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Metabolic and Bariatric surgery (MBS) has become an essential treatment for severe obesity and associated comorbidities, particularly type 2 diabetes mellitus (T2DM), with substantial benefits in weight loss, improved glycemic control, and cardiovascular risk reduction. The International Diabetes Federation (IDF) recognizes MBS as an effective option for individuals with obesity with T2DM due to its ability to improve insulin sensitivity and lower inflammation. These surgeries induce metabolic improvements through distinct mechanisms that affect gut hormone secretion, nutrient absorption, and energy balance. These interventions modulate key gut hormones like glucagon-like peptide-1 (GLP-1), ghrelin, and leptin, which influence appetite, glucose metabolism, and fat storage. Moreover, MBS alters the gut microbiome, contributing to enhanced metabolic function and the resolution of obesity-related conditions. Theories such as the Foregut-Hindgut Hypothesis, Ileal Brake Mechanism, and Gastric Center Hypothesis further try explain these metabolic changes. Understanding these theories and the physiological alterations they provoke is crucial for optimizing patient care and advancing the future of obesity treatments, offering insights into mechanisms that go beyond simple weight loss to address complex metabolic disorders.
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Khan et al. (2025) studied this question.
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