Journal of Obesity

Background. Weight loss and lifestyle interventions are the mainstay of treatment in pediatric NAFLD. There are gaps in the literature on the objective improvement in BMI to meaningfully impact NAFLD in children. Aim. To determine the decrease in BMI associated with a significant decline in ALT and other metabolic parameters. Methods. Retrospective chart review of pediatric patients with the diagnosis of NAFLD. Data were collected at the baseline and 6 and 12 months. A linear regression model was used to assess the percent change in BMI predictive of change in ALT and other metabolic parameters. Results. 281 charts were included. 71% of patients who had up to a 2.5% loss in BMI at 6 months had a decrease in ALT of up to 10 U/L compared to 43% patients who did not have a decrease in BMI up to 2.5% loss at the same time period (). The linear regression model showed that 6-month and 12-month percent changes in BMI are predictive of 6-month and 12-month ALT changes ( and 0.02), respectively. ALT normalization was achieved on 12% of patients with a ≥2.5% decrease in BMI at 6 months compared to 1% of patients that had no decrease of ≥2.5% decrease in BMI at 6 months (). The mean BMI Z-score decline was 0.18 () in the group with a ≥2.5% decrease in BMI at 6 months. Conclusions. BMI loss of up to 2.5% and the mean BMI Z-score 0.18 are associated with a significant decrease in ALT of up to 10 U/L. BMI percent change at 6 months and 12 months is predictive of changes in ALT. These results should help guide providers in clinical practice set objective goals for the management of children with NAFLD resulting from obesity.

Aims. The prevalence of obesity is rapidly increasing during the past decades. While previous research has focused on the early outcome after cardiac surgery or specific complications, the current study covers the whole burden of obesity in the field of cardiac surgery over short term and long term. Endpoints of the study were all-cause mortality, perioperative outcome, and wound-healing disorders (WHDs). Methods. 14.754 consecutive patients who underwent cardiac surgery over a 14 years’ time period were analyzed. BMI classifications were used according to the WHO definition. Results. Mean survival was 11.95 years ± 0.1; CI 95% [12.04–12.14]. After adjustment for clinical baseline characteristics, obesity classes’ I–III (obesity) did not affect 30-day mortality or all-cause mortality during the whole observational period. After adjustment for known risk factors, the risk for WHDs doubled at least in obesity patients as follows: obesity I (OR = 2.06; CI 95% [1.7–2.5]; ), obesity II (OR = 2.5; CI 95% [1.83–3.41]; ), and obesity III (OR = 4.12; CI 95% [2.52–6.74]; ). The same applies to the risk for sternal reconstruction that is substantially elevated in obesity I (OR = 2.23; CI 95% [1.75–2.83]; ), obesity II (OR = 2.81; CI 95% [1.91–4.13]; ), and obesity III (OR = 2.31; CI 95% [1.08–4.97]; ). No significant correlation could be found between obesity and major adverse events in the perioperative course like renal failure, ventilation >24 h, re-exploration, or cerebrovascular events. Conclusions. Cardiac surgery is safe in obesity as short- and long-term mortality are not increased, and major adverse events during the perioperative course are similar to control patients. The burden of obesity lies in substantially increased rates of wound-healing disorders and sternal reconstructions.

Obesity is considered the leading public health problem in the medical sector. The phenotype includes overweight conditions that lead to several other comorbidities that drastically decrease health. Glucagon-like receptor agonists (GLP-1RAs) initially designed for treating type 2 diabetes mellitus (T2DM) had demonstrated weight loss benefits in several clinical trials. In vivo studies showed that GLP-1RA encourages reduced food consumption and consequent weight reduction by stimulating brown fat and enhancing energy outlay through the action of the sympathetic nervous system (SNS) pathways. Additionally, GLP-1RAs were found to regulate food intake through stimulation of sensory neurons in the vagus, interaction with the hypothalamus and hindbrain, and through inflammation and intestinal microbiota. However, the main concern with the use of GLP-1RA treatment was weight gain after withdrawal or discontinuation. We could identify three different ways that could lead to weight gain. Potential factors might include temporary hormonal adjustment in response to weight reduction, the central nervous system’s (CNS) incompetence in regulating weight augmentation owing to the lack of GLP-1RA, and β-cell malfunction due to sustained exposure to GLP-1RA. Here, we also review the data from clinical studies that reported withdrawal symptoms. Although the use of GLP-1RA could be beneficial in multiple ways, withdrawal after years has the symptoms reversed. Clinical studies should emphasize the downside of these views we highlighted, and mechanistic studies must be carried out for a better outcome with GLP-1RA from the laboratory to the bedside.

The “new epidemic,” as WHO calls obesity, is caused by overeating, which, having exceeded the body’s actual needs, accumulates in the form of health-damaging fat deposits. Moving more and eating less is the main remedy, but eating belongs to vital instincts, which are beyond the control of reason. In this sense, eating is different from drinking and breathing because without food it is possible to survive for a few weeks, without water for a few days, without oxygen for a few minutes. The first part of this article provides an overview of obesity and its treatment, focusing on the new anorectic anticipated in the title. The second part focuses on compulsive obesity, typically represented by constitutional obesity and food addiction. The article concludes with a discussion of the pharmacological treatment of compulsive diseases, to which some forms of obesity belong.

Background. Obesity is expected to hinder efferocytosis due to ADAM17-mediated cleavage of the MER tyrosine kinase receptor, producing soluble MER (sMER) that disrupts MERTK binding to cell death markers. However, the intracellular efferocytosis pathway in central obesity remains elusive, particularly the role of low-grade chronic inflammation in its initiation and identification of binding signals that disrupt efferocytosis. Objective. We investigate the efferocytosis signaling pathway in men with central obesity and its relationship with inflammation, cell death, and related processes. Methods. A cross-sectional study was conducted, and clinical data and blood samples were collected from 56 men with central obesity (obese group) and 29 nonobese individuals (control group). Clinical evaluations and predefined biochemical screening tests were performed. The efferocytosis signaling pathway was investigated by measuring phosphatidylserine (PS), ADAM17, TNF-alpha (TNF-α), and sMER. Results. Metabolic syndrome was detected in more than half of the participants in the obese group according to the predefined tests. Mean levels of PS, TNF-α, and sMER were higher in the obese group but not significantly different from those of the control group. Further analysis based on waist circumference (WC) ranges in the obese group revealed a significant increase in PS and sMER levels between the control group and the obese group with WC greater than 120 cm. ADAM17 levels were significantly higher in the obese group than in the control group. PS was positively correlated with WC and ADAM17. ADAM17 was positively correlated with TNF-α and sMER, indicating impaired efferocytosis. Conclusions. Central obesity appeared to cause a disturbance in efferocytosis that began with cell damage and death, along with an enlargement of the WC and an ongoing inflammatory response. Efferocytosis was disrupted by proinflammatory cytokine regulators, which induced the production of sMER and interfered with the efferocytosis process.

Background. Type 2 diabetes mellitus and metabolic syndrome represent two closely intertwined public health challenges that have reached alarming epidemic proportions in low- and middle-income countries, particularly in sub-Saharan Africa. Therefore, the current study aimed to determine the weighted pooled prevalence of metabolic syndrome and its components among individuals with type 2 diabetes mellitus in sub-Saharan Africa as defined by the 2004 National Cholesterol Education Program-Adult Treatment Panel (NCEP-ATP III 2004) and/or the International Diabetes Federation (IDF) criteria. Methods. A systematic search was conducted to retrieve studies published in the English language on the prevalence of metabolic syndrome among type 2 diabetic individuals in sub-Saharan Africa. Searches were carried out in PubMed, Embase, Scopus, Google Scholar, African Index Medicus, and African Journal Online from their inception until July 31, 2023. A random-effects model was employed to estimate the weighted pooled prevalence of metabolic syndrome in sub-Saharan Africa. Evidence of between-study variance attributed to heterogeneity was assessed using Cochran’s Q statistic and the I2 statistic. The Joanna Briggs Institute quality appraisal criteria were used to evaluate the methodological quality of the included studies. The summary estimates were presented with forest plots and tables. Publication bias was checked with the funnel plot and Egger’s regression test. Results. Overall, 1421 articles were identified and evaluated using the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines, and 30 studies that met the inclusion criteria were included in the final analysis. The weighted pooled prevalence of metabolic syndrome among individuals with type 2 diabetes mellitus in sub-Saharan Africa was 63.1% (95% CI: 57.9–68.1) when using the NCEP-ATP III 2004 criteria and 60.8% (95% CI: 50.7–70.0) when using the IDF criteria. Subgroup analysis, using NCEP-ATP III 2004 and IDF criteria, revealed higher weighted pooled prevalence among females: 73.5% (95% CI: 67.4–79.5), 71.6% (95% CI: 60.2–82.9), compared to males: 50.5% (95% CI: 43.8–57.2), 44.5% (95% CI: 34.2–54.8), respectively. Central obesity was the most prevalent component of metabolic syndrome, with a pooled prevalence of 55.9% and 61.6% using NCEP-ATP III 2004 and IDF criteria, respectively. There was no statistical evidence of publication bias in both the NCEP-ATP III 2004 and IDF pooled estimates. Conclusions. The findings underscore the alarming prevalence of metabolic syndrome among individuals with type 2 diabetes mellitus in sub-Saharan Africa. Therefore, it is essential to promote lifestyle modifications, such as regular exercise and balanced diets, prioritize routine obesity screenings, and implement early interventions and robust public health measures to mitigate the risks associated with central obesity.