Background/Objectives: This randomized controlled trial aimed to evaluate the effects of casein-enriched milk (CEM) consumption and its timing (presleep vs. during the day) in the early postoperative period on body composition, muscle strength, physical function, and biochemical parameters in individuals undergoing laparoscopic sleeve gastrectomy (SG). Methods: Forty-five adults (60% female, 40% male; mean age 35.1 ± 9.7 years; mean BMI 41.4 ± 4.9 kg/m²) undergoing SG were randomly assigned to three groups: (1) 15 g protein CEM (12 g casein) presleep, (2) the same CEM during the day, or (3) standard-protein diet without supplementation. The primary endpoint was change in fat-free mass (FFM) at 12 weeks; secondary endpoints included handgrip strength, 30 s sit-to-stand test, and serum total protein, albumin, and prealbumin. Assessments were performed preoperatively and at weeks 4, 8, and 12. Results: No significant differences were found between the groups in terms of body composition, muscle strength, or physical performance measurements (p > 0.05). However, a significant increase in handgrip strength was observed over time in Groups 1 and 2 (p < 0.05), which was not observed in Group 3. Prealbumin levels at week 12 were 0.3 ± 0.0 mg/dL in Group 1 and 0.2 ± 0.0 mg/dL in Group 2, both higher than 0.2 ± 0.0 mg/dL in Group 3 (p < 0.05). No significant differences were found in albumin and total protein levels (p > 0.05). Conclusions: Early postoperative CEM consumption following SG did not significantly affect body composition or physical performance; however, the higher prealbumin levels indicate that this marker may be more sensitive in detecting early protein response, highlighting its potential clinical relevance in monitoring nutritional status after bariatric surgery.

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.

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.

Objective: Surgical weight loss is seen as an option for individuals with obesity. In this case study, it was aimed to evaluate the nutritional status of a vegan obese patient before and after bariatric surgery. Methods: A 26-year-old vegan obese male patient underwent sleeve gastrectomy in May 2016. He was followed up for one month preoperatively and two years postoperatively. The number of individuals adopting vegetarian/vegan lifestyle for various reasons has been increasing recently. To prevent nutrient deficiency after bariatric surgery, lifelong vitamin-mineral supplements and vitamin-minerals-rich food consumption are recommended. Results: A 26-year-old vegan obese male patient body mass index was 38.6kg/m2 and the postoperative 2nd year body mass index was 24.1kg/m2. Preoperative muscle mass was 76.2 kg, postoperative 2nd year 63 kg, preoperative body fat mass was 47.9 kg, postoperative 2nd year 9.2 kg. Conclusion: In this vegan case, preoperative and postoperative medical nutrition treatments were planned considering the type of surgery specific to the individual. Medical nutrition treatment is an important part of the multidisciplinary bariatric surgery process.