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: Impaired glucose tolerance (IGT) is associated with reduced insulin-induced suppression of glucagon concentrations.
    Author: Ahrén B, Larsson H.
    Journal: Diabetologia; 2001 Nov; 44(11):1998-2003. PubMed ID: 11719830.
    Abstract:
    AIMS/HYPOTHESIS: We aimed to examine whether impaired glucose tolerance is associated with reduced suppression of glucagon concentrations. METHODS: Eighty-four non-diabetic women of Caucasian origin and 61 years of age, of whom 48 had normal glucose tolerance (NGT) and 36 had IGT, underwent a 75 g OGTT and a hyperinsulinaemic, euglycaemic clamp with measurement of glucagon, insulin and glucose concentrations. RESULTS: At 2 h after 75 g oral glucose, glucagon concentrations were reduced by 7.1 +/- 1.1 ng/l in NGT vs 8.0 +/- 1.4 ng/l in IGT, (NS). However, the 2 h reductions in glucagon per mmol/l increase in 2 h glucose or per pmol/l increase in 2 h insulin were both impaired in IGT (p = 0.002 and p = 0.043, respectively) because the 2 h increases in glucose and insulin were higher in IGT than in NGT. Furthermore, suppression of glucagon concentrations during a euglycaemic clamp at hyperinsulinaemic concentrations (NGT: 607 +/- 19 pmol/l, IGT: 561 +/- 21 pmol/l) was lower in IGT (13.6 +/- 1.6 ng/l) than in NGT (23.1 +/- 1.2 ng/l; p < 0.001). The suppression of glucagon concentrations during the hyperinsulinaemic, euglycaemic clamp correlated with insulin sensitivity (r = 0.24, p = 0.027) and with the 2 h glucose value during the OGTT (r = -0.52, p < 0.001). CONCLUSION/INTERPRETATION: Impaired glucose tolerance is associated with reduced insulin-induced suppression of glucagon secretion, which could be caused by A-cell insulin resistance. Inappropriately high glucagon secretion could therefore contribute to the metabolic perturbations in IGT.
    [Abstract] [Full Text] [Related] [New Search]