Serum Leptin Levels Research Articles (Page 1)

Omentin-1 (also known as intelectin-1) is a novel adipokine associated with metabolic diseases. However, its physiological role in body composition remains incompletely understood. Therefore, this study aimed to investigate the association between the circulating omentin-1 levels and whole-body and regional body composition parameters measured using dual-energy X-ray absorptiometry (DXA). A population-based cross-sectional survey was conducted among school-aged children in Hamamatsu, Japan. Serum adipokine levels were measured using enzyme-linked immunosorbent assay, and associations between omentin-1 levels and DXA-based parameters were evaluated by multiple regression analysis after adjusting for potential confounding factors. The final study included 392 participants (192 boys, 200 girls, 75.2% of the source population; mean age 11.2 ± 0.3years). Serum omentin-1 levels showed a significantly inverse association with nearly all DXA-based fat mass parameters. Inverse correlations were observed with fat-free soft tissue mass and serum leptin levels, whereas positive correlations were noted with adiponectin levels. The mean values for various body fat parameters, fat-free soft tissue mass, body mass index, and waist circumference were significantly decreased across tertiles of serum omentin-1 levels from lowest to the highest after adjusting for potential confounders. Our results demonstrate that Japanese school-aged children with higher fat mass tended to have lower serum omentin-1 levels. These findings provide crucial insights into the link between omentin-1 levels and body composition, which may contribute to early health interventions for metabolic improvement.

Obesity is a metabolic disorder characterized by excessive fat accumulation due to energy imbalance. This study aimed to evaluate the effects of omega-3 fatty acids (n-3 FAs) on body weight, biochemical parameters, thermogenic gene expression, and adipose tissue morphology in a male C57BL/6 mice model of high-fat diet (HFD)-induced obesity initiated at 4 weeks of age. After a one-week adaptation, mice were randomly divided into four groups: a control group fed a standard diet (CD) and three experimental groups fed a HFD alone or enriched with 1.2% or 2.4% n-3 FAs. All groups were fed ad libitum for 12 weeks. Feed intake and body weight were recorded, and glucose and insulin tolerance tests were performed. Serum glucose, lipid profiles, insulin, leptin, and adiponectin levels were analyzed. Gene expression of uncoupling protein 1 (Ucp1), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (Pgc-1α), PR domain containing 16 (Prdm16), and G protein-coupled receptor 120 (Gpr120) was evaluated in brown adipose tissue (BAT), along with histological assessments of both BAT and white adipose tissue (WAT). n-3 FAs improved serum lipid profiles and glucose metabolism without significant changes in body weight or energy intake. Although no significant differences were observed in the expression of Ucp1, Pgc-1α, and Gpr120, Prdm16 expression was significantly higher in the 1.2% HFD group (p < 0.05). Histological analysis showed that n-3 FAs prevented BAT whitening, promoted WAT browning, and reduced inflammatory infiltration. Ucp1 immunoreactivity was significantly lower in the HFD group compared to the CD group (p < 0.05). These findings suggest that n-3 FAs exerts multifaceted protective effects on adipose tissue at genetic, biochemical, and histological levels, highlighting their potential in the management of diet-induced obesity.

Disclosure: H. Cho: None. H. Jin: None. I. Hwang: None. E. Kim: None.Objective: Leptin, ghrelin, and nesfatin are hormones that play crucial roles in regulating energy balance and metabolism. The objective of this study was to compare the levels of these hormones between patients with growth hormone deficiency (GHD) and idiopathic short stature (ISS) and healthy controls, as well as to evaluate the changes in these hormone levels before and after recombinant human growth hormone (rhGH) therapy in GHD and ISS patients. Methods: A total of 56 prepubescent children aged 5 to 12 years were included in this study, comprising controls (n=17), ISS patients (n=13), and GHD patients (n=26). Clinical parameters and serum levels of leptin, ghrelin, and nesfatin-1 were compared across the groups. Additionally, baseline and 6-month post-GH therapy values were compared in GHD and ISS patients. Results: There were no significant differences in age, BMI, or the levels of leptin, ghrelin, and nesfatin-1 among the three groups. After 6 months of GH therapy, height increased by 5.5 cm in GHD patients and by 5.3 cm in ISS patients. In GHD patients, serum leptin concentrations significantly decreased after 6 months of rhGH therapy (6929 pg/ml ± 8245 pg/ml to 3761 pg/ml ± 4340 pg/ml, p0.037), and leptin was positively correlated with BMI (r=0.672, p0.001). There were no significant changes in ghrelin levels (1367 pg/ml ± 957 pg/ml vs. 1331 pg/ml ± 1431 pg/ml) or nesfatin-1 levels (9.88 ng/ml ± 9.14 ng/ml vs. 7.28 ng/ml ± 5.71 ng/ml) in GHD patients. In ISS patients, leptin (6380 pg/ml ± 5462 pg/ml vs. 2024 pg/ml ± 742 pg/ml), ghrelin (881 pg/ml ± 1273 pg/ml vs. 1015 pg/ml ± 1285 pg/ml), and nesfatin-1 levels (3.03 ng/ml ± 2.31 ng/ml vs. 2.82 ng/ml ± 2.48 ng/ml) showed no significant differences after 6 months of rhGH therapy. Conclusion: While no significant differences in leptin, ghrelin, and nesfatin-1 levels were observed between GHD and ISS patients compared to controls, GH therapy resulted in a significant decrease in leptin levels in GHD patients, which was positively correlated with BMI. These findings provide important insights into the metabolic alterations in GHD patients and the effects of rhGH therapy on these parameters. Further studies with larger sample sizes and extended follow-up periods after growth hormone therapy are necessary to evaluate the long-term effects more comprehensively.Presentation: Sunday, July 13, 2025

Disclosure: G. Scozia: None. D. Menghini: None. D. Fintini: None. S. Cianfarani: None. V. Russo: None. M. Mainardi: None. N. Gianni: None. G. Furini: None. G. Scabia: None. M. Maffei: None. M. Manco: None.Background: In pediatric obesity, altered energy regulation and impaired inhibitory control over food intake are linked to dysfunction in the dorsolateral prefrontal cortex (DLPFC). Lifestyle interventions can potentially restore these brain-metabolic pathways. Leptin, brain-derived neurotrophic factor (BDNF), and eotaxin (CCL11), a chemokine involved in immune signaling, may modulate neural responses to metabolic challenges. Objective: To assess the impact of an 8-week intensive health behavioral treatment (IHBT) on DLPFC activation during oral glucose tolerance testing (OGTT), and to explore the relationship with insulin sensitivity and circulating levels of leptin, BDNF and eotaxin in children with obesity. Methods: Twenty-seven children with obesity (mean age 11 years) underwent functional near-infrared spectroscopy (fNIRS) during OGTT at baseline (T0) and post-IHBT (T1). The IHBT included healthy diet, structured physical activity, and cognitive training. Changes in cerebral blood flow (total Hb, tHb) and oxygenated hemoglobin (O₂Hb) were measured in the DLPFC. Insulin sensitivity was assessed via the Matsuda Index and HOMA-IR; serum eotaxin, leptin, and BDNF levels were also measured by commercial assays. Results: After IHBT, there was a significant increase in bilateral DLPFC activation during OGTT:Left DLPFC: ΔO₂Hb ↑, p < 0.01Right DLPFC: ΔO₂Hb ↑, p < 0.05ΔtHb bilateral ↑, indicating enhanced cortical perfusionImprovement in DLPFC activity correlated with metabolic indices:Positive correlation with Matsuda Index (r = 0.54, p < 0.01)Negative correlation with HOMA-IR (r = -0.47, p < 0.05)Left DLPFC activation at T1 showed sex-related differences, with greater increase in males (p < 0.05)Baseline eotaxin levels were positively associated with DLPFC activation changes at T1 (r = 0.41, p < 0.05), while leptin and BDNF showed no significant associations. Conclusion: An 8-week lifestyle intervention significantly enhanced DLPFC activation during glucose challenge, suggesting improved neural regulation of food-related behavior in children with obesity. The association with eotaxin implicates a potential neuroimmune mechanism whereby inflammatory signaling may influence prefrontal responsiveness to metabolic inputs. Eotaxin may serve as a biomarker of neuroplastic adaptation to behavioral interventions targeting obesity.Presentation: Monday, July 14, 2025

Background/Objectives: The prevalence of obesity globally has increased steadily in the past decades. Obesity, sarcopenic obesity (SO) and nonalcoholic fatty liver disease (NAFLD) commonly coexist. Ursolic acid (UA), a natural pentacyclic triterpenoid, has demonstrated potential anti-obesity properties. This study was designed to evaluate the anti-obesity efficacy of UA in a mouse model of high-fat diet (HFD)-induced obesity, with a particular focus on its impact on muscle function and NAFLD. Methods: Male C57BL/6J mice (6 weeks old) were randomly assigned to three groups (n = 20 per group): a control group (CON) fed a normal chow diet, a high-fat diet group (HFD), and a UA treatment group (UA). The HFD and UA groups received a high-fat diet for 10 weeks to induce obesity. Thereafter, mice in the UA group were administered UA orally once daily for 6 weeks. Results: In HFD-induced obese mice, UA administration significantly reduced body weight (BW), abdominal fat weight and liver weight; improved grip strength and muscle weight; and enhanced lipid profiles, including triglycerides, total cholesterol, low-density lipoprotein cholesterol and free fatty acid levels in serum. UA also improved histological changes in the liver and abdominal adipose tissues, regulated serum GH, IGF-1, T3, T4 and leptin levels and downregulated the inflammation-associated gene expression of TNF-α and IL-1β in abdominal adipose tissue. Conclusions: UA could enhance muscle strength, improve lipid metabolism and hepatic steatosis and might be considered a potential therapeutic agent for managing obesity and related metabolic diseases.

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder connected with insulin resistance (IR), low-grade inflammation, dyslipidemia, and altered adipokine secretion. We evaluated serum levels of leptin, adiponectin, visfatin, resistin, IL-6, and TNF-α in 150 women with PCOS, stratified by IR status (IR, n = 76; non-IR, n = 74), and examined their associations with anthropometric, metabolic, hormonal, inflammatory, and atherogenic parameters. Anthropometric data included body weight, height, BMI, waist circumference, and waist-to-height ratio (WHtR), while IR was assessed using HOMA-IR and the Matsuda index. Serum adipokines were measured using ELISA, and lipid parameters and atherogenic indices-including non-HDL cholesterol, AIP, leptin/adiponectin, and adiponectin/resistin ratios-were calculated. Women with IR had higher levels of leptin, visfatin, resistin, and TNF-α, and lower levels of adiponectin. Leptin correlated positively with weight, WHtR, HOMA-IR, and atherogenic indices. Adiponectin showed the strongest and most consistent associations with anthropometric indices, HOMA-IR, and the Matsuda index. Resistin was linked to IR indices and IL-6, and visfatin correlated negatively with HDL-C and insulin sensitivity. In a multivariate general linear model, WHtR, but not HOMA-IR, remained independently associated with higher leptin levels and with atherogenic indices. These findings suggest that in PCOS, central adiposity rather than IR explains a substantial part of the adverse adipokine and inflammatory profile, thereby contributing to elevated cardiometabolic risk and highlighting the need for targeted treatment strategies.

Changes in attention deficit and adipokine levels in children with sleep-disordered breathing.

Cardiovascular diseases (CVDs) are a leading cause of death globally. Early identification of individuals at elevated risk is essential for improving preventive measures and patient outcomes. Biomarkers like Galectin-1, leptin, and adiponectin are known to play roles in metabolic processes, with a low adiponectin/leptin ratio indicating a heightened cardiometabolic risk. However, the association between Galectin-1, leptin, adiponectin, and the adiponectin/leptin ratio with CVD risk scores is not well understood. This study aims to assess these markers' correlation with CVD risk and their potential utility as predictors. This cross-sectional study assessed 135 healthy adults through questionnaires and blood pressure measurements. Each participant's cardiovascular (CV) risk was estimated, with serum Galectin-1, adiponectin, and leptin levels measured. Comparisons of adipokines levels between age-groups were conducted. The associations between variables were assessed, and linear regression was applied with cardiovascular risk score as the outcome. Statistical significance was set at p < 0.05. After excluding fifteen individuals, 122 subjects (62 males, 60 females; mean age 43.8 years) were included in the study. Leptin levels correlated positively with CV risk score and LDL levels in younger individuals, while the adiponectin/leptin ratio showed a negative correlation with LDL and CV risk scores across age groups. Smoking was a strong predictor of CV risk in younger participants, whereas diabetes, cholesterol/HDL ratio, and leptin were significant predictors in the middle-aged group (p < 0.05). Among measured adipokines, leptin is as a key predictor of cardiovascular risk, alongside established factors like smoking, diabetes, and cholesterol/HDL ratio.

The present study was conducted to assess the hormone's levels (nesfatin-1, leptin, resistin and adiponectin) on some of inflammatory cytokines or the so-called adipokines which exert a variety of biological activities (tumor necrosis factor alpha: TNF-α and interleukin-6 IL6), as well as BMI &amp; lipid profile in serum of obese women in Samarra 10. The present study had included (50) samples, and they were divided into: 25 samples of obese women age ranged between (25-45) years, and (25) samples for the control group that constituted from women with normal weight. The results of the study demonstrated a marked elevation in the levels of leptin and resistin hormonal levels, inflammatory cytokines, i.e., tumor necrosis factor-α (TNF-α) interleukin -6 (IL-6), lipid profile evaluated by body mass index ) as well as significant decline in nesfatin-1 and adiponectin at the significance level represented by mean± SD: (P≤0.05) among obese women compared with control group. Highlights: Obese women showed significantly higher serum levels of leptin, resistin, TNF-α, IL-6, and lipid profile abnormalities compared to controls. Nesfatin-1 and adiponectin levels were markedly reduced in obese patients, indicating impaired appetite regulation and anti-inflammatory response. Findings confirm obesity as a state of chronic low-grade inflammation, linking it to increased risk of diabetes and cardiovascular disease.

IntroductionObesity is caused by excessive storage of adipose tissue and leads to metabolic disorders. Uridine exerts modulatory effects on lipid metabolism, but the regulatory mechanism in obesity needs further research.MethodsIn this study, the effects of uridine supplementation on lipid metabolism were investigated in high-fat diet-induced obese mice. Mice aged at 8 weeks were randomly grouped to receive a control diet (CON, n = 10) or a high-fat diet (HF, n = 24). After 6 weeks of feeding, the HF group was further divided, with half receiving 0.4 mg/mL uridine supplementation in drinking water (HUR, n = 12) for an additional 4 weeks, while the remaining HF mice continued without intervention.ResultsThe results showed that the uridine supplement reduced the liver weight and intra-abdominal white adipose tissue weight in obese mice (p < 0.05). Treatment with uridine and free fatty acid resulted in a significant increase in late and total apoptosis, accompanied by a decrease in early apoptosis of mouse liver organoids (p < 0.05). Moreover, uridine lowered serum levels of triglycerides (TG), total cholesterol (TC), high-density lipoprotein (HDL), leptin, and liver TG content (p < 0.05). In obese mice fed with uridine, the expression of key genes involved in lipid transport [activated fatty acid translocase/cd36 (Fat/cd36) and low-density lipid receptor (Ldlr)], pyrimidine de novo synthesis [dihydroorotate dehydrogenase (Dhodh)], pyrimidine metabolism [uridine phosphorylase 2 (Upp2), ribonucleoside-diphosphate reductase subunit M2 (Rrm2), and thymidine kinase 1 (Tk1)] was improved (p < 0.05). Furthermore, liver metabolomic analysis identified 37 differential metabolites between the HF and HUR groups, primarily enriched in arachidonic acid metabolism and α-linolenic acid metabolism.DiscussionThese findings indicated that uridine supplementation can improve lipid metabolism in obese mice by regulating hepatic gene expression and metabolic pathways.

The response to infection is an energy-demanding process that bolsters cell division and protein synthesis to overcome a rapidly dividing and invasive pathogen. Paradoxically, anorexia, a conserved behavioural response to infection, sharply limits food intake during this period of high energy demand. Leptin, therelease of which from adipocytes is coordinated with the immune response, signals to the hypothalamus to balance energy availability and expenditure with respect to various physiological processes. Congenital deficiency of leptin or its receptor in humans predisposes to infection. Moreover, low serum levels of leptin are associated with poor outcomes in sepsis. Leptin activates pro-opiomelanocortin neurons, which produce melanocortins, a family of peptide hormones that has diverse roles. The melanocortins have targets in many organ systems and their functions include suppressing inflammation and upregulating sympathetic tone. Here, we discuss what is known about leptin and melanocortin signalling in the response to infection, with evidence from preclinical research and human studies. We close by offering insights into how study of these pathways might be translated into therapies for infectious disease as well as new avenues for exploration.

Exercise is crucial for animal survival, enabling them to move, forage, and meet survival needs, as well as maintain fitness and adapt to the environment. The present study aims to explore the effects of long-term forced exercise on the body mass, energy metabolism, and liver metabolomics of Apodemus draco to understand its physiological adaptation mechanisms under exercise stress. Before exercise acclimation, body mass, resting metabolic rate (RMR), non-shivering thermogenesis (NST), and food intake of A. draco in exercise and control groups were measured. After an 8-week exercise acclimation period, these physiological parameters and liver metabolic indices were re-measured. Results showed no significant body mass difference between groups. However, the exercise group had a significant decrease in body fat content (p < 0.01) and serum leptin level (p < 0.01), with a positive correlation between them. RMR and food intake in the exercise group were significantly higher (p < 0.01). Mitochondrial protein (MP) content and cytochrome c oxidase (COX) activity in the liver of exercised animals increased significantly (p < 0.05), while NST and brown adipose tissue-related indicators remained unchanged. Principal component analysis (PCA) of liver metabolites revealed distinct separation between the two groups, indicating good data quality. Differential metabolite analysis showed significant upregulation of metabolites related to lipid, amino acid metabolism, and the tricarboxylic acid (TCA) cycle in the exercise group, like docosahexaenoic acid, glyceric acid, and so forth. In conclusion, long-term forced exercise didn't significantly affect A. draco's body mass, but increased energy intake by reducing body fat and leptin levels. It enhanced RMR and liver mitochondrial metabolic activity, increased obligatory thermogenesis without affecting adaptive thermogenesis, and maintained body weight stability. Liver metabolomics changes suggested multi-dimensional metabolic adaptations of A. draco to exercise. This study provided new insights into the physiological adaptation mechanisms of small rodents under exercise stress.

Obesity or excess visceral adiposity plays a fundamental role in the pathogenesis of heart failure with preserved ejection fraction (HFpEF), but it is not clear that an expanded adipose tissue mass contributes importantly to the evolution and progression of heart failure with reduced ejection fraction (HFrEF). Whereas central adiposity characterizes most patients with HFpEF, obesity was not a remarkable feature of HFrEF in the large-scale trials carried out in the 1980s and 1990s, and studies typically characterized obesity as a protective factor against adverse outcomes. In the general community without apparent heart disease, the finding of obesity or central adiposity precedes and predicts the subsequent occurrence of HFpEF, but not HFrEF. The mass of epicardial adipose tissue-an important source of cardioactive molecules-is expanded in HFpEF, but it is diminished in HFrEF, and the decrease has adverse prognostic significance. An increased waist-to-height ratio (a marker of excess abdominal adiposity) is more strongly associated with adverse heart failure outcomes in HFpEF than in HFrEF. Systemic inflammation [as reflected by elevations of high-sensitivity C-reactive protein (hsCRP)] in the general community presages the development of HFpEF, but not HFrEF, presumably because excess adiposity augments hsCRP in HFpEF, whereas increases in hsCRP in HFrEF may be related to coexisting atherosclerosis or clinical congestion. Whereas obesity is the principal determinant of serum levels of leptin and adiponectin in HFpEF, cardiac and neurohormonal signalling may drive circulating levels of these adipokines in HFrEF. Central obesity identifies patients more likely to respond to mineralocorticoid receptor antagonists in both HFpEF and in HFrEF, but this feature also identifies patients more likely to respond neprilysin inhibition or sodium-glucose cotransporter 2 inhibitors if they have HFpEF, but not HFrEF. Weight loss by incretin-based drugs lowers systolic blood pressure in patients with HFpEF, but potentially not with HFrEF, and such weight loss is accompanied by a reduced risk of worsening heart failure events in patients with HFpEF, but without a similar benefit in HFrEF. Taken collectively, these observations raise important questions about the potential role of obesity and visceral adiposity as contributing factors in the evolution and progression of HFrEF.

Introduction and aim. Acute myocardial infarction (AMI) is a leading cause of mortality. Although traditional risk factors are known, adipokines, such as leptin (LEP) and resistin (RETN), are emerging as potential biomarkers involved in the inflammatory and metabolic processes underlying AMI. This study aimed to evaluate serum LEP and RETN levels in patients with AMI. Material and methods. This case-control study included 60 patients diagnosed with AMI and 60 healthy controls recruited from the Nasiriyah Heart Hospital, Thi-Qar Province. Serum levels of LEP and RETN were measured using an enzyme-linked immunosorbent assay. Results. AMI patients exhibited significantly elevated LEP (3.79±2.0 vs. 1.43±0.7 ng/mL, p&lt;0.001) and RETN (606±325 vs. 289±160 ng/L, p&lt;0.001) compared to controls. Both adipokines were positively correlated with high-sensitive troponin I (Hs-TnI), low-density lipoprotein (LDL-C), and triglycerides (p&lt;0.05). ROC analysis demonstrated a high diagnostic accuracy for LEP (AUC=0.964; cutoff &gt;2.23 ng/mL, derived from internal study data) and moderate accuracy for RETN (AUC=0.878; cutoff &gt;305.9 ng/L). The sensitivity and specificity of the LEP were 93% and 92%, respectively. Conclusion. LEP demonstrated high diagnostic accuracy in our cohort, and its clinical application requires validation in larger prospective studies. The association between RETN and AMI likely reflects inflammatory sequelae rather than predictive utility.

Time-restricted feeding prevents depressive-like behaviors by suppressing changes in the gut microbiota.

Association between brain-gut peptides and depression: A systematic review and meta-analysis.

Inflammatory cytokines negatively impact postoperative reactions and outcomes in abdominal surgeries. This study investigates the effect of general and spinal anesthesia (SA) on the serum levels of leptin, adiponectin, and interleukin-6 (IL-6) 24 hours after cesarean sections (CS) conducted with spinal or general anesthesia (GA). This cross-sectional study was conducted at Sayad Shirazi Hospital in Gorgan, IR. Iran, in 2024. Eighty pregnant women who were scheduled for CS were enrolled in the study. All participants satisfied the criteria for both general and SA, and the method of anesthesia was randomly assigned to each participant. Exclusion criteria included autoimmune diseases, preeclampsia, hypertension, gestational diabetes, a gestational age < 37 weeks, those who received blood transfusions and/or intubation. Participants were divided into two groups based on the anesthesia method after the CS: GA and SA. General anesthesia was administered using propofol and sodium thiopentone combined with atracurium and cis-atracurium. Bupivacaine and ropivacaine were used for SA. Peripheral blood samples were collected 24 hours post-operation to measure IL-6, leptin, and adiponectin levels. A comparison of serum cytokine levels revealed that 24 hours after CS, IL-6, adiponectin, and leptin were significantly higher in the GA than in the SA group (P < 0.001 for all). In the SA group, there were positive and significant correlations among the following variables: IL-6 and leptin (r = 0.641, P < 0.001), IL-6 and adiponectin (r = 0.617, P < 0.001), as well as between leptin and adiponectin (r = 0.742, P < 0.001). In the GA group, a positive and significant correlation was found between the pro-inflammatory cytokines leptin and IL-6 (r = 0.316, P = 0.047). The present research found elevated leptin, IL-6, and adiponectin levels in CS cases that underwent GA.

Background: Obesity, characterized by an abnormal and excessive accumulation of fat, significantly affects health by increasing the probability of chronic diseases and has become a pressing global health issue. Among natural compounds with therapeutic potential, rutin exhibits diverse biological effects, such as antioxidant, anti-inflammatory, and hypolipidemic properties. Objective: The purpose of this work is to evaluate the preventive effects of rutin loaded on chitosan nanoparticles on metabolic and oxidative alterations in male albino rats fed a high-fat diet (HFD). Method: The rats were allocated to four distinct groups: control, HFD, HFD treated with 50 mg/kg rutin, and HFD treated with 50 mg/kg nano-rutin, respectively, for six weeks. Results: Molecular docking analysis revealed that rutin exhibits an inhibitory interaction with PPAR-γ, suggesting its potential role in suppressing adipogenesis and contributing to its preventive effect against obesity. Nano-rutin markedly improved glycemic control, reducing fasting glucose from 161.75 ± 8.37 mg/dL in the HFD group to 133.50 ± 3.55 mg/dL, compared to 92.17 ± 3.53 mg/dL in controls. Serum leptin levels decreased from 28.95 ± 1.06 ng/mL in the HFD group to 15.58 ± 0.65 ng/mL with nano-rutin, approaching the control value of 10.43 ± 0.80 ng/mL. Oxidative stress was also significantly alleviated, as shown by a reduction in malondialdehyde (MDA) from 8.43 ± 0.20 U/µL in HFD rats to 6.57 ± 0.08 U/µL with nano-rutin, versus 1.29 ± 0.13 U/µL in controls. Conclusions: Rutin loaded on chitosan nanoparticles demonstrated protective effects against high-fat diet-induced obesity, mainly through modulation of leptin signaling and oxidative stress pathways. These findings highlight the promise of nano-rutin as a natural agent for preventing metabolic disorders related to obesity.

ABSTRACTThe cafeteria diet (CAFD) model mimics Western dietary patterns, inducing obesity in mice. Blueberry (BB) consumption improves metabolic outcomes due to its anti‐inflammatory and antioxidant properties, though mechanisms remain unclear. This study assessed BB supplementation effects on biometric, metabolic, and hepatic steatosis parameters in CAFD‐fed mice, and analyzed obesity‐related gene expression in adipose tissues, liver, muscle, and hypothalamus. Thirty‐two male C57BL/6 mice were divided into three groups: Control (C, standard diet—SD; N = 10), CAF (CAFD + SD; N = 12), and BB (SD + CAFD + BB; N = 10). BB animals received 22.4 g of freeze‐dried BB per week. After 16 weeks, biometric and glycemic parameters, insulin resistance (IR), hepatic steatosis, oxidative stress markers, and serum leptin, adiponectin, and irisin levels were evaluated. Expression of genes related to apoptosis, lipid and glucose metabolism, oxidative stress, and adipocytokine pathways was analyzed by qPCR. BB supplementation improved biometric, glycemic, IR, hepatic steatosis, and oxidative stress and antioxidant markers compared to CAF. Leptin, adiponectin, and irisin levels decreased in BB mice. Also, BB consumption modulated the expression of obesity‐related genes. BB mitigated CAFD‐induced weight gain, IR, hepatic steatosis, oxidative stress, and obesity‐related gene dysregulation, highlighting its nutrigenomic potential.

Increased serum leptin levels are potentially related to male frontal fibrosing alopecia.