through April 2024 for studies reporting the effect of body mass index (BMI) on the progression of nondysplastic BE or low-grade dysplasia (LGD) to HGD or EAC. A 2-stage dose-response meta-analysis was performed to estimate the dose-response relationship between BMI with malignant progression. Study quality was appraised using a modified Newcastle-Ottawa scale.

Twenty studies reported data on 38,565 patients (74.4% male) in total, of whom 1684 patients were diagnosed with HGD/cancer. Nineteen studies were considered moderate to high quality. Eight cohort studies reported data on 6647 male patients with baseline nondysplastic BE/LGD, of whom 555 progressed to HGD/EAC (pooled annual rate of progression, 0.02%; 95% confidence interval [CI], 0.01%-0.03%), and 1992 female patients with baseline nondysplastic BE/LGD, with 110 progressors (pooled annual rate of progression, 0.01%; 95% CI, 0.01%-0.02%). There was no significant difference in pooled annual rate of progression between males and females (P = .15). Each 5-kg/m2 increase in BMI was associated with a 6% increase in the risk of malignant progression (adjusted odds ratio, 1.06; 95% CI, 1.02-1.10; P < .001; I2= 0%).

Our meta-analysis provides some evidence that obesity as measured by BMI is associated with malignant progression of BE with a dose-response relationship. This finding requires confirmation in future high-quality cohort studies. Future risk prediction models could incorporate measures of obesity to potentially improve risk stratification in patients with BE. PROSPERO, Number: CRD42017051046.

Breast cancer (BC) is the most common malignancy in women, yet the role of beverage consumption in BC risk remains unclear. Additionally, the contribution of anthropo-metabolic biomarkers as mediators is unknown, limiting the development of effective prevention strategies.

This study included 13,567 participants from the Guangzhou Biobank Cohort Study (GBCS), where beverage consumption was assessed at baseline using a food frequency questionnaire. BC cases were identified through cancer registry linkage over a mean follow-up of 14.8 years. Mendelian randomization (MR) analyses were performed to evaluate the causal effects of beverage consumption on BC risk, with a two-step MR approach used to estimate mediation effects.

During follow-up, 243 BC cases were identified. Weekly consumption of ≥ 1 portion of sugar sweetened beverages (SSB), versus < 1 portion, was significantly associated with a higher risk of BC (hazard ratio [HR] 1.58, 95% confidence interval [CI] 1.12-2.23). This association was partly mediated by body mass index (proportion mediated [PM] 4.2%, 95% CI 0.9-17.1%) and uric acid (PM 18.8%, 95% CI 1.5-77.5%). Weekly consumption of > 6 portions of dairy-based milk was associated with a non-significantly higher BC risk (HR 1.41, 95% CI 0.99-2.03), while 3-6 portions of soy milk were associated with a lower BC risk (HR 0.31, 95% CI 0.10-0.98). No significant associations were found for pure fruit juice, coffee, tea, or alcoholic drinks. MR analyses supported the detrimental effect of SSB on BC risk, with high-density lipoprotein cholesterol, polyunsaturated fatty acids to total fatty acids (TFAs) ratio, and omega-6 fatty acids to TFAs ratio mediating 2.44%, 2.73%, and 3.53% of the association, respectively.

This study suggested that SSB consumption was a risk factor for BC and identified key anthropo-metabolic biomarkers mediating this relationship. Reducing SSB consumption and addressing associated metabolic pathways may offer effective strategies for BC prevention.

The increasing prevalence of overweight and obesity not only in adults but also among children and adolescents has become one of the most alarming health problems worldwide. Metabolic disorders accompanying fat accumulation during pathological weight gain induce chronic low-grade inflammation, which, in a vicious cycle, increases the immune response through pro-inflammatory changes in the cytokine (adipokine) profile. Obesity decreases life expectancy, largely because obese individuals are at an increased risk of many medical complications, often referred to as metabolic syndrome, which refers to the co-occurrence of insulin resistance (IR), impaired glucose tolerance, type 2 diabetes (T2D), atherogenic dyslipidemia, hypertension, and premature ischemic heart disease. Metabotropic G protein-coupled receptors (GPCRs) constitute the most numerous and diverse group of cell surface transmembrane receptors in eukaryotes. Among the GPCRs, researchers are focusing on the connection of G protein-coupled receptor 120 (GPR120), also known as free fatty acid receptor 4 (FFAR4), with signaling pathways regulating the inflammatory response and insulin sensitivity. This review presents the current state of knowledge concerning the involvement of GPR120 in anti-inflammatory and metabolic signaling. Since both inflammation in adipose tissue and insulin resistance are key problems in obesity, there is a rationale for the development of novel, GPR120-based therapies for overweight and obese individuals. The main problems associated with introducing this type of treatment into clinical practice are also discussed.

This systematic review and meta-analysis assesses the association between metabolic syndrome and breast cancer (BC) outcomes in BC survivors.

Systematic searches were carried out in PubMed and Embase using variations of the search terms: breast neoplasms (population), metabolic syndrome (exposure), and survival (outcome). Metabolic syndrome was characterized according to the American Heart Association, which includes the presence of three out of five abnormal findings among the risk factors: high blood pressure, high triglycerides, low high-density lipoprotein, high fasting glucose, and central obesity. Data were obtained from observational studies and randomized controlled trials that utilized survival statistics and reported survival ratios to investigate how the presence of metabolic syndrome at the time of BC diagnosis is associated with BC outcomes. Study data were independently extracted by two authors, and effect sizes were pooled using random-effects models.

From the 1019 studies identified in the literature search, 17 were deemed eligible. These encompassed 42,135 BC survivors. The pooled estimates revealed that BC survivors who had metabolic syndrome at the time of their BC diagnosis experienced increased risk of recurrence (HR 1.69, 95% CI: 1.39-2.06), BC mortality (HR 1.83, 95% CI: 1.35-2.49), and shorter disease-free survival (HR 1.57, 95% CI: 1.36-1.81) compared to BC survivors without metabolic syndrome.

Among BC survivors, metabolic syndrome was associated with inferior BC outcomes. This necessitates the creation of clinical guidelines that include metabolic screening for BC survivors. Further research should identify effective interventions to reduce the prevalence of metabolic syndrome among BC survivors to improve metabolic health and BC outcomes.

Metabolic syndrome, a cluster of metabolic disorders comprising dyslipidemia, insulin resistance, elevated blood pressure, and abdominal obesity, is a silent epidemic that may lead to outcomes such as cardiovascular disease, diabetes, and cancer. Due to the increase in the prevalence of these pathologies, the search for better treatments and more efficient drugs is imperative. Species of Artemisia and Salvia genera are excellent examples of noteworthy sources of bioactive products with health applications, their therapeutic properties being well known both in popular medicine and in the scientific community. There are reports of plant extracts or compounds from species belonging to either of these genera, which were able to combat cancer, diabetes, and cardiovascular pathologies. For instance, dihydroartemisinin (analog of artemisin extracted from Artemisia annua L.) can reduce tumor markers p53 and Ki-67 expression levels, leading to a reduction in tumor proliferation. Salvia officinalis L. has antihyperglycemic and lipid profile-improving effects since it decreases total cholesterol, glycosylated hemoglobin, fasting glucose, low-density lipoprotein cholesterol, and triglyceride levels while increasing high-density lipoprotein cholesterol levels. Clinical trials using mixtures (dried powdered plants or extracts) of known medicinal plants are recurrent in published works, in contrast with the scarce clinical trial studies with isolated compounds. Salvia miltiorrhiza Bunge. was by far the most targeted plant in the clinical trials analyzed here. Regarding clinical trials concerning Artemisia, there are more studies aiming to see its effect on diabetes, but the studies about cancer are more advanced. This review aims to give a critical summary of the most interesting and promising results from clinical trials. The abundance of studies with limited statistically significant clinical evidence hinders progress in clinical therapy. This situation demands far greater rigor from the scientific community, researchers, regulatory agencies, editors, and reviewers in conducting and publishing clinical studies.

Body mass index (BMI) may misclassify obesity-related cancer (ORC) risk, as metabolic dysfunction can occur across BMI levels. We hypothesized that metabolic dysfunction at any BMI increases ORC risk compared with normal BMI without metabolic dysfunction. Postmenopausal women (n = 20,593) in the Women's Health Initiative with baseline metabolic dysfunction biomarkers [blood pressure, fasting triglycerides, high-density lipoprotein cholesterol, fasting glucose, homeostatic model assessment for insulin resistance (HOMA-IR), and high-sensitive C-reactive protein (hs-CRP)] were included. Metabolic phenotype (metabolically healthy normal weight, metabolically unhealthy normal weight, metabolically healthy overweight/obese, and metabolically unhealthy overweight/obese) was classified using four definitions of metabolic dysfunction: (i) Wildman criteria, (ii) National Cholesterol Education Program Adult Treatment Panel III, (iii) HOMA-IR, and (iv) hs-CRP. Multivariable Cox proportional hazards regression, with death as a competing risk, was used to assess the association between metabolic phenotype and ORC risk. After a median (IQR) follow-up duration of 21 (IQR, 15-22) years, 2,367 women developed an ORC. The risk of any ORC was elevated among metabolically unhealthy normal weight (HR = 1.12, 95% CI, 0.90-1.39), metabolically healthy overweight/obese (HR = 1.15, 95% CI, 1.00-1.32), and metabolically unhealthy overweight/obese (HR = 1.35, 95% CI, 1.18-1.54) individuals compared with metabolically healthy normal weight individuals using Wildman criteria. The results were similar using Adult Treatment Panel III criteria, hs-CRP alone, or HOMA-IR alone to define metabolic phenotype. Individuals with overweight or obesity with or without metabolic dysfunction were at higher risk of ORCs compared with metabolically healthy normal weight individuals. The magnitude of risk was greater among those with metabolic dysfunction, although the CIs of each category overlapped. Prevention Relevance: Recognizing metabolic dysfunction as a significant risk factor for ORCs underscores the importance of preventive measures targeting metabolic health improvement across all BMI categories.

Obesity, a global health concern, is associated with severe health issues like type 2 diabetes, heart disease, and respiratory complications. It also increases the risk of various cancers, including melanoma, endometrial, prostate, pancreatic, esophageal adenocarcinoma, colorectal carcinoma, renal adenocarcinoma, and pre-and post-menopausal breast cancer. Obesity-induced cellular changes, such as impaired CD8+ T cell function, dyslipidemia, hypercholesterolemia, insulin resistance, mild hyperglycemia, and fluctuating levels of leptin, resistin, adiponectin, and IL-6, contribute to cancer development by promoting inflammation and creating a tumor-promoting microenvironment rich in adipocytes. Adipocytes release leptin, a pro-inflammatory substance that stimulates cancer cell proliferation, inflammation, and invasion, altering the tumor cell metabolic pathway. Adiponectin, an insulin-sensitizing adipokine, is typically downregulated in obese individuals. It has antiproliferative, proapoptotic, and antiangiogenic properties, making it a potential cancer treatment. This narrative review offers a comprehensive examination of the molecular interconnections between obesity and cancer, drawing on an extensive, though non-systematic, survey of the recent literature. This approach allows us to integrate and synthesize findings from various studies, offering a cohesive perspective on emerging themes and potential therapeutic targets. The review explores the metabolic disturbances, cellular alterations, inflammatory responses, and shifts in the tumor microenvironment that contribute to the obesity-cancer link. Finally, it discusses potential therapeutic strategies aimed at disrupting these connections, offering valuable insights into future research directions and the development of targeted interventions.

The aim of our study is to explore the relationship between remnant cholesterol (RC) levels and visceral adipose tissue (VAT) in the US adult population. This cross-sectional study utilized data from 5301 participants aged 20 to 59 years gathered by the National Health and Nutrition Examination Survey (NHANES). RC was determined by deducting both high-density lipoprotein cholesterol (HDL-c) and low-density lipoprotein cholesterol (LDL-c) from total cholesterol (TC), and VAT was measured using dual-energy X-ray absorptiometry. Visceral obesity is defined as a VAT area ≥ 100 cm2. With increasing quartiles of RC levels, the prevalence of visceral obesity rises (16.51% vs. 36.11% vs. 55.66% vs. 74.48%, p<0.001). After adjusting for confounders, RC levels positively correlate with visceral obesity risk (OR=1.039, 95% CI 1.031-1.048, p<0.001). Additionally, individuals with low LDL-c/high RC and those with high LDL-c/low RC showed 2.908-fold (95% CI 1.995-4.241) and 1.310-fold (95% CI 1.022-1.680) higher risk of visceral obesity, respectively, compared to those with low LDL-c/low RC. Receiver Operating Characteristic (ROC) and Decision Curve Analysis (DCA) show RC's superior predictive ability over other lipid markers. Subgroup analysis showed that the relationship between RC and visceral obesity was more ronounced in those with cardiovascular disease. Smooth curve fitting indicated a nonlinear relationship between RC levels and VAT area. Our study highlights that elevated levels of RC are associated with adverse accumulation of VAT. However, the causal relationship between RC and visceral obesity requires additional investigation.

The incidence rate of pancreatic cancer, a fatal illness with a meager 5-year survival rate, has been on the rise in recent times. When individuals accumulate excessive amounts of adipose tissue, the adipose organ becomes dysfunctional due to alterations in the adipose tissue microenvironment associated with inflammation and metabolism. This phenomenon may potentially contribute to the aberrant accumulation of fat that initiates pancreatic carcinogenesis, thereby influencing the disease's progression, resistance to treatment, and metastasis. This review presents a summary of the impact of pancreatic steatosis, visceral fat, cancer-associated adipocytes and lipid diets on the advancement of pancreatic cancer, as well as the reciprocal effects of pancreatic cancer on adipose tissue. Understanding the molecular mechanisms underlying the relationship between dysfunctional adipose tissue and pancreatic cancer better may lead to the discovery of new therapeutic targets for the disease's prevention and individualized treatment. This is especially important given the rising global incidence of obesity, which will improve the pancreatic cancer treatment options that are currently insufficient.

Bevacizumab induces muscle atrophy by changing the gene expression level of muscle tissue. Quantitative computed tomography (QCT) enables precise measurement of various body compositions, including muscle area.

A total of 102 patients with metastatic colorectal cancer (mCRC) undergoing first-line chemotherapy based on bevacizumab were enrolled at thirst Affiliated Hospital of the University of Science and Technology of China. Their body compositions were measured respectively 1 month before and 1 month after the treatment.

Treatment-related decline in skeletal muscle index and visceral fat infiltration significantly affect patient prognosis.

A predictive model constructed by integrating changes in body composition with patient clinical characteristics effectively predicts the 9-month progression-free survival (PFS) of patients with mCRC.

Accurate preoperative risk assessment for major colorectal cancer (CRC) surgery remains challenging. Body composition (BC) and cardiopulmonary exercise testing (CPET) can be used to evaluate risk. The relationship between BC and CPET in patients undergoing curative CRC surgery is unclear.

Consecutive patients undergoing CPET prior to CRC surgery between 2010 and 2020 were identified between two different UK hospitals. Body composition phenotypes such as sarcopenia, myosteatosis, and visceral obesity were defined using widely accepted thresholds using preoperative single axial slice CT image at L3 vertebrae. Relationships between clinicopathological, BC, and CPET variables were investigated using linear regression analysis.

Two hundred eighteen patients with stage I-III CRC were included. The prevalence of sarcopenia, myosteatosis, and visceral obesity was 62%, 33%, and 64%, respectively. The median oxygen uptake at anaerobic threshold (VO2 at AT) was 12.2 mL/kg/min (IQR 10.6-14.2), and oxygen uptake at peak exercise (VO2 peak) was 18.8 mL/kg/min (IQR 15.4-23). On univariate linear regression analysis, male sex (P < 0.001) was positively associated with VO2 at AT. While ASA grade (P < 0.001) and BMI (P = 0.007) were negatively associated with VO2 at AT, on multivariate linear regression analysis, these variables remained significant (P < 0.05). On univariate linear regression analysis, male sex (P < 0.001) was positively associated with VO2 peak, whereas age (P < 0.001), ASA grade (P < 0.001), BMI (P = 0.003), sarcopenia (P = 0.015), and myosteatosis (P < 0.001) were negatively associated with VO2 peak. On multivariate linear regression analysis age (P < 0.001), ASA grade (P < 0.001), BMI (P < 0.001), and sarcopenia (P = 0.006) were independently and negatively associated with VO2 peak.

The novel finding that sarcopenia is independently associated with reduced VO2 peak performance in CPET supports the supposition that reduced muscle mass relates to poor physical function in CRC patients. Further work should be undertaken to assess whether sarcopenia diagnosed on CT can act as suitable surrogate for CPET to further enhance personalized risk stratification.

Severe burn injuries are defined by a prolonged hypermetabolic response characterized by increases in resting energy expenditure, systemic catabolism, and multi-organ dysfunction. The sustained elevation of catecholamines following a burn injury is thought to significantly contribute to this hypermetabolic response, leading to changes in adipose tissue such as increased lipolysis and the browning of subcutaneous white adipose tissue (WAT). Failure to mitigate these adverse changes within the adipose tissue has been shown to exacerbate the post-burn hypermetabolic response and lead to negative outcomes. Propranolol, a non-selective β-blocker, has been clinically administered to improve outcomes of pediatric and adult burn patients, but there is inadequate knowledge of its effects on the distinct adipose tissue depots. In this study, we investigated the adipose depot-specific alterations that occur in response to burn injury. Moreover, we explored the therapeutic effects of β-adrenoceptor blockade via the drug propranolol in attenuating these burn-induced pathophysiological changes within the different fat depots. Using a murine model of thermal injury, we show that burn injury induces endoplasmic reticulum (ER) stress in the epididymal (eWAT) but not in the inguinal (iWAT) WAT depot. Conversely, burn injury induces the activation of key lipolytic pathways in both eWAT and iWAT depots. Treatment of burn mice with propranolol effectively mitigated adverse burn-induced alterations in the adipose by alleviating ER stress in the eWAT and reducing lipolysis in both depots. Furthermore, propranolol treatment in post-burn mice attenuated UCP1-mediated subcutaneous WAT browning following injury. Overall, our findings suggest that propranolol serves as an effective therapeutic intervention to mitigate the adverse changes induced by burn injury, including ER stress, lipotoxicity, and WAT browning, in both adipose tissue depots. KEY MESSAGES: Burn injury adversely affects adipose tissue metabolism via distinct changes in both visceral and subcutaneous adipose depots. Propranolol, a non-selective β-adrenergic blocker, attenuates many of the adverse adipose tissue changes mediated by burn injury.

Body mass index (BMI) is an independent predictor of kidney disease progression in individuals with autosomal dominant polycystic kidney disease (ADPKD). Adipocytes do not simply act as a fat reservoir but are active endocrine organs. We hypothesized that greater visceral abdominal adiposity would associate with more rapid kidney growth in ADPKD and influence the efficacy of tolvaptan.

A retrospective cohort study.

1,053 patients enrolled in the TEMPO 3:4 tolvaptan trial with ADPKD and at high risk of rapid disease progression.

Estimates of visceral adiposity extracted from coronal plane magnetic resonance imaging (MRI) scans using deep learning.

Annual change in total kidney volume (TKV) and effect of tolvaptan on kidney growth.

Multinomial logistic regression and linear mixed models.

In fully adjusted models, the highest tertile of visceral adiposity was associated with greater odds of annual change in TKV of≥7% versus<5% (odds ratio [OR], 4.78 [95% CI, 3.03-7.47]). The association was stronger in women than men (interaction P<0.01). In linear mixed models with an outcome of percent change in TKV per year, tolvaptan efficacy (% change in TKV) was reduced with higher visceral adiposity (3-way interaction of treatment ∗ time ∗ visceral adiposity, P=0.002). Visceral adiposity significantly improved classification performance of predicting rapid annual percent change in TKV for individuals with a normal BMI (DeLong's test z score: -2.03; P=0.04). Greater visceral adiposity was not associated with estimated glomerular filtration rate (eGFR) slope in the overall cohort; however, visceral adiposity was associated with more rapid decline in eGFR slope (below the median) in women (fully adjusted OR, 1.06 [95% CI, 1.01-1.11] per 10 unit increase in visceral adiposity) but not men (OR, 0.98 [95% CI, 0.95-1.02]).

Retrospective; rapid progressors; computational demand of deep learning.

Visceral adiposity that can be quantified by MRI in the coronal plane using a deep learning segmentation model independently associates with more rapid kidney growth and improves classification of rapid progression in individuals with a normal BMI. Tolvaptan efficacy decreases with increasing visceral adiposity.

We analyzed images from a previous study with the drug tolvaptan conducted in patients with autosomal dominant polycystic kidney disease (ADPKD) to measure the amount of fat tissue surrounding the kidneys (visceral fat). We had previously shown body mass index can predict kidney growth in this population; now we determined whether visceral fat was an important factor associated with kidney growth. Using a machine learning tool to automate measurement of fat in images, we observed that visceral fat was independently associated with kidney growth, that it was a better predictor of faster kidney growth in lean patients than body mass index, and that having more visceral fat made treatment of ADPKD with tolvaptan less effective.

Beyond obesity, excess levels of visceral adipose tissue (VAT) significantly contribute to the risk of developing metabolic syndrome (MetS), although thresholds for increased risk vary based on population, regions of interest, and units of measure employed. We sought to determine whether a common threshold exists that is indicative of heightened MetS risk across all populations, accounting for sex, age, BMI, and race/ethnicity. A systematic literature review was conducted in September 2023, presenting threshold values for elevated MetS risk. Standardization equations harmonized the results from DXA, CT, and MRI systems to facilitate a comparison of threshold variations across studies. A total of 52 papers were identified. No single threshold could accurately indicate elevated risk for both males and females across varying BMI, race/ethnicity, and age groups. Thresholds fluctuated from 70 to 165.9 cm2, with reported values consistently lower in females. Generally, premenopausal females and younger adults manifested elevated risks at lower VAT compared to their older counterparts. Notably, Asian populations exhibited elevated risks at lower VAT areas (70-136 cm2) compared to Caucasian populations (85.6-165.9 cm2). All considered studies reported associations of VAT without accommodating covariates. No single VAT area threshold for elevated MetS risk was discernible post-harmonization by technology, units of measure, and region of interest. This review summarizes available evidence for MetS risk assessment in clinical practice. Further exploration of demographic-specific interactions between VAT area and other risk factors is imperative to comprehensively delineate overarching MetS risk.

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.

To investigate the association between visceral obesity and glycemic control in patients with type 2 diabetes mellitus.

A retrospective analysis involved 714 patients diagnosed with type 2 diabetes mellitus from the National Metabolic Management Center from November 2021 to February 2024. Medical data included sociodemographic data, lifestyle behaviors, and anthropometric and biochemical measurements. Multivariate logistic regression analysis was used to analyze their associations.

Among the patients, 251 (35.2%) achieved good glycemic control (HbA1c < 7.0%). On univariate analysis, higher diastolic blood pressure, longer duration of type 2 diabetes mellitus, tobacco smoking, alcohol drinking, insulin treatment, higher levels of fasting plasma glucose, homeostasis model assessment of insulin resistance, triglyceride, total cholesterol, and low-density lipoprotein cholesterol, visceral obesity (visceral fat area ≥ 100cm2) and diabetic peripheral neuropathy were all positively correlated with poor glycemic control; female, older age, higher levels of C peptide and serum uric acid were inversely associated with poor glycemic control (all P < 0.05). On multivariate logistic regression analysis, the results suggested that higher diastolic blood pressure [OR: 1.021, 95% CI (1.002, 1.040), P = 0.030], insulin treatment [currently used: OR = 2.156, 95% CI (1.249, 3.724), P = 0.006], higher level of fasting plasma glucose [OR: 1.819, 95% CI (1.598, 2.069), P < 0.001], and visceral obesity [OR: 1.876, 95% CI (1.158, 3.038), P = 0.011] were risk factors for poor glycemic control.

This study indicated that visceral obesity (visceral fat area ≥ 100cm2) is positively associated with poor glycemic control, and serves as an independent risk factor for poor glycemic control (HbA1c ≥ 7.0%) in patients with type 2 diabetes mellitus. Screening for visceral obesity should be emphasized, and targeted interventions should be taken to improve glycemic control in patients with type 2 diabetes mellitus.

Adipose tissue dysfunction, which is associated with an increased risk of colorectal cancer (CRC), is a significant factor in the pathophysiology of obesity. Obesity-related inflammation and extracellular matrix (ECM) remodeling promote colorectal cancer metastasis (CRCM) by shaping the tumor microenvironment (TME). When CRC occurs, the metabolic symbiosis of tumor cells recruits adjacent adipocytes into the TME to supply energy. Meanwhile, abundant immune cells, from adipose tissue and blood, are recruited into the TME, which is stimulated by pro-inflammatory factors and triggers a chronic local pro-inflammatory TME. Dysregulated ECM proteins and cell surface adhesion molecules enhance ECM remodeling and further increase contractibility between tumor and stromal cells, which promotes epithelial-mesenchymal transition (EMT). EMT increases tumor migration and invasion into surrounding tissues or vessels and accelerates CRCM. Colorectal symbiotic microbiota also plays an important role in the promotion of CRCM. In this review, we provide adipose tissue and its contributions to CRC, with a special emphasis on the role of adipocytes, macrophages, neutrophils, T cells, ECM, and symbiotic gut microbiota in the progression of CRC and their contributions to the CRC microenvironment. We highlight the interactions between adipocytes and tumor cells, and potential therapeutic approaches to target these interactions.

Accurate preoperative prediction of the pathological grade of clear cell renal cell carcinoma (ccRCC) is crucial for optimal treatment planning and patient outcomes. This study aims to develop and validate a deep-learning (DL) algorithm to automatically segment renal tumours, kidneys, and perirenal adipose tissue (PRAT) from computed tomography (CT) images and extract radiomics features to predict the pathological grade of ccRCC.

In this cross-ethnic retrospective study, a total of 614 patients were divided into a training set (383 patients from the local hospital), an internal validation set (88 patients from the local hospital), and an external validation set (143 patients from the public dataset). A two-dimensional TransUNet-based DL model combined with the train-while-annotation method was trained for automatic volumetric segmentation of renal tumours, kidneys, and visceral adipose tissue (VAT) on images from two groups of datasets. PRAT was extracted using a dilation algorithm by calculating voxels of VAT surrounding the kidneys. Radiomics features were subsequently extracted from three regions of interest of CT images, adopting multiple filtering strategies. The least absolute shrinkage and selection operator (LASSO) regression was used for feature selection, and the support vector machine (SVM) for developing the pathological grading model. Ensemble learning was used for imbalanced data classification. Performance evaluation included the Dice coefficient for segmentation and metrics such as accuracy and area under curve (AUC) for classification. The WHO/International Society of Urological Pathology (ISUP) grading models were finally interpreted and visualized using the SHapley Additive exPlanations (SHAP) method.

For automatic segmentation, the mean Dice coefficient achieved 0.836 for renal tumours and 0.967 for VAT on the internal validation dataset. For WHO/ISUP grading, a model built with features of PRAT achieved a moderate AUC of 0.711 (95% CI, 0.604-0.802) in the internal validation set, coupled with a sensitivity of 0.400 and a specificity of 0.781. While model built with combination features of the renal tumour, kidney, and PRAT showed an AUC of 0.814 (95% CI, 0.717-0.889) in the internal validation set, with a sensitivity of 0.800 and a specificity of 0.753, significantly higher than the model built with features solely from tumour lesion (0.760; 95% CI, 0.657-0.845), with a sensitivity of 0.533 and a specificity of 0.767.

Automated segmentation of kidneys and visceral adipose tissue (VAT) through TransUNet combined with a conventional image morphology processing algorithm offers a standardized approach to extract PRAT with high reproducibility. The radiomics features of PRAT and tumour lesions, along with machine learning, accurately predict the pathological grade of ccRCC and reveal the incremental significance of PRAT in this prediction.

Sarcopenic obesity (SO) in patients with gastrointestinal cancer is associated with a poor prognosis. We aimed to investigate the prognostic impact of SO in patients with gastrointestinal cancer, as well as the diagnostic cut-off value of SO in patients with gastrointestinal cancer among Chinese population.

We conducted a consecutive cohort study. Between January 2017 and January 2019, 289 patients diagnosed with gastrointestinal cancer were included in our study. Skeletal muscle area, total fat area, and subcutaneous fat area were measured by CT scan. All patients were followed up for 5 years. Receiver operating characteristic curves (ROC) were adopted to determine the cut-off values of visceral fat obesity for the prediction of sarcopenia. Based on the cut-off values, patients with sarcopenia combined with visceral fat obesity were divided into the SO group, and the others were divided into the non-sarcopenic obesity (NSO) group. Kaplan-Meier curves and univariate and multivariate Cox proportional hazard models were employed to explore the associations of body composition profiles with 5-year overall survival and disease-specific survival.

Obtained from Youden's Index for ROC for the prediction of 5-year survival, skeletal muscle mass index (SMI) ≤40.02 cm2/m2 with VFA ≥ 126.30 cm2 in men and SMI ≤32.05 cm2/m2 with VFA ≥72.42 cm2 in women indicate a risk of poor prognosis in patients diagnosed with gastrointestinal cancer. Patients with SO had poorer 5-year overall survival (OS) than patients with NSO (6.74% vs. 82.84%, p < 0.001), and poorer 5-year DFS (6.74% vs. 81.82%, p < 0.001). In multivariate analysis, we found that the long-term mortality risk was approximately 13-fold higher among patients in the SO group compared to those with no conditions.

Preoperative assessment of SO is useful not only for monitoring nutritional status but also for predicting 5-year OS in gastrointestinal cancer patients.

Neoadjuvant chemotherapy (NT) followed by radical surgery is the standard treatment for locally advanced gastric cancer (GC). The incidence of sarcopenia in upper gastrointestinal tract malignancies is very high, and it may be increased after NT. This study aimed to evaluate the impact of NT on body composition. A retrospective study of patients with locally advanced GC undergoing gastrectomy who had received NT in a tertiary hospital between 2012 and 2019 was conducted. CT measured the skeletal muscle index, total psoas area, and visceral and subcutaneous adipose tissue before and after NT. Of the 180 gastrectomies for GC, 61 patients received NT. During NT, changes in body composition were observed with a decrease in the skeletal muscle mass index (SMMI -2.5%; p < 0.001), and these changes were significantly greater in men (SMMI -10.55%). Before surgery, patients who received NT presented 15% more sarcopenia than those without NT (p = 0.048). In conclusion, patients with locally advanced gastric cancer who receive NT have significant changes in body composition during chemotherapy. These changes, which are at the expense of a loss of muscle mass, lead to an increased incidence of pre-surgical sarcopenia.

Nonalcoholic steatohepatitis (NASH) is a prevalent chronic liver condition. However, the potential therapeutic benefits and underlying mechanism of nicotinate-curcumin (NC) in the treatment of NASH remain uncertain.

A rat model of NASH induced by a high-fat and high-fructose diet was treated with nicotinate-curcumin (NC, 20, 40 mg·kg- 1), curcumin (Cur, 40 mg·kg- 1) and metformin (Met, 50 mg·kg- 1) for a duration of 4 weeks. The interaction between NASH, Cur and Aldo-Keto reductase family 1 member B10 (AKR1B10) was filter and analyzed using network pharmacology. The interaction of Cur, NC and AKR1B10 was analyzed using molecular docking techniques, and the binding energy of Cur and NC with AKR1B10 was compared. HepG2 cells were induced by Ox-LDL (25 µg·ml- 1, 24 h) in high glucose medium. NC (20µM, 40µM), Cur (40µM) Met (150µM) and epalrestat (Epa, 75µM) were administered individually. The activities of ALT, AST, ALP and the levels of LDL, HDL, TG, TC and FFA in serum were quantified using a chemiluminescence assay. Based on the changes in the above indicators, score according to NAS standards. The activities of Acetyl-CoA and Malonyl-CoA were measured using an ELISA assay. And the expression and cellular localization of AKR1B10 and Acetyl-CoA carboxylase (ACCα) in HepG2 cells were detected by Western blotting and immunofluorescence.

The results of the animal experiments demonstrated that NASH rat model induced by a high-fat and high-fructose diet exhibited pronounced dysfunction in liver function and lipid metabolism. Additionally, there was a significant increase in serum levels of FFA and TG, as well as elevated expression of AKR1B10 and ACCα, and heightened activity of Acetyl-CoA and Malonyl-CoA in liver tissue. The administration of NC showed to enhance liver function in rats with NASH, leading to reductions in ALT, AST and ALP levels, and decrease in blood lipid and significant inhibition of FFA and TG synthesis in the liver. Network pharmacological analysis identified AKR1B10 and ACCα as potential targets for NASH treatment. Molecular docking studies revealed that both Cur and NC are capable of binding to AKR1B10, with NC exhibiting a stronger binding energy to AKR1B10. Western blot analysis demonstrated an upregulation in the expression of AKR1B10 and ACCα in the liver tissue of NASH rats, accompanied by elevated Acetyl-CoA and Malonyl-CoA activity, and increased levels of FFA and TG. The results of the HepG2 cell experiments induced by Ox-LDL suggest that NC significantly inhibited the expression and co-localization of AKR1B10 and ACCα, while also reduced levels of TC and LDL-C and increased level of HDL-C. These effects are accompanied by a decrease in the activities of ACCα and Malonyl-CoA, and levels of FFA and TG. Furthermore, the impact of NC appears to be more pronounced compared to Cur.

NC could effectively treat NASH and improve liver function and lipid metabolism disorder. The mechanism of NC is related to the inhibition of AKR1B10/ACCα pathway and FFA/TG synthesis of liver.

Historical maps of racialized evaluation of mortgage lending risk (i.e., redlined neighborhoods) have been linked to adverse health outcomes. Little research has examined whether living in historically redlined neighborhoods is associated with obesity, differentially by race or gender.

This is a cross-sectional study to examine whether living in historically redlined neighborhoods is associated with BMI and waist circumference among Black and White adults in 1985-1986. Participants' addresses were linked to the 1930s Home Owners' Loan Corporation maps that evaluated mortgage lending risk across neighborhoods. The authors used multilevel linear regression models clustered on Census tract, adjusted for confounders to estimate main effects, and stratified, and interaction models by (1) race, (2) gender, and (3) race by gender with redlining differentially for Black versus White adults and men versus women. To better understand strata differences, they compared Census tract-level median household income across race and gender groups within Home Owners' Loan Corporation grade.

Black adults (n=2,103) were more likely than White adults (n=1,767) to live in historically rated hazardous areas and to have higher BMI and waist circumference. Redlining and race and redlining and gender interactions for BMI and waist circumference were statistically significant (p<0.10). However, in stratified analyses, the only statistically significant associations were among White participants. White participants living in historically rated hazardous areas had lower BMI (β = - 0.63 [95% CI= -1.11, -0.15]) and lower waist circumference (β = - 1.50 [95% CI= -2.62, -0.38]) than those living in declining areas. Within each Home Owners' Loan Corporation grade, residents in White participants' neighborhoods had higher incomes than those living in Black participants' neighborhoods (p<0.0001). The difference was largest within historically redlined areas. Covariate associations differed for men, women, Black, and White adults, explaining the difference between the interaction and the stratified models. Race by redlining interaction did not vary by gender.

White adults may have benefitted from historical redlining, which may have reinforced neighborhood processes that generated racial inequality in BMI and waist circumference 50 years later.

In light of ongoing research elucidating the intricacies of obesity and metabolic syndrome, the role of abdominal fat (especially visceral fat) has been particularly prominent. Studies have revealed that visceral adipose tissue can accelerate the development of metabolic syndrome by releasing various bioactive compounds and hormones, such as lipocalin, leptin and interleukin. A retrospective analysis was performed on the clinical data of 167 patients with obesity. Among them, 105 patients who satisfied predefined inclusion and exclusion criteria were included. The parameters evaluated included total abdominal fat area (TAFA), laboratory indicators and anthropometric measurements. Weight reduction was quantified through percent total weight loss (%TWL) and percent excess weight loss (%EWL) postoperatively. Binary logistic regression analysis and receiver operating characteristic (ROC) curve analysis were employed to identify predictors of weight loss. Binary logistic regression analysis emphasized that total abdominal fat area was an independent predictor of %EWL ≥75% (p < 0.001). Total abdominal fat area (p = 0.033) and BMI (p = 0.003) were independent predictors of %TWL ≥30%. In our cohort, %TWL ≥30% at 1 year after surgery was closely related to the abdominal fat area and BMI. Based on these results, we formulated a novel model based on these factors, exhibiting superior predictive value for excellent weight loss.

We aimed to assess the prognostic importance of perinephric fat features in images of patients with non-metastatic renal cell carcinoma (RCC) undergoing surgery.

We enrolled RCC patients who underwent surgical treatment between 2011 and 2019. Two characteristics, including perinephric fat thickness and perinephric fat stranding, were evaluated using preoperative computed tomography or magnetic resonance images. The association between perinephric fat characteristics and disease progression was examined by Kaplan-Meier survival analysis and Cox regression model.

In a multivariate Cox proportional hazards model adjusting for tumor stage, intratumoral necrosis, and neutrophil-to-lymphocyte ratio, we found that patients in the thin perinephric fat group (<1 cm) had a poorer progression-free survival (PFS) compared to the thick perinephric fat group (≥1 cm) (HR 2.8; 95% CI 1.175-6.674, p = 0.02). Additionally, the fat stranding group had a poorer PFS than the non-stranding group (HR 3.852; 95% CI 1.082-13.704, p = 0.037). The non-stranding with thick perinephric fat group exhibits the highest cumulative PFS while the stranding with thin perinephric fat group has the lowest cumulative PFS. In receiver operating characteristic curve analysis, combing these two perinephric fat characteristics with tumor stage can achieve a better discriminatory power than tumor stage alone.

Our study indicates that the evaluation of image-based perinephric fat features is a simple, straightforward, reproducible tool for predicting RCC prognosis and may assist in preoperative risk stratification.

To assess the impact visceral adipose tissue percentage (VAT%) on surgical outcomes during minimally invasive surgery in obese women with endometrial cancer.

Retrospective observational cohort study.

Mie University Hospital, Japan.

Of the 73 women (body mass index [BMI] >30 kg/m2) with obesity and primary endometrial cancer, 52 underwent robotic surgery, while 21 underwent laparoscopic surgery between April 2014 and December 2022.

We investigated the correlation between surgical outcomes (operative time and blood loss) and obesity (BMI and visceral adipose tissue percentage [VAT%]).

Abdominal fat-related parameters were measured at the level of the umbilicus using preoperative computed tomography. A weak negative correlation was found between BMI and VAT% (CC = -0.313, p = .001). Multivariate analysis showed that VAT% had a stronger correlation to total and practical operative time than BMI (β = 0.338 vs 0.267, β = 0.311 vs 0.209, respectively) and was an independent predictor of blood loss. VAT% was an independent predictive marker prolonged for operative time and increased blood loss during lymphadenectomy.

VAT% could be an indicator of surgical outcomes for patients with obesity and endometrial cancer.

Postoperative complications in adhesive small bowel obstruction (ASBO) significantly escalate healthcare costs and prolong hospital stays. This study endeavors to construct a nomogram that synergizes computed tomography (CT) body composition data with inflammatory-nutritional markers to forecast postoperative complications in ASBO.

The study's internal cohort consisted of 190 ASBO patients recruited from October 2017 to November 2021, subsequently partitioned into training (n = 133) and internal validation (n = 57) groups at a 7:3 ratio. An additional external cohort comprised 52 patients. Body composition assessments were conducted at the third lumbar vertebral level utilizing CT images. Baseline characteristics alongside systemic inflammatory responses were meticulously documented. Through univariable and multivariable regression analyses, risk factors pertinent to postoperative complications were identified, culminating in the creation of a predictive nomogram. The nomogram's precision was appraised using the concordance index (C-index) and the area under the receiver operating characteristic (ROC) curve.

Postoperative complications were observed in 65 (48.87%), 26 (45.61%), and 22 (42.31%) patients across the three cohorts, respectively. Multivariate analysis revealed that nutrition risk score (NRS), intestinal strangulation, skeletal muscle index (SMI), subcutaneous fat index (SFI), neutrophil-lymphocyte ratio (NLR), and lymphocyte-monocyte ratio (LMR) were independently predictive of postoperative complications. These preoperative indicators were integral to the nomogram's formulation. The model, amalgamating body composition and inflammatory-nutritional indices, demonstrated superior performance: the internal training set exhibited a 0.878 AUC (95% CI, 0.802-0.954), 0.755 accuracy, and 0.625 sensitivity; the internal validation set displayed a 0.831 AUC (95% CI, 0.675-0.986), 0.818 accuracy, and 0.812 sensitivity. In the external cohort, the model yielded an AUC of 0.886 (95% CI, 0.799-0.974), 0.808 accuracy, and 0.909 sensitivity. Calibration curves affirmed a strong concordance between predicted outcomes and actual events. Decision curve analysis substantiated that the model could confer benefits on patients with ASBO.

A rigorously developed and validated nomogram that incorporates body composition and inflammatory-nutritional indices proves to be a valuable tool for anticipating postoperative complications in ASBO patients, thus facilitating enhanced clinical decision-making.

To explore the association between visceral obesity and short-term postoperative complications in patients with advanced ovarian cancer undergoing cytoreductive surgery.

The medical records of patients with advanced epithelial ovarian cancer were reviewed. The visceral fat area, subcutaneous fat area and total fat area at the L3/4 level were measured on a preoperative single-slice CT scan. The receiver operating characteristic (ROC) curve was used to calculate the optimal cutoff value for the visceral fat area. The relationship between the visceral fat area and the characteristics of ovarian cancer patients were analyzed. Univariable and multivariable logistic regression analyses were performed to investigate relationship between perioperative characteristics and short-term complications.

According to the ROC curve, the best cutoff value of the VFA was 93 cm2. Of the 130 patients, 53.8% (70/130) had visceral obesity. Patients with visceral obesity were older than those with nonvisceral obesity (58.4 years old vs. 52.1 years old, p < 0.001). The proportion of patients with hypertension was higher (35.7 vs. 13.3%, p = 0.003). The total fat area and subcutaneous fat area were larger in patients with visceral obesity (294.3 ± 75.5 vs. 176.2 ± 68.7, p < 0.001; 158.9 ± 54.7 vs. 121.7 ± 52.6, p < 0.001). Compared with patients in the nonvisceral obese group, patients in the visceral obese group were more likely to have postoperative fever (21/70 30.0% vs. 8/60 1.25%, p = 0.023), leading to a longer length of hospital stay (21 days vs. 17 days, p = 0.009). The time from surgery to adjuvant chemotherapy for patients with visceral obesity was shorter (24 days vs. 19 days, p = 0.037). Multivariate analysis showed that visceral obesity (OR = 6.451, p < 0.001) and operation time (OR = 1.006, p < 0.001) were independent predictors of postoperative complications.

Visceral obesity is an important risk factor for short-term postoperative complications in patients with advanced ovarian cancer undergoing cytoreductive surgery.

Segmentation of multiple pelvic structures in MRI volumes is a prerequisite for many clinical applications, such as sarcopenia assessment, bone density measurement, and muscle-to-fat volume ratio estimation. While many CT-specific datasets and automated CT-based multi-structure pelvis segmentation methods exist, there are few MRI-specific multi-structure segmentation methods in literature. In this pilot work, we propose a lightweight and annotation-free pipeline to synthetically translate T2 MRI volumes of the pelvis to CT, and subsequently leverage an existing CT-only tool called TotalSegmentator to segment 8 pelvic structures in the generated CT volumes. The predicted masks were then mapped back to the original MR volumes as segmentation masks. We compared the predicted masks against the expert annotations of the public TCGA-UCEC dataset and an internal dataset. Experiments demonstrated that the proposed pipeline achieved Dice measures ≥65% for 8 pelvic structures in T2 MRI. The proposed pipeline is an alternative method to obtain multi-organ and structure segmentations without being encumbered by time-consuming manual annotations. By exploiting the significant research progress in CTs, it is possible to extend the proposed pipeline to other MRI sequences in principle. Our research bridges the chasm between the current CT-based multi-structure segmentation and MRI-based segmentation. The manually segmented structures in the TCGA-UCEC dataset are publicly available.

We aimed to explore the causal relationship between blood metabolites and the risk of visceral obesity, as measured by visceral adipose tissue (VAT).

Summary statistics for 486 blood metabolites and total, as well as sex-stratified, MRI-derived VAT measurements, adjusted for body mass index (BMI) and height, were collected from previous genome-wide association studies (GWAS). A two-sample Mendelian Randomization (MR) design was used. Comprehensive evaluation was further conducted, including sensitivity analysis, linkage disequilibrium score (LDSC) regression, Steiger test, and metabolic pathway analysis.

After multiple testing correction, arachidonate (20:4n6) has been implicated in VAT accumulation (β = 0.35, 95%CI:0.18-0.52, P < 0.001; FDR = 0.025). Additionally, several blood metabolites were identified as potentially having causal relationship (FDR < 0.10). Among them, lysine (β = 0.67, 95%CI: 0.28-1.06, P < 0.001; FDR = 0.074), proline (β = 0.30, 95%CI:0.13-0.48, P < 0.001; FDR = 0.082), valerate (β = 0.50, 95%CI:0.23-0.78, P < 0.001, FDR = 0.091) are associated with an increased risk of VAT accumulation. On the other hand, glycine (β=-0.21, 95%CI: -0.33-0.09), P < 0.001, FDR = 0.076) have a protective effect against VAT accumulation. Most blood metabolites showed consistent trends between different sexes. Multivariable MR analysis demonstrated the effect of genetically predicted arachidonate (20:4n6) and proline on VAT remained after accounting for BMI and glycated hemoglobin (HbA1c). There is no evidence of heterogeneity, pleiotropy, and reverse causality.

Our MR findings suggest that these metabolites may serve as biomarkers, as well as for future mechanistic exploration and drug target selection of visceral obesity.

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver condition worldwide. NAFLD is often associated with features of Metabolic Syndrome such as obesity and insulin resistance.

The current comprehensive meta-analysis was performed to evaluate the association between circulating Omentin levels and NAFLD. A systematic search in Scopus, Web of Science, PubMed, and Google Scholar databases was conducted to identify relevant studies up until 5th May 2022. The standard mean difference (SMD) values and 95% confidence intervals (CIs) were computed for the association of Omentin levels with NAFLD risk in a random effect model.

The meta-analysis involved 6 case-control studies with a total of 371 cases and 269 controls. Pooled SMD showed no significant difference in serum Omentin between NAFLD and healthy groups (SMD= -0.047 and 95% CI -0.957_0.862 P=0.91). Subgroup analysis based on sample size showed that the average Omentin levels were significantly higher in NAFLD patients in studies with sample size ≥70 (SMD=0.356 CI 0.056_0.655 P=0.02).

Additional well-designed studies with more sample sizes are essential to clarify the potential role of Omentin as a risk marker of NAFLD.

Adipose tissue hypoxia plays a crucial role in the development of chronic low-grade systemic inflammation which has been associated with the pathogenesis of obesity-related diseases. Myricetin is a natural compound present in numerous plant-based foods with presumed anti-inflammatory and beneficial health effects. The impact of this flavonoid on hypoxia-induced expression of inflammatory adipokines and hypoxia-regulated pathways is unknown so far and has been addressed in the present study.

Differentiated human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes were cultured with or without myricetin under normoxic and hypoxic conditions for varying time periods. The effect of hypoxia and myricetin on the expression of the investigated adipokines was measured by real-time RT-PCR. Western blot analysis was used for the detection of transcription factors involved in hypoxia-regulated pathways.

Myricetin interfered in the hypoxia-induced regulation of adipokines and the underlying pathways, which are involved in transmitting the inflammatory response. It strongly repressed hypoxia-induced expression of apelin, leptin, chemerin, asprosin, and DPP-4 and HIF-1α accumulation in the nucleus was diminished. Furthermore, the activation of the key regulators in the inflammatory response NF-κB, Akt, and CREB was suppressed by myricetin under hypoxic conditions. Myricetin also decreased hypoxia-induced accumulation of the pro-tumorigenic transcription factors Snail and Slug in the nucleus.

Taken together, our results indicated that myricetin regulated hypoxia-induced expression of adipokines and hypoxia-regulated pathways in human adipocytes. Our study therefore provided evidence of the anti-inflammatory effects of myricetin in hypoxia-treated human adipocytes.