Plain Language SummaryDespite the increasing interest in combating obesity, its prevalence is increasing worldwide. The success of available management modalities for obesity is often complicated by mental health, eating, and sleeping disorders. Night eating syndrome is a unique eating disorder characterized by excessive calorie intake at night that exceeds one-quarter of the total daily calorie consumption. We conducted a study on 425 individuals with obesity from five healthcare centers in Port Said, Egypt to evaluate the extent and associated factors of night eating syndrome, insomnia, and psychological distress among people with obesity. We found that around one in five individuals with obesity suffered from night eating syndrome or psychological distress, and one in six individuals with obesity had symptoms of insomnia. Notably, night eating syndrome, insomnia, and psychological distress were interrelated. Moreover, fatty liver occurred more frequently in patients with obesity who had night eating syndrome or insomnia highlighting the importance of maintaining circadian rhythms in metabolic disorders. Based on our findings, we recommend that family physicians should routinely assess dietary habits, sleeping disorders, and mental health conditions in people with obesity to enhance the success rate of obesity management in primary care.

Obesity is fundamentally a condition where physiology and behavior of individuals meet the environment, and the emerging global obesity pandemic reflects the contribution of a wide range of cultural, societal, economic and systemic driving forces. Today, different areas of obesity research are relatively separated from each other in discrete silos, with biomedical research determining most of our understanding and solution strategies. This has led to the Y in the road, which means the questionable assumption that effective drug treatment of individual patients is also an effective measure to improve population health. Since human obesity is a condition of population health and planetary impact a better integration of biomedical and public health approaches is based on critical (self-)reflection and communicative understanding of scientists from various research areas who should be on an equal footing.

Bariatric surgery is routinely proposed to patients suffering from obesity including kidney transplant recipients. In this specific population, bariatric surgery has a positive impact in long-term outcomes in terms of patient and graft survival. We report here the cases of 4 patients with five post-kidney transplantation bariatric surgeries who experimented acute renal injury early after surgery. Creatinine rising occurred between day 14 and day 20 after surgery. In all cases, it was due to dehydration leading to a pre-renal acute renal failure. The specific care of kidney transplanted patients is discussed: single kidney associated with pre-existing altered kidney function associated with concomitant use of nephrotoxic drugs. Specific education intervention before surgery associated with careful early management of hydration after surgery is mandatory for these patients.

Introduction: Vertical sleeve gastrectomy (VSG) is considered one of the most effective treatments for sustained weight loss and complete remission of type 2 diabetes mellitus (CR-T2DM). Liver-expressed antimicrobial peptide 2 (LEAP2), a ghrelin receptor antagonist peptide, is a metabolic hormone regulated by VSG. However, it is unknown whether LEAP2 can be used to predict the outcomes of VSG. This study aimed to evaluate LEAP2 as a predictive factor for weight loss and CR-T2DM after VSG. Methods: This retrospective study included 39 Japanese participants with obesity who underwent VSG. Serum LEAP2, des-acyl ghrelin (DAG), and other metabolic and anthropometric parameters were studied before and at 12 months after VSG. Receiver operating characteristics (ROC) curve was generated to evaluate predictive score for weight loss with cut-off value of >50 percent excess weight loss. ROC curve was also generated to assess CR-T2DM. Results: Serum LEAP2 levels were significantly higher in participants with body mass index (BMI) 32–50 kg/m² than in those with normal weight. Participants with BMI >50 kg/m² had lower serum LEAP2 concentrations than those with BMI 32–50 kg/m². VSG caused a significant reduction in serum DAG concentrations, but it did not affect serum LEAP2 concentrations in either male or female participants. Preoperative serum LEAP2 concentration of 2.88 pmol/mL was the optimal cutoff value for predicting weight loss after VSG, with sensitivity of 80.0% and specificity of 75.9%. Preoperative serum LEAP2 level higher than 4.67 pmol/mL predicted CR-T2DM after VSG with sensitivity of 100% and specificity of 58.8%. Conclusion: Preoperative serum LEAP2 could predict weight loss and CR-T2DM as outcomes of VSG.

Introduction: Infections are a major problem after left ventricular assist device (LVAD) implantation that affects morbidity, mortality, and the quality of life. Obesity often increases the risk for infection. In the cohort of LVAD patients, it is unknown if obesity affects the immunological parameters involved in viral defense. Therefore, this study investigated whether overweight or obesity affects immunological parameters such as CD8⁺ T cells and natural killer (NK) cells. Methods: Immune cell subsets of CD8⁺ T cells and NK cells were compared between normal-weight (BMI 18.5–24.9 kg/m², n = 17), pre-obese (BMI 25.0–29.9 kg/m², n = 24), and obese (BMI ≥30 kg/m², n = 27) patients. Cell subsets and cytokine serum levels were quantified prior to LVAD implantation and at 3, 6, and 12 months after LVAD implantation. Results: At the end of the first postoperative year, obese patients (31.8% ± 2.1%) had a lower proportion of CD8⁺ T cells than normal-weight patients (42.4% ± 4.1%; p = 0.04), and the percentage of CD8⁺ T cells was negatively correlated with BMI (p = 0.03; r = −0.329). The proportion of circulating NK cells increased after LVAD implantation patients in normal-weight (p = 0.01) and obese patients (p < 0.01). Patients with pre-obesity showed a delayed increase (p < 0.01) 12 months after LVAD implantation. Further, obese patients showed an increase in the percentage of CD57⁺ NK cells after 6 and 12 months (p = 0.01) of treatment, higher proportions of CD56^bright NK cells (p = 0.01), and lower proportions of CD56^dim/neg NK cells (p = 0.03) 3 months after LVAD implantation than normal-weight patients. The proportion of CD56^bright NK cells positively correlated with BMI (p < 0.01, r = 0.403) 1 year after LVAD implantation. Conclusions: This study documented that obesity affects CD8⁺ T cells and subsets of NK cells in patients with LVAD in the first year after LVAD implantation. Lower proportions of CD8⁺ T cells and CD56^dim/neg NK cells and higher proportion of CD56^bright NK cells were detected in obese but not in pre-obese and normal-weight LVAD patients during the first year after LVAD implantation. The induced immunological imbalance and phenotypic changes of T and NK cells may influence viral and bacterial immunoreactivity.

Introduction: Recent studies suggested that sarcopenia may be a significant comorbidity of diabetes mellitus (DM). Nonetheless, studies with nationally representative data are scarce, and the changing trend of sarcopenia prevalence over time is largely unknown. Therefore, we aimed to estimate and compare the prevalence of sarcopenia in diabetic and nondiabetic US older population, and to explore the potential predictors of sarcopenia as well as the trend of sarcopenia prevalent in the past decades. Methods: Data were retrieved from the National Health and Nutrition Examination Survey (NHANES). Sarcopenia and DM were defined according to corresponding diagnosis criteria. Weighted prevalence was calculated and compared between diabetic and nondiabetic participants. The differences among age and ethnicity groups were explored. Results: A total of 6,381 US adults (>50 years) were involved. The overall prevalence of sarcopenia was 17.8% for US elders, and the prevalence was higher (27.9% vs. 15.7%) in those with diabetes ones than those without. Stepwise regression revealed that sarcopenia was significantly associated with DM (adjusted odds ratio = 1.37, 95% CI: 1.08–1.22; p < 0.05) after controlling for potential confounders including gender, age, ethnicity, educational level, BMI, and muscle strengthening activity. A slight fluctuation but overall increasing trend of sarcopenia prevalence was observed among diabetic elders, while no obvious changing trend was observed in their counterparts in recent decades. Conclusion: Diabetic US older adults face significantly higher risk of sarcopenia when compared with their nondiabetic counterparts. Gender, age, ethnicity, educational level, and obesity were important influencing factors of sarcopenia development.

Introduction: Previous weight loss attempts in young people with obesity may have influenced their beliefs about themselves and contributed to maladaptive eating behaviors. Therefore, we aimed to investigate the association between previous weight loss with self-esteem and different eating behaviors in adolescents and young adults with obesity seeking specialty obesity care. Methods: We performed a cross-sectional study, where a total of 224 participants with obesity, aged 16–25, self-reported the amount and the frequency of previous weight loss of 5 kg or more. Self-esteem was assessed with Rosenberg’s Self-Esteem Scale and eating behavior with the Three-Factor Eating Questionnaire-Revised21. Linear regression was used to analyze associations between the amount of weight loss (no weight loss, 5–10 kg, and >10 kg) and the frequency of weight loss ≥5 kg (0, 1, and ≥2 times) with self-esteem and eating behaviors. Results: We found that both those who had lost 5–10 kg and those who had lost ≥5 kg twice or more, had statistically significantly higher cognitive restraint eating scores β = 7.03 (95% CI: 0.004–14.05) and β = 8.32 (95% CI: 1.20–15.43), respectively, compared to those who reported no previous weight loss. No other statistically significant associations were found. Conclusion: Previous weight loss in adolescents and young adults with obesity may be associated with a higher cognitive restraint eating behavior. Therefore, assessing weight loss history and eating behavior may be beneficial to better individualize obesity treatment.

Introduction: Obesity is associated with an increased risk of inflammatory bowel disease (IBD), whereas not all obese individuals have the same effect. In individuals with obesity, the role of metabolic status in the readmission of IBD remains unclear. Our study aimed to evaluate the association between different obesity metabolic phenotypes and the prognosis of IBD patients. Methods: We conducted a longitudinal cohort study using Nationwide Readmissions Database (NRD) (2018 sample). Out of 12,928,231 discharge records, 63,748 records with a discharge diagnosis of IBD were identified for analysis. Cox proportional hazard ratio (HR) with 95% confidence interval (CI) was calculated, adjusting for potential confounders. Results: During a 180-day follow-up in IBD patients with different obesity metabolic phenotypes, all-cause readmission rate, inpatient mortality rate, unplanned readmission rate, total charge, hospitalized length of stay were statistically different (all p < 0.001). After multivariate Cox regression analysis, IBD patients with metabolically unhealthy nonobese (MUNO) had higher risk of readmission (all-cause and unplanned) (HR 1.04, 95% CI: 1.00–1.08 and HR 1.06, 95% CI: 1.02–1.10), and those with metabolically unhealthy obesity (MUO) had higher risk of unplanned readmission (HR 1.08, 95% CI: 1.02–1.15). In subgroup analysis, both the MUNO group and MUO group had higher risk of readmission (all-cause and unplanned) in the ulcerative colitis (UC) subgroup, but only the MUNO group had higher risk of readmission (all-cause and unplanned) (HR 1.05, 95% CI: 1.00–1.10 and HR 1.06, 95% CI: 1.01–1.12) in the Crohn’s disease (CD) subgroup. Conclusion: Metabolic abnormalities were associated with an increased risk of readmission in patients with IBD, regardless of obesity.

Introduction: Observational studies have shown that obesity is a risk factor for various autoimmune diseases. However, the causal relationship between obesity and autoimmune diseases is unclear. Mendelian randomization (MR) was used to investigate the causal effects of obesity on 15 autoimmune diseases. Methods: MR analysis employed instrumental variables, specifically single-nucleotide polymorphisms associated with obesity measures such as body mass index (BMI), waist circumference, hip circumference, and waist-to-hip ratio. The study utilized UK Biobank and FinnGen data to estimate the causal relationship between obesity and autoimmune diseases. Results: Genetically predicted BMI was associated with risk for five autoimmune diseases. The odds ratio per 1-SD increase in genetically predicted BMI, the OR was 1.28 (95% CI, 1.18–1.09; p < 0.001) for asthma, 1.37 (95% CI, 1.24–1.51; p < 0.001) for hypothyroidism, 1.52 (95% CI, 1.27–1.83; p < 0.001) for psoriasis, 1.22 (95% CI, 1.06–1.40; p = 0.005) for rheumatoid arthritis, and 1.55 (95% CI, 1.32–1.83; p < 0.001) for type 1 diabetes. However, after adjusting for genetic susceptibility to drinking and smoking, the correlation between BMI and rheumatoid arthritis was not statistically significant. Genetically predicted waist circumference, hip circumference, and waist and hip circumference were associated with 6, 6, and 1 autoimmune disease, respectively. Conclusion: This study suggests that obesity may be associated with an increased risk of several autoimmune diseases, such as asthma, hypothyroidism, psoriasis, rheumatoid arthritis, and type 1 diabetes.