Search Results (1,497)

The relationship between epilepsy, obesity, and metabolic syndrome (MetS) has emerged as a rapidly evolving area of neurobiology inquiry. Emerging evidence suggests that epilepsy extends beyond neuronal hyperexcitability, reframing it as a systemic condition characterized by significant metabolic dysregulation. Converging supports a bidirectional relationship while seizures, antiseizure medications (ASM), and neuroinflammation induce exacerbate potentiate epileptogenesis through shared molecular pathways. At the cellular level, chronic epileptic activity induces oxidative stress, mitochondrial dysfunction, and the activation of microglia and astrocytes. This, in turn, leads to the release of pro-inflammatory cytokines including TNF-α, IL-1β, and IL-6. These mediators traverse the blood-brain barrier (BBB), subsequently modifying insulin signaling, and disrupting glucose homeostasis, which collectively fosters a pro-inflammatory and insulin-resistant environment. Furthermore, antiseizure medications such as valproate can exacerbate these effects by directly impairing insulin receptor signaling and altering adipokine production, ultimately contributing to weight gain and systemic metabolic dysregulation. Obesity and MetS induce neuroinflammatory and excitotoxic states that promote seizure onset via leptin resistance, reduced adiponectin levels, and compromised AMP-activated protein kinase (AMPK) signaling. Emerging evidence emphasizes the gut-brain axis as a crucial regulator in this reciprocal interaction. Dysbiosis, altered microbial metabolites (e.g., short-chain fatty acids), and heightened intestinal permeability facilitate systemic inflammation and BBB disruption, enhancing neuronal excitability. Insulin resistance in the brain disrupts synaptic transmission, impairs mitochondrial biogenesis, and compromises redox equilibrium, perpetuating a pathological cycle linking metabolic stress to epileptic activity. This review synthesizes the cellular, molecular, and systemic pathways connecting epilepsy, obesity, and MetS, and proposes that epilepsy be reconceptualized as a neuro-metabolic disorder. Insights into these convergent pathways provide a rationale for novel therapeutic strategies that simultaneously target seizure control and metabolic regulation, encompassing microbiota modulation, antioxidant therapy, and insulin-sensitizing interventions with the overarching aim of restoring neuro-metabolic homeostasis. Full article

High-intensity interval training (HIIT) is widely used to enhance aerobic performance in combat sports, yet the molecular mechanisms underlying training adaptation remain unclear. This study investigated whether changes in circulating myokine–adipokine profiles are associated with aerobic performance adaptation following sport-specific HIIT in trained combat athletes. Forty elite male kickboxers were randomly assigned to a HIIT group (n = 20) or a control group (n = 20). The HIIT group performed an eight-week sport-specific HIIT program in addition to regular training, whereas the control group maintained their usual training routines. Aerobic capacity was assessed using maximal oxygen uptake (VO₂max). Fasting blood samples were collected before and after the intervention to determine circulating apelin, irisin, brain-derived neurotrophic factor (BDNF), myostatin, fibroblast growth factor-21 (FGF21), and adiponectin concentrations. VO₂max increased significantly in the HIIT group compared with the control group (+2.10 ± 1.10 vs. +0.35 ± 0.80 mL·kg⁻¹·min⁻¹, p = 0.001). In addition, apelin, irisin, BDNF, FGF21, and adiponectin increased, whereas myostatin decreased following the intervention. Changes in myostatin were negatively correlated with improvements in VO₂max (r = −0.55, p = 0.007), suggesting that reductions in myostatin may serve as a molecular indicator of aerobic adaptation in combat athletes. Full article

Obesity represents a heterogeneous metabolic disorder characterized by substantial interindividual variation in inflammatory status, insulin sensitivity, and cardiometabolic risk. Traditional anthropometric measures fail to capture this metabolic diversity, limiting risk stratification and personalized intervention strategies. This review critically examines nutritional and metabolic biomarkers that reflect the physiological dysregulation underlying obesity, including adipokines (leptin, adiponectin, resistin), inflammatory markers (C-reactive protein, interleukin-6, TNF-α), insulin resistance indices (HOMA-IR, fasting insulin, HbA1c), and lipid metabolism indicators (LDL cholesterol, triglycerides, HDL cholesterol, and liver enzymes such as ALT and GGT). Among these, elevated CRP, reduced adiponectin, and increased HOMA-IR have demonstrated the strongest clinical utility for early metabolic risk identification. We further evaluate emerging biomarkers—including circulating microRNAs, gut microbiota-derived metabolites (short-chain fatty acids, TMAO, lipopolysaccharides), and bile acid profiles—which offer additional mechanistic insight into diet–microbiome–host interactions. We systematically assess the mechanistic basis, clinical relevance, and nutritional modulation of each biomarker class, emphasizing how dietary composition—particularly fatty acid quality, fiber intake, and overall dietary patterns such as the Mediterranean diet—influences biomarker profiles and metabolic outcomes. Furthermore, we explore how biomarker-based phenotyping enables precision nutrition approaches by identifying individuals most likely to benefit from specific dietary interventions. Integration of multi-biomarker panels with clinical and genetic data holds promise for advancing from population-based dietary guidelines toward individualized nutrition strategies that optimize metabolic health and prevent obesity-related complications. Future research should prioritize validating biomarker-guided intervention frameworks, establishing standardized thresholds across diverse populations, and developing clinically implementable tools for personalized nutritional medicine. Full article

Myeloid differentiation factor 88 (MyD88) signaling plays a central role in inflammatory pathway activation. Adipose-derived interleukin-10 (IL-10), which is induced by insulin and lipopolysaccharides, suppresses hepatic glucose production. This study investigated the role of MyD88/IL-10 signaling in diabetes-induced systemic inflammation and hepatic gluconeogenesis. Stromal vascular fractions (SVFs) were isolated from the adipose tissue of Lepr^db/db and Lepr^db/dbMyD88^−/− mice and treated with IL-10 followed by analysis of inflammatory cytokine expression. IL-10 (10 or 50 ng) was injected into adipose tissue of type 2 DM (T2DM) (Lepr^db/db) mice to investigate its effect on blood dipeptidyl peptidase-4 (DPP4) activity, insulin resistance, and hepatic gluconeogenic signaling. Hepatic inflammatory markers, gluconeogenic gene expression, and metabolic parameters were assessed. Compared with wild-type mice, Lepr^db/db mice exhibited significantly reduced FOXP3 protein expression and IL-10 levels in adipose tissue, accompanied by increased blood DPP4 activity and adiponectin levels, elevated hepatic inflammatory cytokines, and increased G6pc and Pck1 mRNA expression. In contrast, Lepr^db/dbMyD88^−/− mice showed increased Foxp3 protein and PDGFα mRNA expression, decreased IL-6 and CCL2 mRNA expression in SVFs, increased IL-10 levels in adipose tissue, and lower blood adiponectin and ALT levels. MyD88 deletion also attenuated Kupffer cell accumulation, hepatic inflammatory cytokine expression, and gluconeogenic gene expression. In vitro, IL-10 treatment of SVFs from Lepr^db/db mice significantly reduced IL-6 and CCL2 expression and increased Foxp3 mRNA expression. In vivo, adipose IL-10 injection increased Foxp3 and IL-10 expression, expanded Treg cells in SVFs, and activated hepatic Akt signaling, while suppressing pJNK and pNF-κB signaling. These changes were accompanied by reduced blood DPP4 activity, ALT and adiponectin levels, decreased Kupffer cell-derived inflammatory cytokines, reduced hepatic G6pc and Pck1 expression, and improved glucose tolerance. MyD88 signaling induces adipose IL-6 and CCL2, liver inflammation and gluconeogenesis, and blood DPP4 activity by reducing IL-10 and Foxp3 of adipose tissue in T2DM. Enhancing adipose IL-10 induces Treg expansion, inhibits JNK and NF-κB signaling, and alleviates hepatic gluconeogenesis and insulin resistance. MyD88 inhibition or IL-10 elevation in adipose tissue may represent a novel strategy for metabolic syndrome. Full article

Background/Objectives: Fabry disease (FD) is a lysosomal storage disorder characterized by progressive renal and cardiac involvement and an increased burden of cardiovascular and cerebrovascular events. While cardiac magnetic resonance imaging (CMR) has significantly advanced structural assessment, circulating biomarkers reflecting disease-related cardiac manifestations remain incompletely understood. We therefore investigated adiponectin and leptin, two adipokines involved in inflammatory, metabolic, and fibrotic pathways, in relation to cardiac involvement and analyzed long-term lipid trajectories in FD. Methods: This longitudinal observational study included 49 patients with FD with 149 study visits. Circulating adiponectin, leptin, NT-proBNP, and conventional lipid parameters were assessed longitudinally and stratified by FD-specific therapy status and sex. Multivariable linear regression was performed to evaluate independent associations with log-transformed NT-proBNP values. Results: Adiponectin was positively associated with NT-proBNP, reflecting cardiac involvement, independent of age, sex, BMI, and eGFR (p < 0.001). Higher adiponectin levels were observed in patients with left ventricular hypertrophy or low T1 and those with fibrosis, detected by CMR (p = 0.009 and p < 0.001, respectively). This association was mainly seen in patients receiving FD-specific therapy, raising the question of whether this reflects underlying organ involvement or treatment effects. Leptin demonstrated weaker, inverse associations. Adiponectin, leptin, Triglycerides, total cholesterol, and HDL- and LDL-cholesterol levels remained stable over long-term follow-up, irrespective of FD-specific therapy or sex. Conclusions: In FD, adiponectin appears to be associated with cardiac involvement, and conventional lipid parameters remained unchanged over time. These findings suggest that alterations in adipokines, rather than progressive dyslipidemia, may reflect disease-related cardiac manifestations. Full article

Adiponectin is adipokine exhibiting beneficial metabolic action through lipid and carbohydrate metabolism stimulation, as well as anti-inflammatory action. We have determined the role of adiponectin in gastroprotection against the formation of acute gastric lesions induced by ischemia–reperfusion (I/R). Gastric lesions evoked by I/R are a serious clinical entity; however, the participation of reactive oxygen species (ROS) and lipid peroxidation products and the involvement of nitric oxide (NO), neuropeptides released from sensory afferent nerves, and the hormone gastrin in the potential gastroprotective action of adiponectin remains unknown. Therefore, we determined the interplay between capsaicin-sensitive afferent nerves, the NO/NOS system, lipid peroxidation products, and the expression of pro-inflammatory and antioxidative factors in the gastroprotective action of adiponectin against gastric I/R. injury. Wistar rats was administered with adiponectin in graded doses (1–40 μg/kg i.v.) with or without: (a) blockade of nitric oxide (NO) activity by L-nitro-L-arginine (L-NNA) and (b) deactivation of sensory nerves by capsaicin (125 mg/kg s.c. 10 days before experiment conduction). They were then exposed to 30 min of ischemia by clamping of the celiac artery followed by 3 h of reperfusion after clamp release. After 3 h, the rats were euthanized with pentobarbital and their gastric blood flow (GBF) was determined by laser Doppler flowmetry, their blood was withdrawn to assess plasma gastrin levels, and the area of gastric lesions was measured by planimetry. Gastric biopsy samples were excised to determine gastric mucosal levels of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE). In separate groups of animals with chronic gastric fistula, the effect of adiponectin on gastric acid secretion was determined. Adiponectin dose-dependently reduced the gastric lesions induced by I/R and this effect was accompanied by an increase in GBF. Blockade of NO-synthase with L-NNA (20 mg/kg i.p.) reversed the protective effect and the rise in GBF induced by this adipokine, and both these effects were restored when L-arginine was added to L-NNA. Capsaicin denervation also impeded the beneficial action of adiponectin in rats, but these effects were in part restored when exogenous CGRP was combined with adiponectin. Adiponectin dose-dependently decreased gastric acid secretion, the expression of mRNA for pro-inflammatory cytokines, and MDA plus 4-HNE content, while significantly increasing SOD, GSH and plasma gastrin increments. We conclude that adiponectin exerts gastroprotection against I/R-induced gastric lesions, through mechanisms involving NO and neuropeptides such as CGRP being released from sensory nerves, a decrease in lipid peroxidation (MDA+4-HNE), an increase of antioxidative factors (SOD, GSH), and the inhibition of gastric acid secretion. Full article

Background: Adiponectin is a key adipokine involved in glucose and lipid metabolism. Variants in the CDH13 gene have been consistently associated with circulating adiponectin levels. However, limited evidence is available regarding whether these associations differ according to glucose status. We examined the association between CDH13 rs12596316 and adiponectin levels across fasting blood glucose (FBS) categories in a Korean population. Methods: A total of 4865 participants from the Korean Genome and Epidemiology Study were included. Linear regression under an additive genetic model was used to evaluate the association between rs12596316 and adiponectin levels. Logistic regression under a dominant model was used to assess the association with hypoadiponectinemia. Stratified analyses were performed according to BMI and FBS categories. Results: CDH13 rs12596316 was strongly associated with adiponectin levels (β = −0.59, p = 3.30 × 10⁻³¹). Carriers of the TC/CC genotype had a 1.74-fold higher risk of hypoadiponectinemia compared with TT homozygotes after adjustment for age, sex, and BMI. In stratified analyses, the magnitude of association differed across FBS categories, with a stronger association observed in men with FBS ≥ 126 mg/dL (OR = 3.62, p = 0.009) compared with lower FBS groups. However, formal interaction analyses between genotype and fasting glucose categories were not statistically significant. Conclusions: CDH13 rs12596316 is strongly associated with adiponectin levels in this Korean cohort. The strength of association varied across fasting glucose categories, suggesting that the observed association may differ across metabolic subgroups. Full article

Background: Microbial fermentation of non-digestible carbohydrates and proteins produce short-chain fatty acids (SCFAs), which are critical communication signals in the gut–adipose tissue axis. Individual SCFA can differentially modulate the adipocyte secretory profile and adipose tissue metabolic function; however, their dose-dependent effects on adipocyte function in combined inflammatory and hypoxic environmental conditions that reflect the obesity-associated adipose tissue phenotype remain unknown. Methods: Mature 3T3-L1 adipocytes were cultured for 24 h with lipopolysaccharide (LPS; 10 ng/mL) plus 100 µM of cobalt chloride (CoCl₂) to chemically induce hypoxia ± individual SCFAs, namely acetate (Ace), propionate (Pro), and butyrate (But), in a dose-dependent manner (0.25 mM, 0.5 mM, and 1 mM). Results: Ace, Pro and But reduced secretion of IL-6, MCP-1/CCL7 and Rantes/CCL5 in a dose-dependent manner, whereas Pro and But reduced MCP3/CCL7 secretion and only But reduced resistin and increased adiponectin secretion compared to control (p < 0.05). Intracellular protein expression of the ratio of phosphorylated–to–total NFκB p65 was reduced by 1 mM But, whereas the ratio of phosphorylated–to–total STAT3 expression was reduced by 1 mM Ace, Pro and But and 0.5 mM Pro and But compared to control (p < 0.05). There was no difference in insulin-stimulated or non-insulin-stimulated glucose uptake between control and any individual SCFAs (p > 0.05). Conclusions: Adipocyte adipokine secretory function in combined inflammation and hypoxic environmental conditions is dose-dependently attenuated by individual SCFA, which exhibit both individual and overlapping effects. Full article

Background: For decades, the ketogenic diet has been successfully used for the treatment of obesity, metabolic syndrome, and type 2 diabetes. The mechanisms through which it affects metabolism are not fully understood, but the hormonal changes that occur during ketogenic nutrition are likely to play an important role. Objectives: To investigate the effect of the ketogenic diet on various hormones associated with obesity and the accompanying metabolic disorders in childhood. Methods: One hundred children aged 8–18 years with obesity were enrolled. After baseline anthropometric, biochemical, and hormonal testing, they followed a 4-month “well-formulated ketogenic diet.” Fifty-eight of them successfully completed the study with follow-up assessments. Among them, 8 girls had polycystic ovary syndrome (PCOS) and 7 children had Hashimoto’s autoimmune thyroiditis. Results: At the end of the 4-month period, there was a significant decrease in basal insulinemia (p < 0.0001) and in mean morning cortisol levels (p = 0.04), as well as an increase in adiponectin levels (p = 0.04). All girls with PCOS experienced spontaneous menstrual cycles, accompanied by a reduction in testosterone levels. TSH levels showed no change for the whole group (p = 0.13), but there was a significant decrease in T3 (p < 0.0001) and a mild increase in T4 (p = 0.05). Among patients with Hashimoto’s thyroiditis, TSH levels were significantly higher at the end of the study. Conclusions: A short-term, well-formulated ketogenic diet in children with obesity is associated with hormonal changes that support weight loss and improve insulin sensitivity. The diet shows particularly beneficial effects in girls with PCOS and may be considered as part of a comprehensive therapeutic approach in these patients. Monitoring thyroid function during ketogenic nutrition is advisable in patients with hypothyroidism and thyroid disorders. Full article

Adiponectin and omentin are adipose tissue-derived adipokines implicated in insulin sensitivity and cardiometabolic regulation. Their behavior across different stages of dysglycemia, as well as in relation to visceral adiposity and cardiometabolic phenotypes, remains incompletely understood. In this cross-sectional study, circulating adiponectin and omentin levels were evaluated in individuals with prediabetes (PreDM, n = 100) and newly diagnosed type 2 diabetes mellitus (T2DM, n = 128). Associations with insulin resistance-related indices, including the triglyceride–glucose (TyG) index and TyG-derived composites, the visceral adiposity index (VAI), cardiometabolic phenotypes, and cardiovascular risk categories, were assessed using correlation and multivariable regression analyses. Discriminatory performance for metabolically unhealthy obesity was evaluated using receiver operating characteristic (ROC) curve analysis. Both adiponectin and omentin levels were lower in T2DM compared with PreDM (22.05 vs. 30.30 and 25.72 vs. 38.84, p < 0.0001 for both). In PreDMs, omentin showed a significant inverse correlation with the TyG index (weak correlation, ρ = −0.197, p = 0.050), whereas adiponectin demonstrated only weak trends. In multivariable models, VAI and male sex were independent predictors of circulating omentin levels, whereas fasting insulin was not. In contrast, adiponectin did not retain independent associations with metabolic or visceral adiposity indices. In T2DM, adipokine–metabolic associations were largely absent. Neither adipokine differed substantially across cardiometabolic phenotypes or cardiovascular risk categories. ROC analyses revealed modest overall discriminatory performance for metabolically obese phenotypes, with poor discrimination after stratification by glycemic status (area under the ROC curve (AUC) of 0.704 for adiponectin and 0.710 for omentin, and AUC of 0.431 for adiponectin and 0.461 for omentin, respectively). Circulating adipokines appear to exhibit stage-dependent relationships with metabolic dysfunction, being more informative in PreDM than in established T2DM. Omentin may reflect visceral adiposity-related metabolic alterations in early dysglycemia, whereas adiponectin shows limited independent associations. Overall, these findings suggest that adipokines have limited diagnostic or cardiovascular risk-stratification utility when considered in isolation and may be better interpreted within multimarker cardiometabolic assessment frameworks. Full article

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine–metabolic disorder associated with insulin resistance (IR), visceral adiposity, and increased cardiometabolic risk. The visceral adiposity index (VAI) is a validated surrogate marker of adipose tissue dysfunction, but its relationship with circulating neurotrophins and adipokine balance in PCOS remains incompletely understood. In this study, 100 women with PCOS were stratified into lower- (n = 50) and higher-risk (n = 50) groups according to VAI. Anthropometric measures, fasting glucose and insulin concentrations, lipid profile, and serum levels of brain-derived neurotrophic factor (BDNF), nerve growth factor-β (NGFβ), leptin, adiponectin, and resistin were assessed. HOMA-IR, adipokine ratios and atherogenic indices were calculated. Multivariate regression showed that BDNF was independently associated with VAI and non-HDL cholesterol, whereas NGFβ was independently linked to HDL cholesterol and estradiol, highlighting neurotrophin relationships with metabolic and endocrine parameters beyond general adiposity. Correlation heatmap and network analyses demonstrated interconnected clusters linking visceral adiposity, IR, dyslipidemia, adipokine imbalance, and neurotrophins, with the leptin/adiponectin ratio emerging as a central integrative marker. These findings suggest that within a PCOS population, VAI-defined cardiometabolic risk is associated with distinct neurotrophin–adipokine signatures, highlighting neurotrophin–adipokine networks underlying visceral adiposity-driven cardiometabolic and endocrine risk. Full article

Background/Objectives: Fetal growth restriction (FGR) represents a model of adverse intrauterine programming associated with an increased risk of cardiometabolic disorders later in life. We examined the relationships between birth weight, catch-up growth, adipokine signaling, and early cardiometabolic risk in adolescents. Methods: This cross-sectional study included 80 term-born adolescents (40 FGR, 40 controls) matched for age and sex. Anthropometry, blood pressure, lipid profile, fasting glucose, adipokines (leptin, adiponectin), and ghrelin levels were assessed. Associations between birth weight, growth rate, adipokines, and cardiometabolic outcomes were analyzed. Results: Birth weight was not associated with adiposity, lipid profile, blood pressure, or glycemic status (p > 0.05). In contrast, catch-up growth in the FGR group was correlated with increased BMI (ρ = 0.680, p < 0.001), central adiposity (ρ = 0.714, p < 0.001), systolic blood pressure (ρ = 0.448, p = 0.0037) and diastolic blood pressure (ρ = 0.325, p = 0.0409). Mediation analyses showed that the current BMI largely explains the associations between catch-up growth and cardiometabolic risk, systolic blood pressure, and waist circumference (β = 2.832 kg/m² per 1-unit increase in ΔZ; p < 0.001). The hypertensive effect of catch-up growth was amplified in overweight/obese adolescents (β = 8.13 mmHg; p = 0.006). Catch-up growth was independently associated with higher leptin (β = 220 ng/L; p = 0.022) and a higher leptin/ghrelin ratio (β = 2.330; p = 0.034). Conclusions: Postnatal growth acceleration, rather than fetal size alone, drives early cardiometabolic susceptibility following FGR through adiposity-mediated and endocrine pathways. Full article

Background/Objectives: Hepatic encephalopathy (HE) is characterized by hyperammonemia, neuroinflammation, oxidative stress, and blood–brain barrier (BBB) dysfunction, with brain endothelial cells being highly vulnerable to ammonia-induced damage. Adiponectin is a cytoprotective adipokine that may enhance endothelial resilience; however, its specific role under hyperammonemic conditions remains unclear. This study aims to investigate the protective effects of adiponectin on brain endothelial function and BBB integrity. Methods: In vivo, male C57BL/6J mice underwent bile duct ligation (BDL) surgery and received daily intraperitoneal adiponectin injections (10 μg/kg/day) for 6 days, starting 5 days post-surgery. On day 11, brain tissues and serum were collected for molecular and cytokine analyses. In vitro, mouse brain endothelial cells (bEnd.3) were pretreated with adiponectin before exposure to ammonia. Assays for tight junction preservation, mitochondrial membrane potential, reactive oxygen species (ROS) generation, and total RNA sequencing were performed. Results: In BDL mice, adiponectin increased the expression of the tight junction protein claudin-5 and synaptic marker PSD95 across the cortex, hippocampus, and striatum, while reducing pro-oxidant (Cyp2e1, Cyp4a1) and apoptotic (Caspase-9) markers. In vitro, adiponectin pretreatment maintained tight junction proteins, suppressed inflammatory markers, restored mitochondrial membrane potential, and decreased ROS generation in ammonia-exposed bEnd.3 cells. Transcriptomic profiling revealed that adiponectin modulates stress-related gene expression under hyperammonemic conditions. Conclusions: Adiponectin enhances cellular stress resistance and maintains BBB structural integrity under ammonia-induced toxicity. These findings suggest that adiponectin serves as a promising therapeutic target for mitigating neurovascular unit dysfunction in hepatic encephalopathy. Full article

Dietary fat quality, determined by fatty acid composition, plays a central role in regulating adipose tissue function and metabolic homeostasis in obesity. This study examined whether different dietary fat sources modulate the secretory activity, antioxidant capacity, and metabolomic profiles of visceral adipose tissue (VAT) in mice with established high-fat diet (HFD)-induced obesity. Male C57BL/6J mice were rendered obese by long-term feeding with a lard-based HFD and subsequently maintained on isocaloric HFDs containing lard, coconut oil, olive oil, or fish oil. Antioxidant capacity, redox enzyme activities, adipokine levels, and untargeted metabolomic profiles of VAT were analyzed. Fish oil-enriched HFD significantly improved antioxidant potential and partially restored redox enzyme activity compared with the lard-based diet. It preserved adiponectin levels and reduced leptin accumulation in VAT. Multivariate metabolomic analyses showed clear separation of dietary groups and distinct metabolic signatures related to fat quality. Replacement of lard with fish oil induced a coordinated remodeling of the lipid and amino acid metabolism and reduced metabolites linked to mitochondrial overload and oxidative stress, whereas saturated fat-rich diets promoted patterns consistent with metabolic dysfunction. These findings indicate that dietary fat quality reshapes adipose tissue metabolism in obesity and highlights fish oil as a strategy to attenuate adipose tissue dysfunction. Full article

Osteoarthritis (OA) is a prevalent degenerative joint disease which affects millions of patients across the globe. The infrapatellar fat pad (IPFP) harbors diverse cell types with intricate intercellular interactions. Its mesenchymal stem cells (MSCs) and extracellular vesicles (EVs) possess significant biological functions and hold promising applications in regenerative medicine. IPFP exhibits active secretory capacity, releasing adipokines including leptin and adiponectin, along with various cytokines. Furthermore, it contains a rich neural network playing a crucial role in knee pain perception and sensation. Moreover, IPFP and synovium can be considered an integrated unit, exhibiting interactions both with each other and with cartilage. In imaging applications, IPFP is gaining widespread attention as an emerging biomarker. In clinical practice, the decision to resect or preserve IPFP remains a controversial topic. This article will review the latest research regarding the mechanism of IPFP in OA, and discuss its clinical applications, providing a theoretical basis for the prevention and treatment of OA. Full article