Changes in Gut Hormones After Bariatric Surgery

R. P. Vincent; C. W. le Roux

Disclosures

Clin Endocrinol. 2008;69(2):173-179. 

In This Article

Abstract and Introduction

Bariatric surgery is one of the most effective treatments for achieving long-term weight loss in morbidly obese patients. Bariatric surgery causes weight loss through substantial decline of hunger and increased satiety. Recently our understanding of neuroendocrine regulation of food intake and weight gain, especially regarding the role of gut hormones, has significantly increased. The changes in these hormones following bariatric surgery can partly explain the mechanism behind weight loss achieved through these procedures. In this paper, we review the effect bariatric procedures have on different gut hormone levels and how they in turn can alter the complex neuroendocrine regulation of energy homeostasis.

Obesity is fast becoming a major cause of premature death in the developed world. At present one of the most effective therapeutic options available to obtain significant and sustained weight loss is bariatric surgery.[1] The average weight loss in clinical practice after 2years for adjustable gastric banding (GB) is 20%, Roux-en-Y gastric bypass (RYGB) is 30% and biliopancreatic diversion or duodenal switch (BPD) is 35%.[2] The exact mechanism involved in weight loss after the bariatric surgery is not yet clear. However, a number of studies have demonstrated that gut hormones may play a role in weight loss following these procedures.

Energy Homeostasis. Body mass remains remarkably stable in most individuals because, overall energy intake and expenditure are matched through the process of energy homeostasis.[3,4] This homeostatic system defends against weight loss more robustly than against weight gain.[5] When there are alterations of body adiposity, the brain triggers compensatory physiological adaptations that resist weight change. Whereas weight loss increases hunger and decreases metabolic rate, weight gain does not always have the opposite responses.[6] The status of body energy stores is conveyed to the central nervous system by the adiposity-associated hormones leptin, insulin and possibly some gut hormones.[3] Weight loss leads to decreases in catabolic hormone levels and an increase in ghrelin. These changes cause corresponding alterations in brain centres, such as the hypothalamus which is responsible for energy homeostasis. In the arcuate nucleus (ARC) leptin and insulin stimulate the activity of neurones that express the catabolic neuropeptide precursor proopiomelanocortin (POMC), and cocaine and amphetamine-regulated transcript peptide (CART), while inhibiting neurones that produce the anabolic mediators neuropeptide Y (NPY) and agouti-related protein (Agrp).[3,7] The distribution of POMC neurones adjacent to circumventricular organs (CVO), in the ARC of the hypothalamus and in the nucleus of solitary tract (NTS) of the brainstem make them ideally positioned to interact with circulating humoral factors and to receive signals from vagal afferents. Thus, peptides made in the gut and released into the circulation may act directly in the brain after entering through the CVO. Hence the central melanocortin system plays a critical role in the integration of the control of satiety, hunger and energy expenditure.[8] Through these higher centres, the hormones regulate long-term changes in energy stores. Short-term alterations in nutrient status are conveyed to the brain through meal-related gut hormone responses, influenced by gastric distension, as well as variations in levels of nutrient content.[3] Number of the relevant gastro intestinal (GI) signals is stimulated by food intake and contribute to satiation. These meal-related GI signals in turn influence the size and frequency of food intake.

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