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β-cell function

Impact of bypass aids β-cell function post-surgery

Weight loss appears to be the strongest predictor

Although β-cell dysfunction can continue after Roux-en-Y gastric bypass (RYGBP) surgery, the procedure leads to gastrointestinal changes crucial for improved β-cell function after surgery, according to a paper published in the journal Diabetes. They note that pre-surgery β-cell function, weight loss and glucagon-like peptide 1 (GLP-1) response were all predictors of post-surgery β-cell function, with weight loss appearing to be the strongest predictor.

Much is still unknown as to why gastric bypass can result in resolution of type 2 diabetes and although both caloric restriction and weight loss are important contributors, it is also believe that altered gut physiology contributes to the resolution.

Therefore, researchers from St Luke's-Roosevelt Hospital Center, the Albert Einstein School of Medicine, and Columbia University College of Physicians and Surgeons, New York, and the Centre de Recherche Clinique Etienne-Le Bel, Université de Sherbrooke, Sherbrooke, Quebec, Canada, assessed the change in β-cell function up to three years after RYGBP in severely obese individuals with type 2 diabetes who experienced clinical diabetes remission post-RYGBP (OB-DM).

The patients were then compared to  both non-operated, obese normal glucose-tolerant (OB-NGT) and lean NGT (LEAN) patients. They also measured β-cell function during an oral and isoglycaemic glucose challenge to assess if improvements in β-cell function after RYGBP were mediated by the gut

Study

Sixteen severely obese subjects with type 2 diabetes of short duration (mean 3.0 ± 2.6 years) were studied before (OB-DM0; n=16) and at one month (OB-DM1M; n=16), one year (OB-DM1Y; n= 15), two years (OB-DM2Y; n=16 for OGTT, n=14 for iso-IVGC), and three years after RYGBP (OB-DM3Y; n=13).

Eleven severely OB-NGT and seven LEAN subjects were used as control subjects (all OB-NGT control subjects: fasting plasma glucose <5.5mmol/L, 2h postprandial glucose <7.7mmol/L, and HbA1c <6.5%).

Results

The outcomes revealed that weight loss was ~11% at one month, ~31% at one year, and sustained at two and three years. All subjects in OB-DM were in diabetes remission from one month onwards except one subject that did not remit until one year and relapsed (relapse defined as no longer meeting ADA criteria for remission) at three years.

Plasma concentrations of incretins were significantly increased after RYGBP. At all time points after surgery, GLP-1 and GIP peak responses in OB-DM were significantly higher than both control subjects. β-cell function normalised after surgery.

The researchers report that weight loss, pre-surgery β-cell function and GLP-1 response were all significant predictors of post-surgery β-cell function, although weight loss was consistently the strongest predictor. Age, pre-surgery BMI and diabetes duration and control were not significant.

“This study is the first to demonstrate the importance of the oral route to improvements in β-cell function after RYGBP and to show that improvements persist 3 years after surgery,” write the authors. “Despite the important influence of intestinal factors, we cannot discount the contribution of weight loss to improvement in β-cell function after RYGBP.”

They added that future studies comparing β-cell function in a diabetic population, compared with caloric restriction and/or restrictive bariatric surgery will help elucidate the impact of weight loss versus gut-mediated factors.

“RYGBP does not rescue impairment in insulin secretion and β-cell function when the gastrointestinal tract is not engaged,” conclude the authors. “However, oral glucose stimulation rescues impairment rapidly, at one month, and this is sustained up to three years after RYGBP, demonstrating the essential role of the gut in this effect.”

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