Mechanisms of early improvement/resolution of type 2 diabetes after bariatric surgery.
Bariatric surgery represents the main option for obtaining substantial and long-term weight loss in morbidly obese subjects. In addition, malabsorptive (biliopancreatic diversion, BPD) and restrictive (roux-en-Y gastric bypass, RYGB) surgery, originally devised to treat obesity, has also been shown to help diabetes. Indeed, type 2 diabetes is improved or even reversed soon after these operations and well before significant weight loss occurs. Two hypotheses have been proposed to explain the early effects of bariatric surgery on diabetes--namely, the hindgut hypothesis and the foregut hypothesis. The former states that diabetes control results from the more rapid delivery of nutrients to the distal small intestine, thereby enhancing the release of hormones such as glucagon-like peptide-1 (GLP-1). The latter theory contends that exclusion of the proximal small intestine reduces or suppresses the secretion of anti-incretin hormones, leading to improvement of blood glucose control as a consequence. In fact, increased GLP-1 plasma levels stimulate insulin secretion and suppress glucagon secretion, thereby improving glucose metabolism. Recent studies have shown that improved intestinal gluconeogenesis may also be involved in the amelioration of glucose homoeostasis following RYGB. Although no large trials have specifically addressed the effects of bariatric surgery on the remission or reversal of type 2 diabetes independent of weight loss and/or caloric restriction, there are sufficient data in the literature to support the idea that this type of surgery--specifically, RYGB and BPD--can lead to early improvement of glucose control independent of weight loss.
Mingrone
G
G
Department of Internal Medicine, Catholic University, Rome, Italy. gmingrone@rm.unicatt.it
Castagneto-Gissey
L
L
D050110:Bariatric Surgery; D001786:Blood Glucose / Q000378:metabolism*; D031204:Caloric Restriction; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism* / Q000503:physiopathology / Q000601:surgery; D015390:Gastric Bypass; D052216:Glucagon-Like Peptide 1 / Q000378:metabolism*; D005943:Gluconeogenesis; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007421:Intestine, Small / Q000378:metabolism*; D009767:Obesity, Morbid / Q000378:metabolism / Q000601:surgery*; D013270:Stomach / Q000601:surgery*; D015431:Weight Loss
D001786:Blood Glucose; D007328:Insulin; D052216:Glucagon-Like Peptide 1