Oxytocin is expressed throughout the small intestine, suggesting a role for oxytocin in postprandial metabolism. Accordingly, single-dose intranasal oxytocin reduces food intake and improves glucose tolerance. We investigated the effects of a continuous intravenous oxytocin infusion on ad libitum food intake, appetite sensations, and postprandial metabolism. In a randomised, placebo-controlled, double-blind, crossover study, overnight fasted participants with obesity underwent two 4.5-hour intravenous infusions of oxytocin (0.2 international units/min) and placebo (saline), respectively, on separate days interposed by a wash-out period of a minimum of seven days. After 60 min of infusion, participants ingested a standardised liquid mixed meal containing 1.5 g paracetamol (for evaluation of gastric emptying). Appetite sensations were assessed by visual analogue scales, and concentrations of plasma glucose as well as glucose and appetite-regulating hormones were measured. After four hours, food intake (primary endpoint) was assessed by an ad libitum meal test. Twenty-four individuals (12 women, median age 41.5 (interquartile range (IQR) 28.5;55.3) years, body mass index 36.2 (32.1;37.6) kg/m2, mean glycated haemoglobin 34 ± standard deviation (SD) 3.5 mmol/mol) completed the study. Ad libitum food intake was similar between oxytocin and saline infusions (mean 714 ± SD 382 vs. 707 ± 385 kcal). Compared with placebo, oxytocin did not affect sensations of appetite nor circulating glucose, insulin, C-peptide, glucagon, glucagon-like peptide 1, glucose-dependent insulinotropic polypeptide, cholecystokinin, or paracetamol. In individuals with obesity, 4.5-hour intravenous infusion of oxytocin causing supraphysiological plasma concentrations of ~400 pg/mL has no effect on ad libitum food intake, appetite sensations, plasma glucose levels, circulating concentrations of glucose and appetite-regulating hormones, or gastric emptying.

Frailty in aging is a major health challenge, requiring solution. Older people with frailty often exhibit malnutrition and dysregulated feeding. Feeding behavior displays circadian rhythm, while aging and frailty involve rhythm disorders, suggesting possible role of circadian feeding in frailty and treatment. Herbal medicine, Ninjin'yoeito (NYT), reportedly ameliorates frail symptoms. The present study explored impacts of NYT on circadian feeding and psychological/physical functions in aged mice. Here, we report that oral NYT independent of administration timing increases food intake specifically in 18:00-20:00, the pre-active phase, in aged and young mice, an effect mimicked by Chenpi and hesperidin. NYT altered appetite-regulating hormones and neuropeptides in pre-active phase. Repeated NYT administration restored anti-anxiety behavior, memory, and grip strength that declined in aged mice. These effects were blocked by food deprivation and pair-fed to control selectively in 18:00-20:00. These results reveal pre-active phase feeding promotion as a novel avenue to intervene aging-related frailty.

Exploring the evolution of gene networks associated with metabolic/energetic homeostasis can yield key insights into the adaptive landscapes governing the physiology of extant lineages. Here, we investigate a key hormonal module of energy metabolism in reptiles. Ghrelin (GHRL), also known as the 'hunger hormone', is a multifunctional gastric peptide, involved in appetite, food intake and body weight regulation. We examined the genomes of 112 species comprising members of the Squamata, Testudines, Crocodilia and Rhynchocephalia and provided ample evidence that GHRL was independently lost in snakes (32 species), chameleons (four species) and toadhead agamas (two species). In accordance, the enzyme responsible for ghrelin acylation and essential for its activity, MBOAT4 (membrane bound O-acyltransferase domain containing 4), is also eroded in these lineages. We suggest that the loss of this hormonal signalling system parallels critical modifications in energy metabolism, such as lower energy expenditure during rest, possibly linked with their unique ability to undergo large periods of fasting.

The non-degradable poly- and perfluoroalkyl substances (PFAS) are 'Endocrine Disrupting Chemicals' (EDCs), a group of chemicals that interfere with endocrine processes in the human body and potentially have adverse effects on several developmental domains in children. Particularly when PFAS exposure occurs during susceptive periods, including 'the first 1000 days' of life. Human milk is an important PFAS exposure pathway. In contrast to breastfeeding, PFAS have been thought to negatively influence growth, body composition development and metabolic health. However, exact mechanisms are not yet unraveled. Potential pathways might be via appetite regulating hormones (ARHs) and eating behavior. We, therefore, investigated the influence of feeding type (exclusive breastfeeding (EBF), exclusive formula feeding (EFF) or mixed feeding (mix)) on plasma ARHs and eating behavior and also the associations between plasma PFAS levels, ARHs and eating behavior, in infants during the first 2 years of life. This study was embedded in the Sophia Pluto study. We conducted longitudinal follow-up in 371 healthy term-born infants (150 EBF, 97 EFF and 124 mix) during the first 2 years of life. At age 3 months and 2 years, we studied eating behavior via the Baby Eating Behavior Questionnaire (BEBQ) and Child Eating Behavior Questionnaire (CEBQ), respectively. At these timepoints, fasting blood samples were collected in which plasma levels of 5 individual PFAS and 9 ARHs were determined. The associations of plasma PFAS levels and feeding type with ARHs and eating behavior were studied using multiple regression models, corrected for known confounders, such as sex and fat mass SDS. At age 3 months plasma ARH levels differed between children that were EBF, EFF and mix. With EBF-infants having the highest levels of peptide YY (PYY) and the lowest of insulin, amylin and pancreatic polypeptide (PP). These differences disappeared at age 2 years. Higher plasma PFAS levels, corrected for feeding type, at age 3 months were associated with higher adiponectin and lower leptin levels and at age 2 years with lower leptin and insulin levels. When studying eating behavior, we did neither find any differences between EBF, EFF and mix infants at age 3 months nor at age 2 years. At age 3 months, plasma PFAS levels were inversely associated with "food responsiveness", and positively with "slowness in eating". At age 2 years, plasma PFAS levels, corrected for feeding type, were inversely associated with all "food approach" subscales. Our findings could indicate that PFAS exposure does not compromise breastfeeding's health benefits on metabolic health and insulin sensitivity until age 2 years and that PFAS exposure probably effects eating behavior via other pathways than ARHs alone, which warrants further research.

Obesity serves as a predominant factor in the progression of metabolic syndrome and type 2 diabetes mellitus. While sleeve gastrectomy (SG) is a well-established surgical intervention, its impact on appetite-regulating hormones, such as ghrelin (GHRL), is limited. Sleeve gastrectomy combined with fundoplication (SGFD) has emerged as a potential strategy to improve metabolic outcomes by modifying both gastric anatomy and gut-brain signaling. Sixty-five Sprague-Dawley rats were enrolled. After 8 weeks of high-fat feeding, 48 rats developed diet-induced obesity (DIO). These rats were randomized into four experimental groups: DIO control, sham-operated, SG, and SGFD, alongside a normal control cohort. Biochemical indicators, hormonal fluctuations, and insulin responsiveness were analyzed. Molecular expressions were evaluated through quantitative real-time polymerase chain reaction and Western blotting. SGFD reduced body weight (-24.7%), food intake (-28.3%), fasting glucose (-37.5%), triglycerides (-42.6%), and serum GHRL (-51.2%) compared with the DIO group (P<0.01). Gastric GHRL, preproghrelin, and ghrelin O-acyltransferase (GOAT) expression were suppressed. Hypothalamic neuropeptide Y (NPY) was downregulated, and AMP-activated protein kinase (AMPK) signaling was robustly enhanced across various tissues. SGFD also improved insulin receptor substrate-1 (IRS-1), glucose transporter type 4 (GLUT4), β-cell function, hepatic lipid oxidation, and brown adipose thermogenesis. SGFD outperformed SG in most metabolic and molecular outcomes (P<0.05). SGFD provides superior metabolic benefits over SG alone by suppressing GHRL signaling and activating systemic AMPK pathways. SGFD represents a promising surgical strategy for obesity and metabolic syndrome.

Diet is one of the key external factors that can modify hormonal activity across the major endocrine axes and affect metabolic and appetite-regulating hormones including insulin, leptin, ghrelin, and cortisol. A literature search conducted between October and November 2025 using PubMed, Scopus, Web of Science, and Google Scholar identified peer-reviewed studies examining the effects of caloric restriction, macronutrient distribution, glycemic load, micronutrient intake, and structured dietary interventions on endocrine function. The evidence shows that diets high in glycemic load, saturated fats, and low in fiber can disrupt insulin sensitivity, alter leptin and ghrelin signaling, affect cortisol responses, and contribute to thyroid and reproductive hormone imbalances. In contrast, Mediterranean-style and low-glycemic diets, time-restricted feeding, and adequate intake of iodine, selenium, and zinc appear to support metabolic health and more stable hormonal activity. Diet also plays a therapeutic role in endocrine-related conditions including polycystic ovary syndrome, Hashimoto’s disease, acne vulgaris, endometriosis, and thyroiditis, with improvements seen in inflammation, insulin regulation, and hormonal homeostasis. Overall, the review emphasizes that diet can both disturb and restore endocrine balance. Well-structured, nutrient-dense dietary strategies may serve not only as preventive measures but also as valuable tools in supporting long-term hormonal health.

This study examined the effect of adding herbal supplements in the diets of post-partum crossbred cows (Vrindabani cattle; 59.6 ± 0.73 days post-partum) of second to fourth parity (3.1 ± 0.15) on milk yield, milk quality, immune function and antioxidant status. Twenty-four cows were randomly assigned to four groups in a completely randomized design. While the cows in HP, HPL and HEX groups received diets blended with herbal powder (200 gd- 1), herbal pellets (200 gd-1) and methanolic herbal extract (equal to 200 g herbal powder d-1), respectively, the cows in the CON group fed a diet consisting of green fodder, concentrate and wheat straw to meet the requirements for maintenance and milk production (ICAR 2013). The total duration of the experiment was of 120 days. Milk samples were collected fortnightly from each cow to study the udder health, milk composition and quality parameters. Serum antioxidant indices, immunity and mRNA expression of genes (LEP and GHRL) were ascertained. Daily milk yield, 4% Fat corrected milk (FCM), Energy corrected milk (ECM), total milk yield, fat, protein yields and pH were analogous irrespective of treatments, while Diphenyl Picrylhydrazyl (DPPH) value of milk was higher (p < 0.01) in treatment groups. Total antioxidant capacity (TAC) and flavonoids of milk were higher (p < 0.01) in HEX and HP group relative to CON, however, HPL has transitional position. Somatic cell counts in milk were noticeably (p < 0.05) lower in HPL and HEX than CON. The clinical scoring of milk was noticeably (p < 0.05) lower in HP and HPL groups. The cell mediated (CM) immunity was higher (p < 0.05) in HPL. Serum Glutathione Peroxidase (GSH-Px), Glutathione-S-Reductase (GSR) and Superoxide dismutase (SOD) and Catalase (CAT) were noticeably (p < 0.01) higher in HPL, HEX and HP groups relative to CON. LPO was decreased (p < 0.05) in HPL and HP groups relative to CON. The serum TAC (%) was higher (p < 0.01) in treatment groups than CON. The expression of LEP and GHRL gene remained unaffected. It can be deduced that herbal feed supplements in HPL and HP forms in the diet of post-partum cows were found to be promising as a strategy to bolster their overall health status, strengthen immune function and potentially elevate milk quality.

Sex is a critical determinant of health and disease, yet it remains underrepresented in biomedical research. The identification of blood-based biomarkers facilitates early diagnosis and intervention for various diseases; however, sex-differential differences in the plasma proteome have not been sufficiently explored in mouse models. Understanding the molecular features associated with sex is essential for enhancing the translational potential of clinical research. We utilized Olink technology to analyze sex- and strain-differential plasma protein expression in two widely used mouse strains, C57BL/6 and BALB/c. A total of 36 mice (n = 9 per strain and sex) were analyzed using the ‘Olink Target 48 Mouse Cytokine’ and ‘Olink Target 96 Mouse Exploratory’ panels. Differences in normalized protein expression (NPX) were compared between groups, and proteins with a P-value < 0.05 were considered significantly different. Our analysis identified 55 strain-differential proteins and 33 sex-differential proteins among the 87 proteins analyzed in mouse plasma. Importantly, LPL (Lipoprotein lipase) and GHRL (Appetite-regulating hormone) were also more highly expressed in females in human datasets, suggesting a conserved sex-biased expression pattern across species. This study characterized sex- and strain-differential differences in the plasma proteomes of C57BL/6 and BALB/c mice. Among the identified proteins, LPL and GHRL were significantly elevated in females, consistent with human gene and plasma protein expression trends. These findings highlight the presence of sex-based molecular differences in energy and lipid metabolism and provide a valuable foundation for future mechanistic studies.

Some nuclei of the hypothalamus are known for their important roles in maintaining energy homeostasis and regulating food intake. Moreover, obesity has been associated with hypothalamic inflammation and morphological alterations, as indicated by increased volume. However, the reversibility of these changes after bariatric surgery-induced weight loss remains underexplored. The aim of this study was to characterize volume changes in hypothalamic subunits up to 2 years following bariatric surgery. A secondary objective was to explore whether changes in hypothalamic subunit volumes were associated with changes in metabolic parameters and levels of gastrointestinal appetite-regulating hormones. Participants with severe obesity undergoing bariatric surgery were recruited. They completed high-resolution T1-weighted brain magnetic resonance imaging (MRI) before bariatric surgery and at 4, 12, and 24 months post-surgery. Blood samples collected during the fasting and postprandial states were analyzed for concentrations of glucagon-like peptide 1 (GLP-1), peptide YY (PYY), and ghrelin. The hypothalamus was segmented into five subunits per hemisphere using a publicly available automated tool. Linear mixed-effects models were employed to examine volume changes between visits and their associations with variables of interest. A total of 73 participants (mean age 44.5 ± 9.1 years; mean body mass index (BMI) 43.5 ± 4.1 kg/m2) were included at baseline, with 22 participants completing 24-month follow-up. Significant volume reductions were observed in the whole left hypothalamus 24 months post-surgery. More specifically, decreases were noted in both the left anterior-superior and left posterior subunits at 12 and 24 months post-surgery (all p < 0.05, after false discovery rate (FDR) correction). Smaller volumes in these subunits were significantly associated with a greater percentage of total weight loss (both subunits p < 0.001), as well as with higher postprandial PYY levels (both subunits p < 0.05). These findings suggest that some hypothalamic morphological alterations observed in the context of obesity could potentially be reversed following bariatric surgery-induced weight loss.

BackgroundNuts generally blunt the postprandial increases in glucose levels and increase satiety, while yogurt studies yield inconclusive results regarding post-meal hunger. This study investigated the effects of high-protein, and high-fat snacks, specifically Greek yogurt, and peanuts, on satiety, gut hormones, and insulin secretion in women with overweight and obesity. The hypothesis posited that peanuts would exhibit a more beneficial impact on satiety, gut hormones, and insulin levels compared to Greek yogurt.MethodsThe two-arm parallel randomized trial involved fifty participants aged 30–40 years with a BMI between 25 and 35 kg/m2, randomly divided into peanut (n = 25) and Greek yogurt (n = 25) groups. After three days of adhering to 1200 Kcal diet, appetite sensations were gauged using a visual analog scale (VAS) upon arrival, and at 30- and 60-min post-snack. Pre- and post-snacking, plasma levels of cholecystokinin (CCK), Peptide Tyrosine-Tyrosine (PYY), Glucagon Like Peptide-1 (GLP-1), Ghrelin (GHRL), and insulin were analyzed.ResultsRevealed that Greek yogurt induced a statistically significant increase in satiety 30 min after consumption and markedly elevated postprandial insulin levels compared to peanuts. Moreover, notable intergroup differences in postprandial insulin concentrations were observed in the Greek yogurt group. The peanut group had no significant alterations in PYY, GLP-1, CCK or GHRL levels. Pre-snacking, GHRL levels exhibited a positive association with abdominal circumference, weight, and fat mass, while CCK levels displayed a negative association with abdominal circumference, weight, and fat mass.ConclusionGreek yogurt may enhance satiety and thus has the potential to positively influence body weight in individuals with overweight and/or obesity. Further research is required to elucidate appetite control mechanisms.Trial registrationThe study was registered on ClinicalTrials.gov (No. NCT 04518930).

ABSTRACT Nesfatin-1, initially identified as an appetite-regulating hormone, has also been detected in various cancer tissues and implicated in tumorigenesis. However, its role in the proliferation and migration of lung cancer cells remains unclear. This study aims to investigate the effects of nesfatin-1 on the proliferation and migration of human lung cancer cells and elucidate the underlying molecular mechanisms. The expression of nesfatin-1 protein and NUCB2 mRNA was detected in the immortalized normal human bronchial cell line BEAS-2B and the non-small-cell lung cancer cell line H1299. Immunohistochemical staining revealed the localization of nesfatin-1 binding sites in both cell lines. Nesfatin-1 treatment significantly increased the proliferation and migration of BEAS-2B cells but not of H1299 cells. The expression levels of cell proliferation-related genes, such as TGFα, PXN, MTOR, and CCND1, were upregulated in BEAS-2B cells, with no significant changes observed in H1299 cells. In addition, phosphorylation of FAK, PI3 K, and AKT was increased in BEAS-2B cells, whereas only FAK phosphorylation was increased in H1299 cells. To further assess the role of endogenous nesfatin-1, NUCB2 expression was silenced using small interfering RNA. Knockdown of NUCB2 suppressed proliferation and migration of BEAS-2B cells, as well as their expression of TGFα, PXN, MTOR, and CCND1; however, it had no significant effect on H1299 cells. These results suggest that nesfatin-1 promotes proliferation and migration in normal lung epithelial cells but not in lung cancer cells. Further research is needed to elucidate the molecular mechanisms underlying the differential effects of nesfatin-1 on normal and cancerous lung cells.

The primary aim of this study was to evaluate the effect of ingestion of a standardized meal on gastric content volume and gastric emptying time in healthy normal weight people and those with obesity. Secondary aims were to evaluate the effect of the meal on superior mesenteric artery blood flow, small bowel water content, subjective satiety, and concentrations of appetite and motility-regulating hormones (PYY, ghrelin, GLP-1, and GLP-2), blood glucose and insulin in the participants. Ten normal weight male participants and ten with obesity were recruited. After fasted measurements participants consumed a test meal [∼500 g portion, 145 kcal (606 kJ)/100 g]. T50 gastric emptying time, gastric content volume, superior mesenteric artery blood flow and small bowel water content were measured using magnetic resonance imaging. Blood PYY, ghrelin, GLP-1, GLP-2, insulin and glucose were measured along with composite satiety scores. Measurements were repeated at regular intervals for up to 300 min. At screening, there were no differences between the groups apart from greater body weight and body mass index in those with obesity. Median ± SD T50 gastric emptying time was not different between normal weight participants and those with obesity (148 ± 16 min vs. 170 ± 15 min, respectively, P = 0.87). Gastric content volume, blood glucose, PYY, ghrelin, active GLP-1 and total GLP-2 concentrations, superior mesenteric artery blood flow, and small bowel water content, when fasted and in response to eating did not differ between groups (all P > 0.05). Repeated measures ANOVA showed no difference in postprandial blood glucose concentrations (P = 0.486) over time between the groups, but postprandial serum insulin was significantly higher (P = 0.015) in those with obesity. Composite satiety scores were significantly higher in the normal weight group immediately after eating and in the postprandial period (P = 0.015). Lower meal-stimulated satiety in males with obesity could lead to greater habitual dietary intake and further weight gain and, therefore, be an important driver for the maintenance of obesity in individuals without comorbidities.

Blunted cold pressor test-induced cortisol but not total ghrelin response in women with bulimia nervosa following a standardized sweet-fat liquid meal.

Aim: Dopaminergic neurons and dopamine transporters show variations in Attention Deficit Hyperactivity Disorder (ADHD). Furthermore, Ghrelin and leptin, hormones recognized for their neurotrophic effects, are significant in central nervous system regulation, influencing neuronal survival and development. Material and Methods: This study aimed to examine the potential relationship between Attention Deficit Hyperactivity Disorder (ADHD) and polymorphisms in the GHRL (rs34911341) and LEP (rs7799039) genes. The research sample consisted of 29 children diagnosed with ADHD and 24 age-matched healthy controls. Genotypic analysis was conducted using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Results: A significant difference in genotype distribution for the GHRL gene rs34911341 polymorphism was observed between the ADHD group and healthy controls (p = 0.036), whereas allele frequencies did not show a statistically significant difference (p = 0.207). In contrast, analysis of the LEP gene rs7799039 polymorphism revealed no significant differences in either genotype (p = 0.579) or allele frequencies (p = 0.558) between the two groups. Conclusion: These findings suggest a potential role for the GHRL rs34911341 polymorphism in the development or presentation of ADHD. Further research is required to elucidate the mechanisms underlying this association.

Study ObjectivesWeight gain after continuous positive airway pressure (CPAP) initiation in obstructive sleep apnea (OSA) is common, but its mechanism and relevance remain unclear. This open-label randomized trial evaluated CPAP effects on energy expenditure, intake, body composition, physical activity, and appetite-regulatory hormones.MethodsPatients with OSA were randomized (1:1) to 12-week CPAP or inactive control. The primary outcome was resting energy expenditure (REE). Secondary outcomes included dietary intake, eating behavior, fat mass (FM), fat-free mass (FFM), and activity count. Tertiary outcomes included appetite-regulatory hormones. CPAP effects were assessed as baseline-adjusted between-group differences using intention-to-treat (ITT) analysis; Per-protocol analysis (completers) served as sensitivity analysis.ResultsOf 52 randomized participants, 45 completed the study. In ITT analysis, CPAP had no effect on REE (8.6 kcal/day [95% CI = −51.5 to 68.7]; p = .774) or caloric intake (144.4 kcal/day [95% CI = −123.1 to 411.9]; p = .283). Although insignificant in morning, CPAP significantly increased evening body weight (p = .017) and body mass index in morning and evening (p = .040 and .030). CPAP also increased FFM, raised acylated ghrelin and insulin-like growth factor 1, and reduced cortisol and cognitive restraint. No changes were observed in macronutrient intake, FM, activity, insulin resistance, leptin, or neuropeptide Y. Per-protocol findings were similar.ConclusionsCPAP-induced weight gain, probably primarily from FFM, occurred without measurable changes in REE, activity, or significant increases in caloric intake. Accompanying hormonal and behavioral changes suggest a subtle positive energy balance. This gain may not reflect adverse metabolic effects and supports evaluating CPAP’s metabolic impact through body composition, not weight alone.Clinical trial registrationRegistry: ClinicalTrials.gov; Name: Validation of Sleep Healthcare System; URL: https://clinicaltrials.gov/study/NCT04252482; Identifier: NCT04252482.Statement of SignificanceThe physiological basis and clinical relevance of weight gain following CPAP therapy remain insufficiently defined. This study found that CPAP-induced weight gain was probably primarily due to increases in FFM, without measurable changes in REE, physical activity, or significant increases in reported caloric intake. Given the potential underestimation in dietary reporting, the observed gain—together with hormonal and behavioral changes—suggests a subtle positive energy balance. These findings indicate that post-CPAP weight gain may not reflect adverse metabolic effects and highlight the value of assessing body composition, rather than weight alone, in clinical follow-up.

IntroductionAlthough the literature suggests a strong association between attention deficit hyperactivity disorder (ADHD) and obesity, the underlying mechanisms remain unclear. Eating attitudes and appetite-regulating hormones (ARH) are considered to play a role in this relationship. Recent studies have shown that ARH may be linked to executive functions, and dysregulation of these hormones may help explain the connection between ADHD and obesity.ObjectivesWe aimed to investigate the levels of ARH, executive functions, eating attitudes, and ADHD symptoms in adults with ADHD compared to healthy controls.MethodsThe study included 44 drug-naive non-obese adults with ADHD who had no comorbid psychiatric diagnoses and 44 healthy controls matched for age, gender, education, and body mass index (BMI). All participants were diagnostically assessed using the Structured Clinical Interview for DSM-5 Disorders-Clinician Version. Also, participants completed the Adult ADHD Self-Report Scale, the Mind Excessively Wandering Scale, the Hospital Anxiety and Depression Scale, and the Eating Attitude Test (EAT). A battery of neuropsychological tests—Stroop Test (ST), Cancellation Test, Serial Digit Learning Test (SDLT), Wisconsin Card Sorting Test (WCST), and Judgment of Line Orientation Test (JLOT)—was administered. The serum samples obtained from fasting blood, after centrifugation were stored at -80°C until the time of analysis, at which point ARH levels (insulin, leptin, neuropeptide Y, orexine A, ghrelin, adiponectin) were measured using the ELISA method. The study was approved by Selçuk University Local Ethics Committee with the decision numbered 2023/328.ResultsAdults with ADHD exhibited worse ADHD symptoms, disordered eating attitudes, more severe anxiety and depression, and reduced executive functioning compared to healthy controls. Although ADHD groups showed more disordered eating attitudes compared to healthy controls, there was no significant difference in ARH levels between the two groups; however, these hormone levels were associated with specific parameters from ST, SDLT, WCST, and JLOT. Linear regression analyses to identify factors associated with each ARH separately revealed significant F values, except for ghrelin, which explained a unique variance ranging from 23.5% to 36%. These results indicated that visuospatial ability was associated with each ARH levels, even after controlling for age, gender, years of education, body mass index, severity of disordered eating attitudes, and the absence of an ADHD diagnosis.ConclusionsOur findings suggest that dysregulation of ARH may associate cognitive processes related to executive functioning independent of disordered eating attitudes, BMI, and ADHD diagnosis. However, these hormones may be mediating factors in relation between ADHD and obesity, and to figure out this relation, longitudinal clinical studies with larger samples are needed.Disclosure of InterestNone Declared

This study aimed to construct a nomogram to identify risk factors for malnutrition in patients with chronic heart failure (CHF) and to explore the correlation between Ghrelin (GHRL), Myostatin (MSTN), C-reactive protein (CRP) and High-sensitivity C-reactive protein (Hs-CRP) to further elucidate the potential pathophysiological mechanisms linking malnutrition/sarcopenia and inflammation. A total of 128 patients with congestive heart failure (CHF) admitted to the Cardiology Department of Guang'anmen Hospital, China Academy of Chinese Medical Sciences, between February 2022 and February 2023, were included in the study. Based on their MNA-SF scale scores, the patients were classified into two groups: the malnutrition group (107 patients) and the non-malnutrition group (21 patients). Univariate and multivariate logistic regression analyses were performed to identify risk factors for malnutrition in CHF patients, which facilitated the development of a nomogram. Correlation analysis was also conducted to explore the relationships between GHRL, MSTN, CRP, and Hs-CRP. Logistic regression analysis identified age, right upper limb diameter, simplified anorexia scale score, and MSTN as significant risk factors for malnutrition in CHF patients (P < 0.05). The nomogram exhibited strong discriminative power during internal validation, with an AUC of 0.917 (95% CI: 0.8439-0.990), a Hosmer-Lemeshow test result of χ2 = 7.966 (P = 0.336), a maximum Youden index of 0.701, an optimal cutoff value of 2.207, sensitivity of 77.7%, and specificity of 92.3%. Calibration curve analysis showed that the nomogram's predictions closely matched the ideal outcomes. Decision curve analysis (DCA) demonstrated that when the threshold probability exceeded 0.1, the nomogram's clinical net benefit surpassed those of the "full intervention" and "no intervention" strategies, highlighting its strong clinical applicability. Additionally, MSTN was positively correlated with CRP and Hs-CRP, while GHRL was negatively correlated with MSTN, CRP, and Hs-CRP. Significant differences were observed between MSTN, GHRL, and CRP (P < 0.05). This study supports the hypothesis that age, right upper limb diameter, simplified anorexia scale score, and MSTN are significant risk factors for malnutrition in CHF patients. The nomogram developed in this study demonstrated robust predictive value for identifying malnutrition in this population. Furthermore, the proposed inflammation-GHRL/MSTN-appetite improvement/muscle growth-CHF improvement pathway offers a potential regulatory mechanism,which represents a promising direction for research into the mechanisms of malnutrition and muscle loss disorders in patients with CHF.

Adolescent obesity is a growing global health concern, often refractory to conventional interventions. While bariatric surgery remains the most effective treatment, its invasiveness and long-term implications limit its use in pediatric patients. Endoscopic sleeve gastroplasty (ESG) has recently emerged as a minimally invasive alternative. This narrative review aims to provide a comprehensive overview of ESG in adolescents, addressing efficacy, safety, mechanisms of action, comparisons with other therapies, and current guideline recommendations. We conducted a narrative review of studies on ESG in individuals under 21years of age. Literature searches were performed using PubMed, Scopus, EMBASE, and Web of Science for English-language articles published up to April 2025. Studies were included if they reported on ESG outcomes, safety, mechanisms, indications, or expert consensus. Available pediatric data, primarily from a single-center cohort of 109 adolescents, show a total body weight loss (TBWL) of 14.4% at 6months, 16.2% at 12months, and 13.7% at 24months. ESG demonstrated a favorable safety profile, with minor adverse events (abdominal pain, nausea) in 2-3% and no severe complications or growth impairment. Mechanistically, ESG induces weight loss via gastric restriction and delayed gastric emptying, without altering nutrient absorption or appetite-regulating hormones. Comparisons with other modalities show ESG outperforms lifestyle therapy and pharmacotherapy in TBWL, with fewer complications than laparoscopic sleeve gastrectomy. ESG is cost-effective in class II obesity and may be reversible or combined with medical therapies. Despite promising results, ESG remains supported by Level IV evidence and is recognized in only a few pediatric guidelines. ESG offers a safe, anatomy-preserving, and moderately effective treatment option for adolescents with moderate-to-severe obesity. It may serve as a valuable bridge between conservative therapy and surgery. However, long-term data and randomized controlled trials are needed to define its role within standardized pediatric obesity care pathways.

K-757 and K-833 are novel full agonists of GPR40 and GPR119, respectively, which are nutrient receptors co-expressed on both pancreatic beta cells and gut enteroendocrine cells that signal through complementary mechanisms. We sought to assess the effects on glucose control and body weight following co-administration of K-757 and K-833. We conducted two randomized, double-blind, placebo-controlled Phase 1 studies in overweight-obese subjects with T2DM maintained on metformin to characterize the effects on secretion of gut incretin and appetite-regulating hormones, glucose control and body weight following combined therapy with K-757 and K-833. In Study 1 (28 days in duration) K-757/K-833 was titrated to 60/100 mg BID. In Study 2 (42 days in duration) K-757/K-833 was titrated to 240/200 mg QD. Twenty-five subjects were enrolled in Study 1 (12 on placebo and 13 on K-757 + K-833) and 24 in Study 2 (6 on placebo and 18 on K-757 + K-833). By design, baseline A1C was higher in Study 1 compared with Study 2. After 28 days of dosing (Study 1), the combination of K-757 + K-833 resulted in placebo-corrected LS mean reductions from baseline in 24 h-WMG, FPG, A1C and body weight of 77.3 mg/dL, 64.0 mg/dL, 0.55% and 1.61%, respectively. After 42 days of dosing (Study 2), the combination of K-757 + K-833 resulted in placebo-corrected LS mean reductions from baseline in FPG, A1C and body weight of 25.2 mg/dL, 0.26% and 4.95%, respectively. Co-agonism of GPR40 and GPR119 with K-757 and K-833 elicits rapid, robust and glucose-dependent glucose lowering and modest weight loss in patients with T2DM on stable metformin.

Short sleep has been linked to overweight, possibly via alterations in appetite-regulating hormones, but findings are inconsistent. Sex differences may contribute to this variability. This systematic review examines whether sex modifies the hormonal response to sleep curtailment. PubMed, Embase, Cochrane, CINAHL, and PsycINFO were searched for English-language experimental studies published before December 2024. Included studies assessed at least one appetite-regulating hormone and presented sex-specific analyses. Studies involving health conditions affecting sleep, circadian misalignment, or additional interventions were excluded. Risk of bias was assessed using the Revised Cochrane Risk-of-Bias tool (RoB 2). Eight studies (n = 302 participants) met inclusion criteria. A narrative synthesis of the findings was conducted for each hormone separately to explore potential differences in their response to sleep restriction. Some sex-related variations in hormonal response to sleep restriction have been observed for leptin (four studies, n = 232), insulin (three studies, n = 56), glucagon-like peptide-1 (one study, n = 27), ghrelin (three studies, n = 87), adiponectin (two studies, n = 71) and thyroxine (two studies, n = 41). However, findings were inconsistent with no clear patterns. No sex-related differences were found for glucagon or PYY, though data were limited. Findings suggest sex may influence hormonal responses to sleep restriction, but inconsistencies highlight the need to consider factors such as BMI and energy balance. Well-controlled, adequately powered studies are needed to clarify these effects.