Background Children engaged in aesthetic sports face performance demands and parental dietary influence during critical developmental windows. This study examined associations between parental nutrition knowledge and children's eating behaviours and nutrient intakes in young female aesthetic gymnasts. We hypothesised that higher parental nutrition knowledge would be associated with reduced desire to drink sweetened beverages, lower emotional overeating, and more favourable dietary patterns. Methods A cross-sectional survey was conducted with 119 parent–child dyads recruited from aesthetic gymnastics clubs (children aged 6–12 years; 100% female). Parental nutrition knowledge was assessed with the General Nutrition Knowledge Questionnaire (GNKQ) and children's eating behaviours with the Children's Eating Behaviour Questionnaire (CEBQ; eight subscales). Dietary intake was assessed by a single 24-hour recall administered by a registered dietitian and analysed using BeBiS 8.1 software. Multiple linear regression models were fitted for each CEBQ subscale with GNKQ score, maternal education, paternal education, child age and BMI as predictors. The Benjamini–Hochberg procedure controlled the false discovery rate across multiple comparisons. Results GNKQ score (M = 85.8 ± 15.6; possible range 0–116) was a significant independent predictor of children’s Desire to Drink (β = −0.381, t = − 3.790, p < 0.001) and Emotional Overeating (β = −0.140, t = − 2.057, p = 0.040) in regression models adjusting for child age, BMI, and parental education. Paternal education was independently associated with higher Emotional Overeating (β = 0.142, p = 0.023) and Emotional Undereating (β = 0.234, p = 0.037). Higher parental knowledge was also associated with greater fibre, protein, and micronutrient intakes. Mean daily energy intake was 1123 ± 273 kcal, substantially below estimated requirements for active girls in this age range. Conclusions Parental nutrition knowledge is independently and inversely associated with children’s desire to drink sweetened beverages and with emotional overeating in young gymnasts, after controlling for demographic covariates. The very low energy intake observed raises concern for Relative Energy Deficiency in Sport (REDs). Nutrition education programmes targeting parents and coaches in aesthetic gymnastics are warranted.

Inflammatory bowel diseases (IBD) are chronic inflammatory disorders that arise from the complex interplay among genetic predisposition, immune dysregulation, environmental factors, and disruption of intestinal epithelial barrier integrity. Increasing evidence suggests that endoplasmic reticulum (ER) stress may represent an important mechanistic pathway in this multifactorial pathogenesis. Experimental evidence indicates that dietary patterns and nutrient-derived factors may modulate ER stress responses. In this review, the role of ER stress in IBD is discussed from a mechanistic perspective, with particular emphasis on the effects of nutrition on ER stress pathways and the relationship between these interactions and IBD pathogenesis. The available findings are evaluated according to whether they derive from direct human IBD studies, experimental colitis models, intestinal cellular systems, or indirect non-intestinal models. Evidence derived predominantly from experimental and non-intestinal metabolic models indicates that high-fat and high-fructose exposures can activate PERK- and IRE1-associated signaling and CHOP-related terminal responses; however, their direct effects on intestinal UPR signaling and epithelial barrier integrity in human IBD have not been established. In contrast, polyunsaturated fatty acids, flavonoids, polyphenols, and certain micronutrients have been reported to modulate selected UPR markers and support cellular adaptation in experimental systems, although differences in dose, bioavailability, and study model limit clinical extrapolation. Collectively, current evidence suggests that ER stress may represent an important mechanistic pathway linking nutrition and intestinal inflammation, although direct causal evidence linking nutritional exposures to mucosal ER stress and clinical outcomes in humans remains limited. Controlled dietary studies incorporating standardized, pathway-specific mucosal biomarkers are required before this mechanistic framework can inform personalized nutritional strategies or ER-stress-targeted interventions.

Background/Objectives: Obesity after kidney transplantation impairs graft function, but the time course of lean tissue loss after sleeve gastrectomy in this population is poorly described. Methods: A 46-year-old woman underwent sleeve gastrectomy five years after kidney transplantation and was followed for 33 months with bioelectrical impedance analysis (BIA) and three 24-h dietary recalls per visit. Results: Weight fell from 103.4 to 69.4 kg by month 6, with mild regain to 71.9 kg at month 33. BIA-derived fat-free mass, BIA-predicted total muscle mass and BIA-derived skeletal muscle mass reached their lowest recorded values at month 3, each 21.3% below baseline, and were essentially unchanged at month 6; fat-free mass loss corresponded to 34.1% of the weight lost by month 6, above the thresholds proposed for excessive loss in a bariatric cohort which are research rather than clinical definitions. This early loss coincided with three concurrent exposures: energy restriction (521 and 466 kcal/day at months 1 and 3), protein intake below target during a period of aversion to protein-rich foods (33.2 g/day against a 60 g/day target), and absence of structured physical activity; anaemia was present throughout and may have contributed to both. Graft function was clinically stable but not unchanged, with estimated glomerular filtration rate 25% below baseline at month 33 and persistent proteinuria; biopsy was not performed. Conclusions: Early postoperative nutritional vulnerability was temporally associated with substantial lean tissue loss. The estimates are BIA-derived and hydration-dependent, muscle function was not assessed, and the concurrent exposures cannot be separated in a single case, so no causal relationship can be inferred.

Most existing reviews treat endoplasmic reticulum (ER) stress as one mechanism among several in leptin resistance. This review advances a different claim: ER proteostasis may act as a central convergence node, translating metabolic, inflammatory, developmental, and nutrient-derived signals into a shared effector signature. In common obesity, leptin responsiveness is blunted despite hyperleptinaemia—the principal obstacle to leptin-based therapy. Leptin resistance is examined at the intersection of intracellular signalling networks (JAK2/STAT3, PI3K/Akt, MAPK, AMPK, mTOR, FoxO1, SOCS3, and PTP1B), hypothalamic ER stress, and the unfolded protein response (UPR). This narrative synthesis incorporates 22 primary studies, with PRISMA 2020 principles used to document study selection transparently. The ER shapes leptin signalling at three levels: receptor biogenesis (SEL1L–HRD1 ERAD), receptor bioavailability (CHOP-mediated soluble receptor), and post-receptor inhibition (SOCS3/PTP1B). Distinct stressors converge on a narrow effector set (CHOP, SOCS3, and PTP1B) whose direction of effect is context-dependent, and receptor quality control can operate without activation of the PERK arm, indicating that the ER’s role is not confined to the canonical stress response. The framework yields three testable hypotheses with an explicit falsification criterion and proposes that leptin resistance comprises phenotypically distinct subtypes. The evidence base is entirely preclinical (17 rodent in vivo; 5 in vitro studies); translation to humans remains untested.

Most existing reviews treat endoplasmic reticulum (ER) stress as one mechanism among several in leptin resistance. This review advances a different claim: ER proteostasis may act as a central convergence node, translating metabolic, inflammatory, developmental, and nutrient-derived signals into a shared effector signature. In common obesity, leptin responsiveness is blunted despite hyperleptinaemia—the principal obstacle to leptin-based therapy. Leptin resistance is examined at the intersection of intracellular signalling networks (JAK2/STAT3, PI3K/Akt, MAPK, AMPK, mTOR, FoxO1, SOCS3, PTP1B) and hypothalamic ER stress and the unfolded protein response (UPR). This narrative synthesis incorporates 22 primary studies, with PRISMA 2020 principles used to document study selection transparently. The ER shapes leptin signalling at three levels: receptor biogenesis (SEL1L–HRD1 ERAD), receptor bioavailability (CHOP-mediated soluble receptor), and post-receptor inhibition (SOCS3/PTP1B). Distinct stressors converge on a narrow effector set (CHOP, SOCS3, PTP1B), and receptor quality control can operate independently of ER stress, demonstrating that the ER's role is not confined to a stress response. The framework yields three testable hypotheses with an explicit falsification criterion, and proposes that leptin resistance comprises phenotypically distinct subtypes. The evidence base is entirely preclinical (17 rodent in vivo; 5 in vitro studies); translation to humans remains untested.