Insulin resistance and insulin secretion in morbidly obese patients before and six months after bariatric surgery
Miriam Promintzer1, Gerhard Prager2, Marietta Stadler3, Christian Anderwald1, Martina Mandl1, Soheila Shakeri Manesch2, Peter Nowotny1, Martin Georg Bischof1, Bernhard Ludvik1, Anton Luger1 & Michael Krebs1
Recent case reports describe hyperinsulinemic hypoglycemia after gastric bypass. The aim of this study was the assessment of insulin resistance and insulin secretion in non-diabetic morbidly obese patients before and six months after bariatric surgery.
In 8 non-diabetic morbidly obese patients (OB:6f/2 m, age:42±3a, BMI:47.29±2.2 kg/m2) and 6 controls (CON:4f/2 m, age:43±0a, BMI:23.8±0.5 kg/m2) we performed a frequently sampled oral glucose tolerance test (75 g, 3-hOGTT). The OGTT was repeated in 4 patients (3 Roux-en-Y gastric bypass, 1 gastric band) 6 months after surgery. Before bariatric surgery fasting plasma levels of glucose were comparable between OB and CON while fasting insulin and c-peptide were higher in OB (insulin:OB:27.0±5.6/CON:7.0±0.6 μU/ml, P=0.01; c-peptide:OB:4.3±0.7/ CON:1.3±0.1 ng/ml, P=0.003). During the OGTT peak plasma glucose and insulin concentrations were significantly higher in OB (glucose: OB:196.1±15.6/CON:130.5±9.6 mg/dl, P=0,006; insulin:OB:119.7±21.6/CON:58.6±9 μU/ml, P=0.039). 6 months after bariatric surgery fasting and early postprandial glucose concentrations were unchanged, while insulin and c-peptide were lower at fasting and higher after glucose load. Insulin resistance, assessed by HOMA-IR and OGIS, improved after bariatric surgery. After glucose load insulin and c-peptide secretion was adapted to insulin resistance prior surgery but was excessively elevated after bariatric surgery (adaptation index: before:119±16/after surgery:228±53, P<0.05, CON:114.5±19.6 total-nmol*m-2, P=0.8, for before surgery vs. CON). Conclusion: Non-diabetic morbidly obese patients exhibit preserved adaptation of insulin secretion to severe insulin resistance. Six months after bariatric surgery elevated fasting insulin and c-peptide were normalized. In the early postprandial state, however, hyperglycemia remained unchanged, while secretion of insulin and c-peptide was excessive and not adapted to improved insulin resistance. Thus, this dissociation between increase of insulin secretion on the one hand and amelioration of insulin resistance on the other hand might put patients at risk for late postprandial hypoglycemia.