Is Glucagon-like peptide-1 for real?

Is Glucagon-like peptide-1 for real?

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Surgery for Obesity and Related Diseases ] (2014) 00–00

Editorial

Is Glucagon-like peptide-1 for real? Received February 9, 2014; accepted February 10, 2014

The initial wave of enthusiasm for the metabolic underpinning of bariatric surgery was dampened by subsequent emergence of human and animal data that lacked specificity and was fraught with methodological flaws. The present study reports preliminary and associative data on serum levels of leptin, peptide YY (PYY) and Glucagon-like peptide-1 (GLP-1) in response to luminal stimulation with an electrolyte solution. Because of many confounding factors, these particular experiments are complex and yield data with large variability. Notwithstanding, the temporal increase in PYY and GLP-1 is noticeable and may be a focal point for additional experimentation. GLP-1 secretion can be stimulated by other types of food and is rapidly degraded by peptidases thereby suggesting that its control of glucose homeostasis and hepatic insulin sensitivity may be in part through neural pathways. The work by Buchwald and Ikramuddin lays the foundation for a wide variety of proposals that address those mechanisms in addition to the central question of whether the increase in GLP-1 after diversionary procedures is mechanistically linked to remission of diabetes. Recently published data [1] show that blocking the GLP-1 receptor with exendin has a limited effect on post-

prandial glucose control in diabetic-obese patients who had undergone RYGB; these data suggest that sustained remission of diabetes may involve GLP-1 independent mechanisms. As bariatric surgeons, we have a unique window through which we witness rapid resolution of diabetes and therefore we should exploit every opportunity for translational collaborative research. Disclosures XXX Michel M. Murr* University of South Florida Tampa, Florida Reference [1] Jiménez A, Casamitjana R, Viaplana-Masclans J, Lacy A, Vidal J. GLP-1 action and glucose tolerance in subjects with remission of type 2 diabetes after gastric bypass surgery. Diabetes Care 2013;36:2062–9.

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* Correspondence: Dr. Michel M. Murr, University of South Florida, 5 Q5 Tampa General Circle, Tampa, FL 33606.

http://dx.doi.org/10.1016/j.soard.2014.02.006 1550-7289 r 2014 Published by Elsevier Inc. on behalf of American Society for Metabolic and Bariatric Surgery.