Search Results (1,333)

Obesity is an epidemic that currently impacts many nations. The persistence of this disease is shaped by both genetic and epigenetic factors that extend beyond calorie balance. Research in the past year has revealed that epigenetic and cellular memory within adipose tissue can predispose individuals to weight regain after initial fat loss, as shown by studies indicating persistent transcriptional and chromatin changes even after fat mass reduction. Independent studies also demonstrate long-lasting metabolic shifts, such as those triggered by glucose-dependent insulinotropic polypeptide receptor (GIPR)-induced thermogenesis and sarcolipin (SLN) stabilization that also support a form of “metabolic memory” that is associated with sustained weight loss. At the neural level, rare variants in synaptic genes like BSN (Bassoon presynaptic cytomatrix protein), a presynaptic scaffold protein, and APBA1 (amyloid beta precursor protein binding family A member 1), a neuronal adaptor involved in vesicular trafficking, disrupt communication in feeding circuits, elevating obesity risk and illustrating how synaptic integrity influences food intake regulation. Similarly, the spatial compartmentalization of metabolic signaling within neuronal cilia is emerging as crucial, with cilia-localized receptors G protein-coupled receptor 75 (GPR75) and G protein-coupled receptor 45 (GPR45) exerting opposing effects on energy balance and satiety. Meanwhile, genome-wide association studies (GWAS) have advanced through larger, more diverse cohorts and better integration of environmental and biological data. These studies have identified novel obesity-related loci and demonstrated the value of polygenic risk scores (PRS) in predicting treatment responses. For example, genetic variants in GLP-1R (glucagon-like peptide-1 receptor) and GIPR (glucose-dependent insulinotropic polypeptide receptor) may modulate the effectiveness of incretin-based therapies, while PRS for satiation can help match individuals to the most appropriate anti-obesity medications. This review focuses on studies in the last two years that highlight how advances in obesity genetics are driving a shift toward more personalized and mechanism-based treatment strategies. Full article

Background/Objectives: Gut microbiota has been implicated in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD) and cardiovascular disease (CVD). This study aimed to identify associations between gut dysbiosis and MASLD, regarding body mass index (BMI) and subclinical coronary atherosclerosis (SCA). Methods: We conducted a cross-sectional study of 202 patients with MASLD who had no previous history of CVD. The severity of MASLD was evaluated using a magnetic resonance imaging-based method, and SCA was measured by assessing coronary artery calcification (CAC). Gut microbiota was assessed in fecal specimens using sequencing targeting the V4 region of the 16S rRNA gene. Results: Our results demonstrated that gut microbial profiles between low- and high-BMI groups (<30 vs. ≥30 kg/m²) differed significantly in beta-diversity, but not in alpha-diversity indices. At the genus level, we identified Megamonas, Sutterella, Catenibacterium, and Odoribacter, enriched in the high BMI group. Compared to the low CAC group (<100 AU), MASLD patients with high CAC scores (≥100 AU) exhibited enrichment in Ruminococcus gnavus, Bacteroides, and Lachnoclostridium, along with depletion of several short-chain fatty acid (SCFA)-producing bacteria, such as Faecalibacterium. Multivariate analysis demonstrated that older age, the presence of diabetes, high BMI, fibrosis stage F3-F4, and high plasma trimethylamine oxide (TMAO) levels were independently associated with a high CAC score in patients with MASLD. Conclusions: These data indicated that gut dysbiosis and related metabolites, in association with advanced liver disease, were potential contributors to the progression of SCA in obese patients with MASLD. Full article

Background/Objectives: Obesity is a chronic metabolic disorder characterized by the excessive expansion of adipose tissue and impaired energy homeostasis. Natural products, such as plant extracts, are gaining attention as potential anti-obesity agents. This study aimed to evaluate and compare the anti-obesity effects of ginger (Zingiber officinale Roscoe) extract alone and as a mixture with long pepper (Piper longum L.) extract in a mouse model of high-fat diet-induced obesity. Methods: Male ICR mice were fed a high-fat diet to induce obesity and were orally administered ginger extract (60 mg/kg/day) or a 1:1 mixture of ginger and long pepper extracts (30 mg/kg/day each) for 8 weeks. Body weight, fat mass, glucose tolerance, and serum lipid levels were measured. Results: Ginger extract alone significantly reduced body weight gain and visceral and subcutaneous fat accumulation and improved glucose homeostasis and serum lipid profiles compared to the high-fat diet group. These effects were more pronounced than those observed with the mixture group. Ginger extract upregulated lipolytic markers via activation of the protein kinase A (PKA) signaling pathway and increased expression of uncoupling protein 1 (UCP1), indicating browning of white adipose tissue. Conclusions: Ginger extract alone exhibited significant anti-obesity effects compared to the mixture with long pepper extract. These findings suggest that ginger extract may serve as a promising natural agent for the prevention and management of obesity-related metabolic dysfunction. Full article

Obesity represents a significant global public health challenge, which not only elevates the risk of mortality but also increases the likelihood of chronic diseases. The ongoing obesity epidemic has led to a growing recognition of the detrimental effects of excessive adipose tissue accumulation on male reproductive health. Substantial evidence indicates that obesity adversely affects sperm quality, thereby impairing male fertility. Specifically, obesity is associated with compromised spermatogenesis, erectile dysfunction, and detrimental effects on offspring fertility parameters. These effects are mediated through various mechanisms, including alterations in the hypothalamic–pituitary–gonadal axis, inflammation within the reproductive system, localized caloric excess in reproductive tissues, epigenetic modifications, disruptions in gut microbiota, and heightened oxidative stress levels. While the molecular alterations associated with obesity have been extensively documented, the precise mechanisms by which obesity influences male reproductive function remain inadequately understood. This article aimed to review the classification and distribution of adipose tissue in obesity, the impact of obesity on male fertility, and the potential mechanisms through which obesity affects male reproductive health, thereby offering insights into the prevention and treatment of obesity-related male fertility issues. Full article

Background: Type 2 diabetes (T2D), the most common form of diabetes, is associated with a significantly elevated risk of cardiovascular and cerebrovascular complications. However, circulating metabolic signatures that reliably predict the transition to insulin resistance, and are potentially linked to increased vascular risk, remain incompletely characterized. Rodent models, particularly those induced by a high-fat diet (HFD) combined with low-dose streptozotocin (STZ), are widely used to study the progression of T2D. However, the systemic metabolic shifts associated with this model, especially at the plasma level, are poorly defined. Methods: In this study, we performed untargeted liquid chromatography–mass spectrometry (LC-MS)-based metabolomic profiling on plasma samples from control, HFD-only (obese, insulin-sensitive), and HFD + STZ (obese, insulin-resistant) C57BL/6 mice. Results: In the HFD + STZ cohort, plasma profiles showed a global shift toward lipid classes; depletion of aromatic and branched-chain amino acids (BCAAs); accumulation of phenylalanine-derived co-metabolites, consistent with gut–liver axis dysregulation; elevations in glucose, fructose-6-phosphate, and nucleoside catabolites, indicating impaired glucose handling and heightened nucleotide turnover; increased free fatty acids, reflecting membrane remodeling and lipotoxic stress; and higher cAMP, thyroxine, hydrocortisone, and uric acid, consistent with endocrine and redox imbalance. By contrast, HFD-only mice exhibited elevations in aromatic amino acids and BCAAs relative to controls, a pattern compatible with early obesity-associated adaptation while insulin signaling remained partially preserved. KEGG analysis revealed disturbances in carbohydrate metabolism, amino acid degradation, nucleotide turnover, and hormone-related pathways, and HMDB mapping linked these changes to T2D, obesity, heart failure, and renal dysfunction. Conclusion: Collectively, these findings delineate insulin resistance-specific plasma signatures of metabolic inflexibility and inflammatory stress in the HFD + STZ model, distinguishing it from HFD alone and supporting its utility for mechanistic studies and biomarker discovery. Importantly, this plasma metabolomics study shows that insulin-sensitive and insulin-resistant states exhibit distinct variation in circulating metabolites and cardiovascular risk factors, underscoring the translational value of plasma profiling. Full article

Polyphenols have been widely recognized for their potential anti-obesity effects. This study aimed to evaluate the impact of a polyphenol compound-epigallocatechin-3-gallate, quercetin, and rutin (EQR) on obesity-related parameters and gut microbiota composition. After four weeks of high-fat diet (HFD) induction, the obese Wistar male rats received EQR treatment for an additional four weeks. EQR supplementation significantly reduced body weight gain, feed efficiency, adipose tissue accumulation, and liver lipid content in obese rats. Additionally, it enhanced fecal short-chain fatty acid (SCFA) levels and modulated gut microbiota composition. Specifically, EQR treatment significantly induced Fusobacteria, Fusobacteriaceae, Christensenellaceae, Christensenellaceae R-7 group, Lachnoclostridium, Enterorhabdus, and Parvibacter levels and reduced Deferribacteres and Mucispirillum levels. Gene expression analysis in liver, white adipose tissue (WAT), and brown adipose tissue (BAT) revealed that EQR upregulated the expression of liver PPAR-α, WAT SIRT-1, and BAT PGC-1α, while downregulating liver PPAR-γ, liver FATP-1, and WAT FAS, indicating its role in promoting fatty acid oxidation and thermogenesis, as well as suppressing lipid synthesis and transport. In conclusion, EQR demonstrated significant anti-obesity effects by modulating gut microbiota and lipid metabolism, suggesting its potential as a functional ingredient for obesity management. Full article

Background/Objectives: Gestational diabetes mellitus (GDM) complicates approximately 14% of pregnancies worldwide, its prevalence rising with increasing maternal age and obesity. While maternal hyperglycemia is traditionally associated with fetal overgrowth and large-for-gestational-age (LGA) neonates, emerging evidence indicates that GDM may also contribute to small-for-gestational-age (SGA) outcomes. Methods: A comprehensive literature search was conducted using multiple databases, including PubMed, Web of Science, and ScienceDirect, to identify studies related to gestational diabetes mellitus, fetal growth outcomes such as small for gestational age and large for gestational age, and associated pathophysiological mechanisms. Results: This narrative review explores the mechanisms by which GDM influences fetal growth, emphasizing the dual risk of excessive and restricted intrauterine growth. Fetal macrosomia typically results from chronic maternal hyperglycemia, leading to increased transplacental glucose delivery and fetal hyperinsulinemia. In contrast, SGA outcomes are a consequence of vascular and endothelial dysfunction, placental insufficiency, or excessively restrictive glycemic control that limit the availability of nutrients. Both extremes of fetal growth carry a myriad of significant perinatal and long-term metabolic risks. Conclusions: Understanding the diverse pathways through which GDM affects fetal growth is essential for developing individualized clinical strategies. Full article

Background/Objectives: The relationship between systemic health and ocular diseases is well-documented, with various body metrics potentially playing significant roles in the pathogenesis of cataracts, glaucoma, and age-related macular degeneration (AMD). However, comprehensive studies linking these metrics with ocular health are sparse. This study aims to explore the associations between height, weight, waist circumference, and BMI with the prevalence and current status of cataracts, glaucoma, and AMD in a large cohort. Methods: We used data from Korean National Health and Nutrition Survey (KNHANES 2015–2021), a national, cross-sectional health examination and survey, for which representative data on the health, nutritional status, and physical activities of the Korean general population are collected by the Korea Centers for Disease Control and Prevention (KCDC). We compared height, weight, waist circumference, and BMI among patients with diagnosed and current cataracts, glaucoma, and AMD versus those without these conditions. Statistical analyses included t-tests and Pearson correlation analyses to examine the relationships between body metrics and ocular diseases. Results: Our findings indicate that shorter height and lower weight are associated with diagnosed cataracts and glaucoma but not with their current status. A greater waist circumference was observed in patients with diagnosed cataracts, glaucoma, and AMD compared to controls, suggesting central obesity as a potential associated factor. No significant differences in BMI were found in patients with current ocular diseases. Additionally, certain body metrics were correlated with refractive errors and visual acuity, suggesting broader implications for ocular health. Conclusions: The study highlights significant associations between body metrics and the risk of developing cataracts, glaucoma, and AMD. AMD was found to be more closely related to systemic diseases, such as diabetes and hypertension, than to body metrics. These findings suggest that interventions targeting obesity and metabolic health could potentially reduce the risk or severity of these common ocular conditions. Further research is needed to confirm these relationships and explore underlying mechanisms. Full article

Obesity is strongly associated with an increased risk of heart failure. Recent studies indicate that epicardial adipose tissue plays a critical role in the development of obesity-related cardiomyopathy. This distinct visceral fat depot, located between the myocardium and the visceral pericardium, is involved in direct cross-talk with the adjacent myocardium, influencing both its structural integrity and electrophysiological function. This review aims to provide an up-to-date overview of the morphological, metabolic, immunological, and functional alterations of this adipose compartment in the context of obesity, and to explore its contribution to the pathogenesis of heart failure. Moreover, the article synthesizes current evidence on the potential cardioprotective effects of emerging anti-obesity pharmacotherapies—particularly GLP-1 and dual GLP-1/GIP receptor agonists—on metabolic pathways associated with epicardial fat that are implicated in obesity-induced cardiomyopathy. Further clinical trials are required to clarify the impact of these therapies on the course and prognosis of heart failure, as well as on the epidemiology and societal burden of the disease. Full article

Obesity is a global problem, increasing interest in adipose tissue (AT) biology. One of the techniques for analyzing visceral adipose tissue (VAT) and phase angle (PhA) is bioelectrical impedance analysis (BIA). PhA is considered an indicator of cell integrity and health and can be a prognostic marker in diseases and clinical conditions. The aim of the study was to assess the nutritional status and level of visceral fat area (VFA) to investigate the association between phase angle (PhA) and content of visceral adipose tissue in young adults. Our cohort consisted of 292 young adults (18–25), both sexes. Body composition was performed by the inBody 770 analyzer. We confirmed the relationship between PhA and gender (female vs. male: 5.3 vs. 6.5; p < 0.001) and BMI (female vs. male: 22.56 kg/m² vs. 23.78 kg/m²; p = 0.013). A total of 20.2% of examined students had a VFA of more than 100 cm² (Visceral Obesity, VO). We demonstrated a dependence between VFA and PhA value (PhA = 5.4 (VFA > 100 cm²) vs. PhA = 5.7 (VFA < 100 cm²), p = 0.003). Students with VO and normal BMI had a significantly lower PhA than those with VO and BMI ≥ 30 kg/m² (p = 0.021). PhA may be a useful indicator for assessing nutritional status and physiological differences related to gender, BMI, and visceral obesity in young adults. Full article

Background/Objectives: Adolescence is a critical period for the early detection of metabolic syndrome (MetS), a condition that increases the risk of cardiometabolic diseases in adulthood. Timely identification of at-risk adolescents enables targeted prevention strategies. This study aimed to analyze the discriminative capacity and accuracy of six biochemical and/or anthropometric indices related to lipid metabolism and adiposity for the early detection of MetS in a sample of Spanish adolescents. Methods: A cross-sectional study carried out according to the STROBE guidelines. A sample of 981 adolescents aged 11–16 years old were randomly recruited from schools in Southeastern Spain. The presence or absence of MetS was determined according to the International Diabetes Federation criteria. The following biochemical and/or anthropometric indices were evaluated: triglyceride glucose index, visceral adiposity index, logarithm children’s lipid accumulation product, triglyceride glucose-body mass index, triglyceride glucose-waist circumference, and triglyceride glucose-waist-to-hip ratio. Results: The triglyceride glucose-waist-to-hip ratio and triglyceride glucose-body mass index parameters were the strongest indicators associated with MetS in boys and girls, respectively, after adjusting for several factors. Moreover, all evaluated indices showed optimal AUC values, with the visceral adiposity index and triglyceride glucose-waist circumference index exhibiting the highest discriminative capacity in both genders. Conclusions: The evaluated biochemical and anthropometric indices—particularly visceral adiposity index and triglyceride-glucose-waist circumference—show promise as accessible biomarkers for identifying adolescents at metabolic risk. These indices may serve as practical tools in preventive health strategies aimed at improving metabolic health by screening adolescents at risk of MetS, thereby helping to reduce the future burden of non-communicable diseases. Full article

Background: Asprosin is a relatively recently discovered glucogenic adipokine secreted during fasting that plays an important role in various biochemical processes in the body, including those connected with obesity and insulin resistance. The aim of this exploratory study was to investigate the associations between selected hormonal, anthropometric, and lifestyle-related parameters and serum asprosin concentration. As studies concerning fertility and asprosin have so far been limited to men or women with PCOS, its role in the general female population remains largely unexplored. The direction of this exploration was thus pointed toward possible connections with female fertility. Methods: The case-control study group included 56 women of reproductive age (25–42 years), who were patients of the Reproductive Health Clinic and the Clinic of Endocrinology, Diabetology, and Internal Medicine of the Medical University of Białystok, Poland. The levels of selected hormones, including anti-Müllerian hormone (AMH), estradiol, sex hormone-binding globulin (SHBG), and testosterone, body composition parameters, and a lifestyle parameter—night fasting duration—were assessed to test their associations with serum asprosin concentration. Results: A weak negative correlation was found between AMH level and serum asprosin concentration, suggesting a potential link between asprosin and ovarian reserve. Furthermore, a moderate positive correlation was found between the percentage of total body water (TBW) and serum asprosin concentration. No significant associations were observed between the levels of the other tested hormones and serum asprosin concentration, or between body composition parameters or night fasting duration and serum asprosin concentration. The multivariate model designed in the study shows that AMH, TBW, and night fasting duration explain 23.4% of asprosin variability. Conclusions: Although the nature of the study is exploratory, the findings indicate that the role of asprosin in the female population—particularly its role in fertility—requires further research. Not only is the number of available studies on asprosin insufficient, but the results of this study partly contradict what is known about the hormone from previous studies, which were largely performed with male cohorts. In addition, the results of this study suggest that asprosin may indeed be involved in mechanisms related to female fertility, particularly those connected with ovarian reserve. Nevertheless, studies performed in larger, more homogeneous populations are necessary to confirm the role of asprosin in women, including its association with female fertility. Full article

Background/Objectives: Prior research suggest that poor working memory significantly contributes to the growth of overweight and obesity. This study investigated the behavioral and neural aspects of general and food-specific working memory in females with overweight or obesity (OW/OB). Method: A total of 54 female participants, with 26 in the OW/OB group and 28 in the normal-weight (NW) group, completed a general and a food-related two-back task while an EEG was recorded. Results: In the general task, the OW/OB group showed significantly poorer performance (higher IES) than the NW group (p = 0.018, η² = 0.10), with reduced theta power during non-target trials (p = 0.040, η² = 0.08). No group differences were found for P2, N2, or P3 amplitudes. In the food-related task, significant group × stimulus interactions were observed. The OW/OB group showed significantly higher P2 amplitudes in high-calorie (HC) versus low-calorie (LC) food conditions (p = 0.005, η² = 0.15). LPC amplitudes were greater in the OW/OB group for HC targets (p = 0.036, η² = 0.09). Alpha power was significantly lower in OW/OB compared to NW in HC non-targets (p = 0.030, η² = 0.09), suggesting a greater cognitive effort. Conclusions: These findings indicate that individuals with OW/OB exhibit deficits in general working memory and heightened neural responses to high-calorie food cues, particularly during non-target inhibition. The results suggest an interaction between reward salience and cognitive control mechanisms in obesity. Full article

Background/Objectives: The receptor for advanced glycation end products (RAGEs) has been implicated in obesity and metabolic dysfunction. However, its precise role in diet-induced obesity remains unclear. Methods: In this study, we investigated the metabolic consequences of RAGE knockout (RAGE KO) in mice subjected to a Western diet (WD). Results: Our findings demonstrate that RAGE KO mice remained significantly leaner than their wild-type (WT) counterparts when fed a WD, exhibiting reduced body weight gain and smaller adipocyte size. Indirect calorimetry revealed that RAGE KO mice had increased oxygen consumption and locomotor activity compared to WT mice, indicating enhanced energy expenditure. Mitochondrial respiration assays indicated significantly greater oxygen consumption in RAGE KO animals. Additionally, systemic inflammation markers, such as TNF-α, were significantly lower in RAGE KO mice when fed a WD, indicating a reduction in diet-induced inflammatory responses. Conclusions: These findings suggest that RAGE plays a key role in metabolic homeostasis, and its deletion confers resistance to obesity and metabolic disruption induced by a Western diet. Targeting RAGE may provide a novel therapeutic approach for combating obesity and related metabolic disorders. Full article

Metabolic dysfunction-associated fatty liver disease (MASLD) is a chronic, non-communicable spectrum of diseases characterized by lipid accumulation. It is often asymptomatic, and its prevalence varies by region, age, gender, and economic status. It is estimated that 25% of the world’s population currently suffer from MAFLD, and 20 million patients will die from MAFLD-related diseases. In the last 20 years, tea and anti-obesity research have indicated that regularly consuming tea decreases the risk of cardiovascular disease, stroke, obesity, diabetes, and metabolic syndrome (MeS). In this review, we aimed to present studies concerning the influence of matcha extracts and epigallocatechin-3 gallate (EGCG) supplements on metabolic functions in the context of MAFLD in human and animal studies. The published data show promise. In both human and animal studies, the beneficial effects on body weight, cholesterol levels, and liver metabolism and function were noted, even in short-period experiments. The safety levels for EGCG and green tea extract consumption are marked. More experiments are needed to confirm the results observed in animal studies and to show the mechanisms by which green tea exerts its effects. The preliminary data from research concerning microbiota or epigenetic changes observed after polyphenols and green tea consumption need to be expanded. To improve the efficiency and availability of green tea or supplement consumption as a treatment for MAFLD patients, more research with larger groups and longer study durations is needed. Full article