These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Elevated plasma glucose-dependent insulinotropic polypeptide associates with hyperinsulinemia in metabolic syndrome.
    Author: Calanna S, Urbano F, Piro S, Zagami RM, Di Pino A, Spadaro L, Purrello F, Rabuazzo AM.
    Journal: Eur J Endocrinol; 2012 May; 166(5):917-22. PubMed ID: 22391044.
    Abstract:
    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 hence 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 glucose tolerance test (OGTT, 75  g) and 60' intravenous glucose tolerance test (IVGTT, 0.3  g/kg), we studied α and β cell function, insulin resistance, and incretin levels in 96 subjects with normal fasting glucose and normal glucose tolerance to OGTT, with (MS+, n=29) and without MS (MS-, n=67). RESULTS: MS+ individuals showed in comparison with MS-: higher insulinogenic index (IG30) and higher area under the curve (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 ΔAIRG and AUC (0-10) for insulin during the IVGTT; increased AUC (0-60) for insulin during the IVGTT (P=0.04); 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; and delayed glucagon suppression after the OGTT. CONCLUSION: NGT subjects with MS showed increased GIP secretion that could be responsible for the delayed glucagon suppression during the OGTT, thereby suggesting a role for incretins in regulating glucose homeostasis in this condition.
    [Abstract] [Full Text] [Related] [New Search]