Abstract
Postprandial hypoglycemia is a complication following gastric bypass surgery, which frequently remains undetected. Severe hypoglycemic episodes, however, put patients at risk, e.g., for syncope. A major cause of hypoglycemia following gastric bypass is hyperinsulinemic nesidioblastosis. Since pancreatic islets in nesidioblastosis overexpress insulin-like growth factor 1 (IGF-1) receptor α and administration of recombinant IGF-1 provokes hypoglycemia, our main objective was to investigate the occurrence of post-load hypoglycemia one year after bariatric surgery and its relation to pre- and post-operative IGF-1 serum concentrations. We evaluated metabolic parameters including 2 h 75 g oral glucose tolerance test (OGTT) and measured IGF-1 serum concentration in thirty-six non-diabetic patients (29 f/7 m), aged 41.3±2.0 y with a median (IQR) BMI of 30.9 kg/m2 (27.5–34.3 kg/m2), who underwent elective bariatric surgery (predominantly gastric bypass, 83%) at our hospital. Post-load hypoglycemia as defined by a 2 h glucose concentration <60 mg/dl was detected in 50% of patients. Serum insulin and C-peptide concentration during the OGTT and HOMA-IR (homeostatic model assessment–insulin resistance) were similar in hypoglycemic and euglycemic patients. Strikingly, pre- and post-operative serum IGF-1 concentrations were significantly higher in hypoglycemic patients (p = 0.012 and p = 0.007 respectively). IGF-1 serum concentration before surgery negatively correlated with 2 h glucose concentration during the OGTT (rho = −0.58, p = 0.0003). Finally, IGF-1 serum concentrations before and after surgery significantly predicted post-load hypoglycemia with odds ratios of 1.28 (95%CI:1.03–1.55, p = 0.029) and 1.18 (95%CI:1.03–1.33, p = 0.015), respectively, for each 10 ng/ml increment. IGF-1 serum concentration could be a valuable biomarker to identify patients at risk for hypoglycemia following bariatric surgery independently of a diagnostic OGTT. Thus, IGF-1 testing could help to prevent a significant complication of gastric bypass surgery.
Highlights
Bariatric surgery is currently the most effective treatment to achieve and maintain clinically significant long-term weight-loss in severely obese subjects [1]
After short venous stasis and venipuncture, blood was collected into evacuated vials and the samples were transferred to the Department of Laboratory Medicine of the Medical University of Vienna, where serum concentrations of triglycerides, total, HDL- and LDL-cholesterol, alanine transaminase (ALT), GGT, hemoglobin A1c (HbA1c), glucose, insulin and C-peptide were determined by routine laboratory analyses
Glucose concentration during the course of the 2 hOGTT was drastically changed in the postoperative setting, with significantly lower concentrations after the first hour, which is reflected by the reduced area under the curve (AUC) - Figure 1A, Table 1
Summary
Bariatric surgery is currently the most effective treatment to achieve and maintain clinically significant long-term weight-loss in severely obese subjects [1]. Postprandial, severe and recurrent hypoglycemia is a late complication of Roux-en-Y gastric bypass surgery (RYGB) [3] and could contribute to the post-operative increase in mortality unrelated to disease. Postoperative hypoglycemia seems to be caused by post-prandial hyperinsulinemia, accompanied or not by pancreatic nesidioblastosis [9,10,11], or altered incretin release [12,13,14], even though other causes cannot be ruled out [9]. Therapeutic approaches to prevent hypoglycemia following RYGB are not standardized and comprise dietary interventions, drugs, such as acarbose, diazoxide or verapamil as well as invasive procedures such as subtotal or total pancreatectomy [16,17]. In order to prevent post-prandial hypoglycemia, pre-operative individual risk assessment would be imperative. Factors predicting the onset of post-load hypoglycemia following bariatric surgery are widely unknown
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