Elevated Plasma Glucose-dependent Insulinotropic Polypeptide Associates with Hyperinsulinemia in Metabolic Syndrome

Background and aims: Metabolic syndrome (MS) is a high risk condition for type 2 diabetes, a disease characterized by insulin resistance and insulin secretion abnormalities. Insulin resistance has been widely characterized in MS subjects while insulin secretion has been poorly investigated. The present study was undertaken to further investigate the α and β cell function and entero-insular axis in this pre-diabetic condition.Materials and Methods: Using 120´ oral (75g-OGTT) and 60´ intravenous (0,3g/kg-IVGTT) glucose tolerance tests, we studied α and β cell function, insulin resistance, incretin levels in 96 subjects with normal fasting glucose and normal glucose tolerance to OGTT, with (n=29) and without MS (n=67).Results: MS+ individuals showed in comparison with MS-: higher insulinogenic index (IG30) and higher AUC (0-120) for glucose and insulin during the OGTT, p<0.05; higher AUC (0-10) for glucose (p<0.05) but similar first phase insulin secretion (p=ns) as measured by AIRG and AUC (0-10) for insulin during the IVGTT; increased (p=0.04) AUC (0-60) for insulin during the IVGTT; higher GIP levels at 30'(p=0,03), 60'(p=0,01), 90'(p=0,003) and 120'(p=0,004); higher AUC (0-120) for GIP (p=0,007); similar AUC (0-120) for GLP-1 during the OGTT; delayed glucagon suppression after OGTT.Conclusion: NGT subjects with metabolic syndrome showed increased GIP secretion that could be responsible for the delayed glucagon suppression during the OGTT, suggesting a role of incretins in regulating glucose homeostasis in this condition.