Abstract
To describe glucose metabolism in the late, weight stable phase after Roux-en-Y Gastric Bypass (RYGB) in patients with and without preoperative type 2 diabetes we invited 55 RYGB-operated persons from two existing cohorts to participate in a late follow-up study. 44 (24 with normal glucose tolerance (NGT)/20 with type 2 diabetes (T2D) before surgery) accepted the invitation (median follow-up 2.7 [Range 2.2–5.0 years]). Subjects were examined during an oral glucose stimulus and results compared to preoperative and 1-year (1 y) post RYGB results. Glucose tolerance, insulin resistance, beta-cell function and incretin hormone secretion were evaluated. 1 y weight loss was maintained late after surgery. Glycemic control, insulin resistance, beta-cell function and GLP-1 remained improved late after surgery in both groups. In NGT subjects, nadir glucose decreased 1 y after RYGB, but did not change further. In T2D patients, relative change in weight from 1 y to late after RYGB correlated with relative change in fasting glucose and HbA1c, whereas relative changes in glucose-stimulated insulin release correlated inversely with relative changes in postprandial glucose excursions. In NGT subjects, relative changes in postprandial nadir glucose correlated with changes in beta-cell glucose sensitivity. Thus, effects of RYGB on weight and glucose metabolism are maintained late after surgery in patients with and without preoperative T2D. Weight loss and improved beta-cell function both contribute to maintenance of long-term glycemic control in patients with type 2 diabetes, and increased glucose stimulated insulin secretion may contribute to postprandial hypoglycemia in NGT subjects.
Highlights
The mechanisms responsible for improving T2D glucose metabolism are still being debated, but early after surgery, the combined effects of caloric restriction and an exaggerated postprandial GLP-1 release, improving hepatic insulin sensitivity and beta-cell function, respectively, are among the most likely explanations[4]
To address the development of these glycemic disturbances, we studied the effects of Roux-en-Y Gastric Bypass (RYGB) on glycemic control as well as measures of insulin sensitivity, beta-cell function and body weight late after RYGB surgery in patients with normal glucose tolerance (NGT) or T2D prior to surgery, and results were compared to preoperative and 1-year (1 y) post RYGB results
Patients lost to follow-up did not differ from participants with respect to preoperative age, bmi, hba1c or diabetes duration or with respect to 1 y postoperative Excess body weight loss (EBWL). 3 patients (2 T2D/1 NGT) in cohort 2 refused the oral glucose tolerance test (OGTT) postoperatively due to a general distaste for the oral stimulus, previous problems with malfunctioning iv access and/or lack of time
Summary
The mechanisms responsible for improving T2D glucose metabolism are still being debated, but early after surgery, the combined effects of caloric restriction and an exaggerated postprandial GLP-1 release, improving hepatic insulin sensitivity and beta-cell function, respectively, are among the most likely explanations[4]. Fasting plasma glucose >7.0 mM and/or 2 hour OGTT plasma glucose >11.1 mM and/or Treatment with ≥1 antidiabetic agents. In persons with normal glucose tolerance (NGT) before the operation, a late complication to RYGB is postprandial hypoglycemia[14]. This has been linked to exaggerated insulin release in response to rapid increases in postprandial glucose and GLP-1 concentrations[15,16]
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