Insulin sensitivity and secretion modifications after bariatric surgery.
Type 2 diabetes mellitus is increasing over time as result of the obesity epidemics. In fact, the prevalence of Type 2 diabetes across Europe in 2010 was estimated to be 8.2% of the population and its projection for 2030 sees figures of 10.1%. This increase in the number of diabetic individuals has also dramatically raised the health expense, with spending on diabetes in Europe in 2010 accounting for 10% of the total healthcare cost. A meta-analysis of the literature evidenced that the clinical and laboratory manifestations of Type 2 diabetes are resolved in 78.1%, and are improved in 86.6% of obese patients (body mass index >35 kg/m²) after bariatric surgery. However, a gradation of effects of different surgical techniques in improving glucose control does exist, with the largest and durable effects observed in prevalently malabsorptive procedures. The outcome of bariatric surgery on insulin sensitivity and secretion is different in relation to the type of operation performed. In fact, while Roux-en-Y Gastric Bypass enhances insulin secretion after a meal thus improving glucose metabolism, Bilio-Pancreatic Diversion acts through the amelioration of insulin sensitivity allowing a subsequent reduction of insulin hypersecretion, which is a typical feature of the insulin resistance state. Gastric banding action is mediated uniquely through the weight loss, and the effect of sleeve gastrectomy is still to be elucidated. Incretin secretion is dramatically increased under nutrient stimulation after gastric bypass leading, probably, to an overstimulation of pancreatic β-cells resulting in the increase of insulin secretion.
Department of Internal Medicine, Catholic University of Rome, Rome, Italy.
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Castagneto-Gissey
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Mingrone
D000818:Animals; D050110:Bariatric Surgery / Q000379:methods*; D015992:Body Mass Index; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000378:metabolism / Q000517:prevention & control; D005753:Gastric Mucosa / Q000378:metabolism*; D054439:Ghrelin / Q000378:metabolism; D005934:Glucagon / Q000378:metabolism; D052216:Glucagon-Like Peptide 1 / Q000378:metabolism; D050416:Glucagon-Secreting Cells / Q000378:metabolism; D006801:Humans; D054795:Incretins / Q000378:metabolism; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism*; D009767:Obesity, Morbid / Q000150:complications / Q000378:metabolism / Q000601:surgery*
D054439:Ghrelin; D054795:Incretins; D052216:Glucagon-Like Peptide 1; D005934:Glucagon