Brown adipose tissue (BAT) exhibits greater resilience against inflammation compared to white adipose tissue. However, chronic consumption of a high-fat diet can render brown adipocytes vulnerable to proinflammatory conditions, leading to a decline in their thermogenic capacity and subsequent dysfunction. The analysis of the effects of type fatty acids intake must be important in the context of the dietary pattern and obesity. This study aims to investigate the impact of a low-carbohydrate/high-fat diet, enriched with different types of fatty acids, on mitochondrial activity on brown adipose tissue in obese mice. Male mice were allocated into different dietary groups: a control diet (CTL), and a high-fat diet (HFD) for a duration of 10 weeks to induce obesity. Subsequently, the HFD group was subdivided into the following categories for an additional 6 weeks: HFD with a low carbohydrate content enriched with saturated fatty acids; HFD with a low carbohydrate content enriched with fish oil; HFD with a low carbohydrate content enriched with soybean oil; and HFD with a low carbohydrate content enriched with olive oil. The findings indicated that in comparison to a low-carbohydrate diet rich in saturated fats, diets rich in unsaturated fatty acids-particularly omega-6 (n-6) and omega-9 (n-9)-resulted in elevated expression of UCP1, a marker of BAT activity. Moreover, there was an increase in the expression of PGC1-α, a protein involved in mitochondrial biogenesis, and enhanced functionality of the oxidative phosphorylation system within BAT mitochondria. These results suggest that n-6 and n-9 fatty acids may confer greater benefits to BAT functionality than saturated fats within the context of a low-carbohydrate diet. Therefore, this study revealed some molecular components that mediate BAT mitochondria function influenced by different fatty acids in a low carbohydrate diet, making it an important therapeutic target in obesity.

Lipedema is an abnormal accumulation of adipose tissue, predominantly observed in women, characterised by symmetrical fat deposition and tactile sensitivity in the extremities, affecting both sides of the body. This condition can lead to significant pain, impairing daily activities and causing substantial discomfort.

While the etiology of the disease is not yet fully understood, genetic predisposition, hormonal fluctuations, a stressful lifestyle, as well as traumatic events are considered potential triggers. Lipedema remains a condition with low diagnostic awareness as well as is frequently misdiagnosed as obesity or lymphedema. While obesity is a risk factor for lipedema, the abnormal fat deposition characteristic of the disease can occur across a wide spectrum of body weights, from underweight to overweight individuals. Specific patterns of adipose tissue distribution may be associated with signs of inflammation as well as heightened pain perception, as well as individuals with eating disorders, such as anorexia, may additionally be affected. Ketogenic diets have emerged as a promising therapeutic option for lipedema. Characterized by low carbohydrate as well as high fat content, ketogenic diets facilitate metabolic improvements by reducing insulin resistance as well as supporting weight loss. Furthermore, they may mitigate tissue damage associated with lipedema by decreasing inflammation as well as oxidative stress levels.Nevertheless, current scientific data regarding the mechanisms of action as well as therapeutic efficacy of ketogenic diets are limited, necessitating further research to expand their clinical application.

Sporadic Alzheimer's disease (AD), which accounts for the majority of cases, is sturdily influenced by lifestyle factors such as dietary habits, obesity, and diabetes, leading to its classification as Type 3 diabetes. To model this pathological link, our AD-like model was developed by feeding Wistar male rats a high-fat diet with fructose in drinking water (HFFD) for 8 weeks, followed by a single dose of lipopolysaccharide (LPS). This group was compared with a normal control group fed a standard diet and a β-hydroxybutyrate (BHB)-treated group (125 mg/kg, p.o.), administered starting 3 h after LPS and continuing for 1 week. The results demonstrate that BHB treatment illuminated cognitive gains, as indicated by the Y-maze, Morris water maze, and novel object recognition tests. In addition, it preserved hippocampal cytoarchitecture, reduced neurodegeneration, and attenuated amyloid plaques and phosphorylated Tau deposition. Cellularly, BHB restored critical molecular mechanisms, including increased lysosomal-associated membrane protein 2A (LAMP2A) hippocampal content as the main marker of chaperone-mediated autophagy (CMA), along with the chaperon protein Hsp70. Moreover, BHB alleviated neuroinflammation by inhibiting the nucleotide-binding domain, leucine-rich-containing family, and pyrin domain-containing-3 (NLRP3) inflammasome activation alongside the downstream targets cleaved caspase-1 and IL-1β/IL-18 cytokines. BHB also reduced pyroptotic markers, caspase-11 and gasdermin-N, and microglia-induced inflammation as it shifted microglial polarization toward the neuroprotective M2 phenotype. Finally, BHB normalized hippocampal neurotransmitter levels of the inhibited acetylcholine and serotonin. These findings support BHB as a promising, multifaceted treatment for AD, highlighting the roles of CMA, Hsp70, and 5-HT in slowing disease progression and improving cognitive function.

The ketogenic diet (KD) has attracted attention in recent years for its potential anticancer effects. KD is a dietary structure of high fat, moderate protein, and extremely low carbohydrate content. Originally introduced as a treatment for epilepsy, KD has been widely applied in weight loss programs and the management of metabolic diseases. Previous studies have shown that KD can potentially inhibit the growth and spread of cancer by limiting energy supply to tumor cells, thereby inhibiting tumor angiogenesis, reducing oxidative stress in normal cells, and affecting cancer cell signaling and other processes. Moreover, KD has been shown to influence T-cell-mediated immune responses and inflammation by modulating the gut microbiota, enhance the efficacy of standard cancer treatments, and mitigate the complications of chemotherapy. However, controversies and uncertainties remain regarding the specific mechanisms and clinical effects of KD as an adjunctive therapy for cancer. Therefore, this review summarizes the existing research and explores the intricate relationships between KD and cancer treatment.

Objective: This study aimed to review the structural concepts, definition, classification, and macronutrient and food composition of carbohydrate-restricted diets (CRDs) for individuals with type 2 diabetes mellitus (T2DM). Methods: A scoping review was conducted following Joanna Briggs Institute guidelines. Searches were performed in Scopus, PubMed, Web of Science, and Embase, including texts published in Portuguese, English, and Spanish. Official documents from governments, regulatory agencies, and international diabetes organizations were also consulted. Results: In total, 79 articles and 17 official documents were analyzed. The following structural concept was identified: restricted carbohydrate intake decreases the need for endogenous and exogenous insulin, contributing to the maintenance of glycemic control, and justifies its consideration among the nutritional therapy options for individuals with T2DM. CRDs varied in definition, classification, and macronutrient composition. Studies failed to provide detailed information on the food composition of diets, precluding an in-depth understanding of metabolic effects. The existence of several approaches with varying recommendations makes it difficult to generalize the results. International CRD guidelines for T2DM adopt divergent definitions, compromising interpretation, recommendation, and even adherence. Conclusions: Although the concept of CRDs justifies their adoption within the nutritional therapy choices for T2DM, the multiple denominations can hinder understanding and comparison between studies. The lack of information on food composition and carbohydrate types compromises the assessment of the effects and adherence to CRD-based nutritional interventions. We emphasize the need for methodologically consistent studies that evaluate CRDs based on fresh and minimally processed foods with a low glycemic index to support official diabetes guidelines and organizations.

Dravet syndrome (DS) is a severe and catastrophic epilepsy with childhood onset. The incidence and prevalence of sudden unexpected death in epilepsy (SUDEP) are significantly higher in DS patients than in general epileptic populations. Although extensive research conducted, the underlying mechanisms of SUDEP occurring in DS patients remain unclear. This review focuses on the link between DS and SUDEP and analyzes the potential pathogenesis. We summarize the genetic basis of DS and SUDEP and elucidate the pathophysiological mechanisms of SUDEP in DS. Furthermore, given the drug-resistant nature of this disorder, the pharmacological approach has limited efficacy and often causes side effects, therefore, the non-pharmacological approaches and precise treatment can reduce the risk of SUDEP in this condition, open a new window to cure this disease, and provide a widened landscape of treatment options for patients.

Type 2 diabetes mellitus is a complex, pervasive disease that creates a health and financial burden. The goal is to head off progression to insulin requirement, and dietary changes have been recognized as a first-line intervention in the treatment protocol. Four evidence-based nutritional options are reviewed and their benefits for metabolic consequences.

We conducted a comprehensive search of relevant literature using the PubMed database for recent systematic reviews, meta-analyses, and original research articles.

The Mediterranean and plant-based diets have demonstrated benefits for the prevention and treatment of diabetes, weight reduction, lipid improvements, and overall cardiovascular risk reduction. A low carbohydrate diet is another viable option for hemoglobin A1c (HbA1c) reduction, though it is not as uniformly defined and is difficult to maintain long term. The ketogenic diet is similarly very restrictive and produces significant HbA1c reductions.

Type 2 diabetes prevention and treatment is crucial in this widespread disease. The first-line treatment is lifestyle modifications with dietary interventions being at the forefront. With a unique clinical model and a variety of dietary options, our program strives for individualized evidence-based care. Nutritional modifications are the best initial approaches to overcoming insulin resistance and hyperinsulinemia. All dietary modifications, like any medical intervention, require education on benefits vs risks.

The ketogenic diet (KD), high in fat and low in carbohydrates, was introduced in the 1920s as a non-pharmacological treatment for refractory epilepsy. Although its mechanism of action is not fully understood, beneficial effects have been observed in neurological diseases such as epilepsy, Alzheimer's disease, and Parkinson's disease.

This review examines the impact of the ketogenic diet and its molecular and neuroglial effects as a complementary therapy for neurological diseases.

KD is associated with neuroprotective and antioxidant effects that improve mitochondrial function, regulate neurotransmitter flow, and reduce neuroinflammation and oxidative stress. Glial cells play an essential role in the utilization of ketone bodies (KBs) within the central nervous system's metabolism, particularly during ketosis induced by the KD. Thus, the KD represents a broad and promising strategy that involves both neurons and glial cells, with a molecular impact on brain metabolism and neuroinflammatory homeostasis.

Multiple molecular mechanisms have been identified to explain the benefits of the KD in neurological diseases; however, further experimental and clinical studies are needed to address various molecular pathways in order to achieve conclusive results.

In recent times, there has been growing interest in understanding the factors contributing to prolonged and healthy lifespans observed in specific populations, tribes, or countries. Factors such as environmental and dietary play significant roles in shaping the ageing process and are often the focus of inquiries seeking to unravel the secrets behind longevity. Among these factors, diet emerges as a primary determinant, capable of either promoting or mitigating the onset of age-related diseases that impact the ageing trajectory. This review examines the impact of various diet types on ageing and age-related conditions, including cardiovascular disease, cancer, neurodegenerative disorders, and metabolic syndrome. Different dietary patterns, such as the Mediterranean diet, the Japanese diet, vegetarian and vegan diets, as well as low-carbohydrate and ketogenic diets, are evaluated for their potential effects on longevity and health span. Each diet type is characterized by distinct nutritional profiles, emphasizing specific food groups, macronutrient compositions, and bioactive components, which may exert diverse effects on ageing processes and disease risk. Additionally, dietary factors such as calorie restriction, intermittent fasting, and dietary supplementation are explored for their potential anti-ageing and disease-modifying effects. Understanding the influence of various diet types on ageing and age-related diseases can inform personalized dietary recommendations and lifestyle interventions aimed at promoting healthy aging and mitigating age-associated morbidities.

The ketogenic diet (KD) is a special high-fat, very low-carbohydrate diet with the amount of protein adjusted to one's requirements. By lowering the supply of carbohydrates, this diet induces a considerable change in metabolism (of protein and fat) and increases the production of ketone bodies. The purpose of this article is to review the diversity of composition, mechanism of action, clinical application and risk associated with the KD. In the last decade, more and more results of the diet's effects on obesity, diabetes and neurological disorders, among other examples have appeared. The beneficial effects of the KD on neurological diseases are related to the reconstruction of myelin sheaths of neurons, reduction of neuron inflammation, decreased production of reactive oxygen species, support of dopamine production, repair of damaged mitochondria and formation of new ones. Minimizing the intake of carbohydrates results in the reduced absorption of simple sugars, thereby decreasing blood glucose levels and fluctuations of glycaemia in diabetes. Studies on obesity indicate an advantage of the KD over other diets in terms of weight loss. This may be due to the upregulation of the biological activity of appetite-controlling hormones, or to decreased lipogenesis, intensified lipolysis and increased metabolic costs of gluconeogenesis. However, it is important to be aware of the side effects of the KD. These include disorders of the digestive system as well as headaches, irritability, fatigue, the occurrence of vitamin and mineral deficiencies and worsened lipid profile. Further studies aimed to determine long-term effects of the KD are required.

The ketogenic diet (KD) has been explored for diabetes management; however, a quantitative synthesis of its specific effects on diabetes has not yet been conducted. This study aims to examine the current status and research hotspots of KD in diabetes management from 2005 to 2024, providing a reference for future research.

We retrieved articles published between 2005 and 2024 from the Web of Science database and analyzed them using R software, VOSviewer, and CiteSpace.

This study includes 432 relevant publications. From 2005 to 2024, the volume of literature in this field has shown a steady upward trend, with a notable increase from 2017 to 2021, and a slight decline observed from 2021 to 2023. The United States is the leading country in terms of the number of publications, followed by China, Australia, and Canada. The United States not only leads in publication volume but also maintains a broader international collaboration network. Nutrients and the American Journal of Clinical Nutrition are the most frequently published and cited journals. Current research hotspots primarily focus on the impact of KD on blood glucose control, insulin resistance, and lipid metabolism in diabetic patients. Mechanistic studies on KD in diabetes management concentrate on aspects such as the "regulation of genes by β-hydroxybutyrate," "anti-inflammatory effects," and "oxidative stress." The role of the gut microbiome is also emerging as an important research area. Currently, exploring the application of KD in managing different age groups and types of diabetes has become a significant research trend.

As an emerging dietary intervention, KD is gradually attracting widespread attention from researchers around the world and is expected to become a major research focus in the future for diabetes management and control. This paper provides a systematic review and analysis of the current research status and hotspots of KD in diabetes management, offering important references and insights for future research in related fields.

The ketogenic diet (KD) is a popular option for managing body weight, though its influence on glucose and lipid metabolism was still inconclusive. Gut microbiota is modulated by dietary pattens and has been associated with the changes of metabolic homeostasis induced by KD. Here, we found that two types of KDs, KD1 (8.8% carbohydrate, 73.4% fat, 17.9% protein, 5.7 kcal/g) and KD2 (0.4% carbohydrate, 93.2% fat, 6.4% protein, 6.7 kcal/g), induced changes of gut microbiota and its metabolites, contributing to glucose intolerance but not lipid accumulation in mice. Following a 2-week intervention with KDs, mice fed on KD1 displayed symptoms related to obesity, whereas KD2-fed mice exhibited a decrease in body weight but had severe hepatic lipid accumulation and abnormal fatty acid metabolism, while both KDs led to significant glucose intolerance. Compared to the mice fed on a standard chow diet, the conventional mice fed on both KD1 and KD2 had significant shifted gut microbiota, lower levels of short chain fatty acids (SCFAs) and composition alteration of cecal bile acids. By using an antibiotic cocktail (ABX) to deplete most of the gut microbiota in mice, we found the disturbances induced by KDs in lipid metabolism were similar in the ABX-treated mice to their conventional companions, but the disturbances in glucose metabolism were absent in the ABX-treated mice. In conclusion, these findings suggest that ketogenic diets disrupted glucose and lipid metabolism, at least in mice, and highlight the gut microbial culprits associated with KD induced glucose intolerance rather than lipid accumulation.

This study examined the effect of a low-carbohydrate diet (LCD) and a low-carbohydrate ketogenic diet (LCKD) on diabetic retinopathy in high-fat diet-induced diabetes mellitus in rats and studied the mechanisms of action. Rats were divided into four groups: the Control group, which was fed a normal diet for 16 weeks; the HFD group, which was fed a high-fat diet (HFD) for the first 8 weeks and then switched to a normal diet for 8 weeks; the HFD+LCD group, fed a HFD for 8 weeks followed by an LCD for 8 weeks, and the HFD+LCKD group, which was fed a HFD for 8 weeks followed by an LCKD for 8 more weeks. Both the LCD and the LCKD effectively reduced the final body and total fat weights and decreased fasting serum levels of glucose, insulin, hemoglobin A1 (HbA1C), triglycerides, cholesterol, and LDL-c. They also reduced the levels of malondialdehyde (MDA), tumor necrosis factor-α, vascular endothelial factor, caspapse-3, and bax. In the HFD rats, we found increased serum levels of β-Hydroxybutyrate and upregulated expression of Bcl2, glutathione, superoxide dismutase, and hemeoxygenase-1. Moreover, the LCD and LCKD significantly reduced mRNA levels of Kelch-like ECH-associated protein 1 (Keap1) and enhanced mRNA and nuclear concentrations of nuclear factor erythroid factor 2 (Nrf2). All these effects were associated with improved layers of the retina in the HFD - LCD and HFD + LCKD rats but not in HFD animals. The impact of the LCKD was always more profound on all measured parameters and on improving the structure of the retina compared to the LCD. In conclusion, the LCKD is superior to the LCD in preventing diabetic retinopathy in HFD-fed rats. Mechanistically, our results suggest that the hypoglycemic and hypolipidemic conditions and the Nrf2-dependent antioxidant and anti-inflammatory effects may be involved in the preventative effects of the LCD and LCKD.

Polycystic ovary syndrome (PCOS) affects up to 20 % of reproductive-age individuals and is strongly linked to obesity. The impacts of ketogenic diet on fertility in people with PCOS are unknown. This study aims to determine the effect of a ketogenic diet on restoration of regular menstrual cycles and fertility.

After approval from the Institutional Review Boards of Cleveland Clinic, a retrospective analysis was conducted using the electronic health record system. We analyzed data from thirty patients (n = 30) with polycystic ovary syndrome who followed a ketogenic diet for at least 3 months at the Cleveland Clinic, Cleveland, Ohio, USA. Main outcomes were percentage of women with restoration of regular menstrual cycles and pregnancy rate.

All women (n = 30) had restoration of regular menstrual cycles. The overall pregnancy rate of women desiring pregnancy (n = 18) was 55.6% (n = 10). Pregnancy rate was 38.5% for women on metformin and 100% for those who were not (P = 0.036). Pregnancy rate was 62.5% for women using ovulation induction agents and 50.0% for those who did not (P = 0.66). Percent weight change between the pregnant and non-pregnant groups did not significantly differ [-8.1 ± 6.2, vs -6.4 ± 8.4, P = 0.64, respectively].

This study reports a higher rate of pregnancy with the ketogenic diet in women with PCOS compared to existing literature.

Dietary regulation has been recognized for its profound impact on human health. The convergence of cardiovascular, kidney, and metabolic disorders at the pathophysiological level has given rise to cardiovascular-kidney-metabolic (CKM) syndrome, which constitutes a significant global health burden. Maternal dietary nutrients play a crucial role in fetal development, influencing various programmed processes. This review emphasizes the effects of different types of dietary interventions on each component of CKM syndrome in both preclinical and clinical settings. We also provide an overview of potential maternal dietary strategies, including amino acid supplementation, lipid-associated diets, micronutrients, gut microbiota-targeted diets, and plant polyphenols, aimed at preventing CKM syndrome in offspring. Additionally, we discuss the mechanisms mediated by nutrient-sensing signals that contribute to CKM programming. Altogether, we underscore the interaction between maternal dietary interventions and the risk of CKM syndrome in offspring, emphasizing the need for continued research to facilitate their clinical translation.

Ketogenic diets (KD) have shown remarkable effects in many disease areas. It has been demonstrated in numerous animal experiments that KD is effective in the treatment of Alzheimer's disease (AD). But the clinical effect of treating AD is uncertain.

To systematically review the impact of KD on cognitive function in AD.

We conducted a search of three international databases-PubMed, Cochrane Library, and Embase-to retrieve RCTs on the KD intervention for AD from the inception of the databases through October 2023. Two reviewers searched and screened the literature, extracted and checked relevant data independently, and assessed the risk of bias of the included studies. The meta-analysis was carried out utilizing RevMan 5.3 software.

A total of 10 RCTS involving 691 patients with AD were included. There were 357 participants in the intervention group and 334 participants in the control group. The duration of the KD intervention ranged from a minimum of 3 months to a maximum of 15 months. Meta-analysis results showed that KD could effectively improve the mental state of the elderly (NM scale) [MD = 7.56, 95%CI (3.02, 12.10), P = 0.001], MMSE [MD = 1.25, 95%CI (0.46, 2.04), P = 0.002], and ADAS-Cog [MD = -3.43, 95%CI (-5.98, -0.88), P = 0.008]. The elevation of ketone body (β-hydroxybutyric) [MD = 118.84, 95%CI (15.20, 222.48), P = 0.02] may also lead to the elevation of triglyceride [MD = 0.19, 95%CI (0.03, 0.35), P = 0.02] and low density lipoprotein [MD = 0.31, 95%CI (0.04, 0.58), P = 0.02].

Research conducted has indicated that the KD can enhance the mental state and cognitive function of those with AD, albeit potentially leading to an elevation in blood lipid levels. In summary, the good intervention effect and safety of KD are worthy of promotion and application in clinical treatment of AD.

This study was designed to evaluate the impact of VLCKD on cardiovascular risk factors in patients with T2DM.

Until March 2024, extensive searches were conducted on PubMed, Scopus, Web of Science, Embase, and other relevant databases. The purpose was to identify clinical trials examining the impact of VLCKD on glycemic control, lipid profile, and blood pressure. The GRADE (Grading of Recommendations Assessment, Development, and Evaluation) method was used to assess the evidence's degree of certainty.

Our initial search found a total of 2568 records and finally 29 trials were included in final analysis. Our results showed that adherence from VLCKD led to significant reduction in fasting blood sugar (WMD= -11.68 mg/dl; 95% CI: -18.79, -4.56; P = 0.001), HbA1c (WMD= -0.29; 95% CI: -0.44, -0.14; P < 0.001), HOMA-IR(WMD= -0.71; 95% CI: -1.14, -0.29; P = 0.001), insulin (WMD= -1.45; 95% CI: -2.54, -0.36; P = 0.009), triglyceride (WMD= -17.95; 95% CI: -26.82, -9.07; P < 0.001), systolic blood pressure (WMD= -2.85, 95% CI: -4.99, -0.71; P = 0.009) and diastolic blood pressure (WMD= -1.40; 95% CI: -2.66, -0.13; P = 0.03). We also found a significant increase in high-density lipoprotein (HDL) level after adherence from VLCKD diet (WMD = 3.93, 95% CI: 2.03, 5.84; P = 0.000). We couldn't find any significant differences between groups in term of LDL and total cholesterol levels.

People following a VLCKD experience a more significant improvement in cardiovascular risk factors when compared to individuals on control diets.

This is a protocol for a Cochrane Review (intervention). The objectives are as follows: To assess the effects of a low-carbohydrate diet in adults with type 2 diabetes mellitus.

Epilepsy is a common neurological disorder characterized by recurrent epilepsy episodes. As a non-pharmacological treatment, the ketogenic diet has been widely applied in treating epilepsy. However, the exact therapeutic mechanism of the ketogenic diet for epilepsy remains unclear. This study investigates the molecular mechanisms of the ketogenic diet in regulating fatty acid metabolism and activating the ADCY3-initiated cAMP signaling pathway to enhance neuronal inhibition and thereby treat epilepsy.

Meta-analysis reveals that the ketogenic diet is superior to the conventional diet in treating epilepsy. Animal experiments demonstrate that the ketogenic diet is more effective than the conventional diet in treating epilepsy, with the best results achieved using the classic ketogenic diet. Transcriptome sequencing analysis identifies six essential genes, among which ADCY3 shows increased expression in the ketogenic diet. In vivo experiments confirm that the activation of the cAMP-PKA signaling pathway by ADCY3 enhances neuronal inhibition and improves epilepsy control.

Clinical observations indicate that the ketogenic diet improves patient epilepsy episodes by regulating the ADCY3-initiated cAMP signaling pathway.

Diabetes mellitus is a collection of metabolic disorders marked by elevated levels of glucose in the blood due to irregularities in the generation or functioning of insulin. Medical nutrition therapy and weight loss are crucial elements in the management of diabetes and the prevention of complications. Several diets have become popular over time for the goal of achieving weight loss, but their popularity has declined due to a lack of reliable scientific evidence. This study classifies popular diets into three categories: diets that manage the composition of macronutrients, diets that restrict specific foods or food groups, and diets that manipulate meal timing. The review includes research studies that investigated the effects of popular diets on the prevention, management, and complications of diabetes. It is clear that different popular diets can have positive effects on both preventing and treating diabetes and preventing and treating complications related to diabetes. However, it is not practical to determine which diet is the most effective option for preventing or controlling diabetes. Thus, the main focus should be on common underlying factors that support well-being, such as decreasing the intake of refined grains and added sugar, choosing non-starchy vegetables, and giving priority to whole foods over processed foods whenever possible, until there is stronger evidence supporting the specific benefits of different dietary patterns.

All recent guidelines on cardiovascular prevention have highlighted the role of a healthy diet and lifestyle advocating an holistic approach to reduce the cardiovascular burden among the population. Despite these efforts, registries have reported that only a minority of healthcare professionals provide advice on diet and lifestyle, and, in most cases, counseling is suboptimal for several reasons. Cardiovascular benefits linked to lifestyle and nutrition seem to be underestimated by many patients and doctors. This overview aims to summarize well-established benefits related to lifestyle and nutrition, discuss the current debates in this field in order to improve awareness among the medical community and promote better implementation of non-pharmaceutical measures to prevent the occurrence of atherothrombotic events, by reducing cardiovascular risk factors such as hypertension, diabetes, dyslipidemia, and obesity.

Diabetes is often associated with reduced muscle mass and function. The ketogenic diet (KD) may improve muscle mass and function via the induction of nutritional ketosis. To test whether the KD is able to preserve muscle mass and strength in a mouse model of type 2 diabetes (T2DM), C57BL/6J mice were assigned to lean control, diabetes control, and KD groups. The mice were fed a standard diet (10% kcal from fat) or a high-fat diet (HFD) (60% kcal from fat). The diabetic condition was induced by a single injection of streptozotocin (STZ; 100 mg/kg) and nicotinamide (NAM; 120 mg/kg) into HFD-fed mice. After 8-week HFD feeding, the KD (90% kcal from fat) was fed to the KD group for the following 6 weeks. After the 14-week experimental period, an oral glucose tolerance test and grip strength test were conducted. Type 2 diabetic condition induced by HFD feeding and STZ/NAM injection resulted in reduced muscle mass and grip strength, and smaller muscle fiber areas. The KD nutritional intervention improved these effects. Additionally, the KD altered the gene expression of nucleotide-binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome- and endoplasmic reticulum (ER) stress-related markers in the muscles of diabetic mice. Collectively, KD improved muscle mass and function with alterations in NLRP3 inflammasome and ER stress.

Diabetes mellitus is a condition caused by a deficiency in insulin production or sensitivity that is defined by persistent hyperglycemia as well as disturbances in glucose, lipid, and protein metabolism. Uncurbed diabetes or incessant hyperglycemic condition can lead to severe complications, including renal damage, visual impairment, cardiovascular disease, neuropathy, etc., which promotes diabetes-associated morbidity and mortality rates. The therapeutic management of diabetes includes conventional medications and nutraceuticals as complementary therapies. Nutraceuticals are bioactive compounds derived from food sources that have health-promoting properties and are instrumental in the management and treatment of various maladies. Nutraceuticals are clinically exploited to tackle DM pathogenesis, and the clinical evidence suggests that nutraceuticals can modulate biochemical parameters related to diabetes pathogenesis and comorbidities. Hypoglycemic medicines are designed to mitigate DM in traditional medicinal practice. This review intends to emphasize and comment on the various therapeutic strategies available to manage this chronic condition, conventional drugs, and the potential role of nutraceuticals in managing the complexity of the disease and reducing the risk of complications. In contrast to conventional antihyperglycemic drugs, nutraceutical supplements offer a higher efficacy and lesser adverse effects. To substantiate the efficacy and safety of various functional foods in conjunction with conventional hypoglycemic medicines, additional data from clinical studies are required.

Worldwide obesity and cardiovascular diseases have encouraged the adoption of new and efficient dietary strategies. Among various proposed diets, ketogenic diets, both the very-low-calorie ketogenic diet (VLCKD) and the low-calorie ketogenic diet (LCKD), have been suggested in recent years as an effective nutritional approach for obesity management. The VLCKD and the LCKD are characterized by a low carbohydrate content (<50 g/day), 1-1.5 g of protein/kg of ideal body weight, less than 20-30 g of lipids, and a daily intake of about 800 calories for VLCKD and about 1200-1400 calories for LCKD. The purpose of our narrative review is to offer an overview of the most impactful studies in the scientific literature regarding VLCKD and LCKD to discuss their short- and long-term effects (less than 12 months and more than 12 months respectively) on weight loss, metabolic and cardiovascular aspects. Articles we focused on were cohort studies, case-control studies, cross-sectional studies, randomized controlled trials, and meta-analyses. Results indicate that VLCKD and LCKD could be helpful to ameliorate metabolic and cardiovascular risk factors such as weight loss, glucose, and cholesterol levels, both in the short and long term. Further research in this area may include more randomized controlled trials to gather more data.

Currently, the lack of comparative studies between weekly and daily formulations of glucagon-like peptide-1 receptor agonists (GLP-1RAs) for glucose excursion is worth investigation.

To investigate the effects of weekly and daily formulations of GLP-1RA on glucose excursion and inflammation in overweight and obese patients with type 2 diabetes.

Seventy patients with type 2 diabetes mellitus who were treated at our hospital between January 2019 and January 2022 were enrolled in this retrospective analysis. All patients were treated with metformin. We evaluated changes in blood glucose levels and a series of important indicators in patients before and after treatment with either a weekly or daily preparation of GLP-1RA (group A; n = 33 and group B; n = 37).

The degree of decrease in the levels of fasting blood glucose, mean blood glucose, mean amplitude of glycemic excursions, total cholesterol, triglycerides, tumor necrosis factor-α, interleukin-6, and high-sensitivity C-reactive protein after treatment in group A was higher than that in group B (P < 0.05), whereas the 2-h postprandial blood glucose levels decreased more so in group B than in group A (P < 0.001). However, there were no statistically significant differences in the levels of glycated hemoglobin, standard deviation of blood glucose, coefficient of variation, absolute mean of daily differences, percentage of time with 3.9 mmol/L < glucose < 10 mmol/L, and high- and low-density lipoproteins between the two groups (P > 0.05). The incidence of adverse reactions was significantly lower in group A than in group B (P < 0.05).

The effect of the weekly preparation of GLP-1RA in controlling blood glucose levels in the patients, suppressing inflammation, and reducing adverse reactions was significantly higher than that of the daily preparations, which is worthy of clinical promotion.

The role of pescadillo1 (PES1) in regulating vascular permeability has been unknown. This study probes the role of PES1 and its mediated molecular mechanism in modulating vascular hyperpermeability in diabetic mice. Male C57BL/6J and db/db mice were fed a standard diet and a ketogenic diet (KD). Meanwhile, mouse vascular endothelial cells (MVECs) were treated with β-hydroxybutyric acid (β-HB), Pes1 siRNA or a Pes1 overexpression plasmid. Additionally, knockout (KO) of Pes1 in mice was applied. After 12 weeks of feedings, enhanced vascular PES1 expression in diabetic mice was inhibited by the KD. The suppression of PES1 was also observed in β-HB-treated MVECs. In mice with Pes1 KO, the levels of vascular VEGF and PES1 were attenuated, while the levels of vascular VE-cadherin, Ang-1 and Occludin were upregulated. Similar outcomes also occurred after the knockdown of Pes1 in cultured MVECs, which were opposite to the effects induced by PES1 overexpression in MVECs. In vitro and in vivo experiments showed that high glucose concentration-induced increases in vascular paracellular permeability declined after MVECs were treated by β-HB or by knockdown of Pes1. In contrast, increases in vascular permeability were induced by overexpression of Pes1, which were suppressed by coadministration of β-HB in cultured endothelial cells. Similarly declines in vascular permeability were found by Pes1 knockdown in diabetic mice. Mechanistically, β-HB decreased PES1-facilitated ubiquitination of VE-cadherin. The KD suppressed the diabetes-induced increase in PES1, which may result in vascular hyperpermeability through ubiquitination of VE-cadherin in type 2 diabetic mice.

The ketogenic diet (KD) is a potential nutritional therapy that is frequently utilized in various conditions. More and more studies are being done on KD in recent years. However, as far as we know, few studies have made an effort to offer a thorough synthesis and assessment of this topic. This paper aims to do a rigorous and thorough evaluation of the knowledge structure, development trend, and research hotspot of scientific outputs connected to KD. The bibliographic records connected to KD from January 1, 2001 to April 22, 2022 were collected using the core collection database of Web of Science. The complex data input, that consisted of the amount of publications, journals, authors, institutions, countries, keywords and cited references, was generated and analyzed visually using CiteSpace. A total of 2676 literatures on the KD were published between 2001 and 2022. The most KD-related publications were found in Epilepsia and Epilepsia Research. The authors with the most KD-related papers are Kossoff EH and Rho J. The United States is the country with the most publications, and Johns Hopkins University, Johns Hopkins University Hospital, and Johns Hopkins Medical Institutions are the institutions with the most articles. The high frequency keywords are "KD," "ketone body," "children," "efficacy," "weight loss," "low carbohydrate diet," "metabolism," "epilepsy," "beta hydroxybutyrate," and "modified atkins diet." The 2018 study by Kossoff EH on epilepsia and the 2017 study by Puchalska P on ketone body metabolism earned 127 and 114 citations, respectively. The results of this bibliometric analysis provide information on the state and trends in KD and may be used by researchers to pinpoint hot issues and discover new areas of study.

Since daily dietary habits can affect cognitive function, dietary patterns such as the Mediterranean-DASH Intervention for Neurodegenerative Delay diet have been proposed as interventions to slow cognitive decline. However, because dietary habits vary widely among different food cultures, it is necessary to establish dietary pattern intervention methods that are appropriate for each population. Therefore, in this study, the dietary patterns of elderly Japanese individuals were classified using cluster analysis, and their relationship with cognitive function was investigated. We then modeled the dietary patterns and applied them to another cohort of elderly Japanese individuals to determine whether differences in dietary patterns could predict cognitive decline. One hundred and fifty older adults ≥ 65 years of age in the community were recruited. Their daily food intake and cognitive function were measured using the brief-type self-administered diet history questionnaire and Montreal Cognitive Assessment, respectively. K-means cluster analysis identified a high-carbohydrate (HC) dietary pattern with high cereal intake and a protein-balanced (PB) dietary pattern with high intake of legumes, vegetables, seafood, meat, and eggs. Cognitive function was significantly higher in the PB group than in the HC group. Furthermore, to classify the new data into HC and PB patterns, a classification model was created by discriminant analysis using food groups with significantly different intakes among dietary patterns. Next, we recruited 267 new older adults ≥ 65 years of age and measured food intake and cognitive function assessed using the memory performance index score. Individuals with cognitive decline were identified and their detailed cognitive functions were assessed using the neurocognitive index score. Cognitive function was significantly impaired in the HC pattern in both the general elderly and cognitively impaired cohorts. These findings suggest that a dietary pattern of low carbohydrate and high protein intake is associated with good cognitive function in elderly Japanese individuals. Classification by these dietary patterns can predict cognitive reservation in community-dwelling older adults.

The exponentially growing frequency of diagnosing diabetes mellitus means that a verification of the previous dietetic approach to treating the disease seems justified. The simultaneous growth of interest in the ketogenic diet and the development of knowledge in this field have contributed to the increasingly frequent application of the ketogenic diet in diabetes treatment. This paper also deals with that issue; its aim includes an extensive analysis of the influence of the ketogenic diet on the prophylaxis and treatment of diabetes. The paper has been prepared based on a wide, meticulous analysis of the available literature on the subject. Among other findings, a favorable effect of that nutrition model has been demonstrated on the values of glycated hemoglobin, glucose, insulin, or other metabolic parameters in diabetes patients. The effect of the ketogenic diet on the pharmacotherapy of type 1 and type 2 diabetes has been presented and compared with the standard nutritional management plan recommended for that disease. Further research is needed in this field, especially studies with a long follow-up period. The discussed articles report interesting therapeutic advantages to the ketogenic diet in comparison with standard diets.

Dietary risk factors play a fundamental role in the prevention and progression of atherosclerosis and PAD (Peripheral Arterial Disease). The impact of nutrition, however, defined as the process of taking in food and using it for growth, metabolism and repair, remains undefined with regard to PAD. This article describes the interplay between nutrition and the development/progression of PAD. We reviewed 688 articles, including key articles, narrative and systematic reviews, meta-analyses and clinical studies. We analyzed the interaction between nutrition and PAD predictors, and subsequently created four descriptive tables to summarize the relationship between PAD, dietary risk factors and outcomes. We comprehensively reviewed the role of well-studied diets (Mediterranean, vegetarian/vegan, low-carbohydrate ketogenic and intermittent fasting diet) and prevalent eating behaviors (emotional and binge eating, night eating and sleeping disorders, anorexia, bulimia, skipping meals, home cooking and fast/ultra-processed food consumption) on the traditional risk factors of PAD. Moreover, we analyzed the interplay between PAD and nutritional status, nutrients, dietary patterns and eating habits. Dietary patterns and eating disorders affect the development and progression of PAD, as well as its disabling complications including major adverse cardiovascular events (MACE) and major adverse limb events (MALE). Nutrition and dietary risk factor modification are important targets to reduce the risk of PAD as well as the subsequent development of MACE and MALE.

Ketogenic diets appear promising for obesity, diabetes, cancer, and other illnesses. Because older patients are more likely to contend with such illnesses and because of a paucity of dietary outcomes among these patients, we examined ketogenic diets in older patients.This multisite study focused on patients (≥65 years of age) on a ketogenic diet. Medical records were identified with the keywords "keto," "ketogenic," and "Atkins." Records were reviewed in detail with extraction of direct quotations to substantiate observations.We report on 200 consecutive patients with a median age of 70 years. Reasons for diet included weight loss, diabetes, and cancer; the majority remained on the diet for >1 month. In 134 (67%: 95% confidence interval: 60, 73%), the ketogenic diet appeared beneficial: 93 of 117 (79%) who sought weight loss lost weight ("She has lost 15 pounds and plans to lose another 8"); 36 of 67 (54%) who sought glucose control appeared to achieve the latter ("He has gone on a ketogenic diet and has been able to bring his sugars down significantly"); and 5 of 8 (63%) who sought improved cancer outcomes appeared to derive them ("He attributes part of the control of his cancer and increased QOL to adopting the keto for cancer diet"). Adverse events occurred in 30 patients (15%): dyslipidemia (n = 14), constipation (n = 9), sub-therapeutic international normalized ratio (n = 3), pancreatitis (n = 2), diarrhea (n = 1), and fatigue (n = 1).Trials that test ketogenic diets for a variety of illnesses should enroll older adults.

To assess the pleiotropic effects of ketogenic diets (KD) on glucose control, changes in medication, and weight loss in individuals with type 2 diabetes, and to evaluate its practical feasibility RECENT FINDINGS: KD results in improved HbA1c already after 3 weeks, and the effect seems to persist for at least 1 year. This is associated with a reduction in glucose-lowering medications. The weight loss observed after a short time period seems to be maintained with a long-term diet. Adequate support (supportive psychological counseling, enhancing positive affectivity, reinforcing mindful eating) is necessary to achieve a benefit and to assure adherence. Despite the documented decrease in HbA1, a definitive causal effect of KD remains to be proven. KD should be performed under strict medical supervision. Future research should clarify how compliance can be maximized and how ketosis can be optimally monitored.

Insulin mimic can promote transporting glucose to muscle tissue and accelerate glucose consumption. It is commonly occurring in many functional foods or traditional medicines. Anti-diabetes molecules from food sources are highly safe and suitable for long-term use to prevent early diabetes. The leaves of Acer truncatum was found glucose uptake promotion in our phenotypic screening. However, its bioactive components and mechanism are still unclear. We collected leaves from trees of different ages (2, 3, 4, 7 and 11 years old) and profiled the ingredients by LC-MS/MS. The essential active component (myricitrin) was acquired following bio-guide on a whole organism Zebrafish (Danio rerio). Its content in the leaves was not affected by tree ages. Therefore, myricitrin can serve as a quality mark for functional foods derived from A. truncatum leaves. The transcriptomic and metabolomic analysis in Zebrafish explored the differentially expressed genes and metabolites. Based on joint-pathway enrichment and qRT-PCR verification, the critical bioactive component myricitrin was found to affect toll-like receptors signaling pathways to regulate glucose uptake. Our findings disclosed a bioactive marker (myricitrin) in A. truncatum leaves and explored its regulation mechanism, which rationalized the anti-diabetes function of the herbal food.