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Enhanced glucagon‐like peptide‐1 (GLP‐1) response to oral glucose in glucose‐intolerant HIV‐infected patients on antiretroviral therapy
Author(s) -
Andersen O,
Haugaard SB,
Holst JJ,
Deacon CF,
Iversen J,
Andersen UB,
Nielsen JO,
Madsbad S
Publication year - 2005
Publication title -
hiv medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.53
H-Index - 79
eISSN - 1468-1293
pISSN - 1464-2662
DOI - 10.1111/j.1468-1293.2005.00270.x
Subject(s) - medicine , impaired glucose tolerance , incretin , endocrinology , glucagon like peptide 1 , insulin , diabetes mellitus , glucose tolerance test , glucagon , area under the curve , antiretroviral therapy , human immunodeficiency virus (hiv) , insulin resistance , type 2 diabetes , viral load , immunology
Objectives We investigated whether the incretin hormones glucagon‐like peptide‐1 (GLP‐1) and glucose‐dependent insulinotropic polypeptide (GIP), which are major regulators of glucose tolerance through the stimulation of insulin secretion, contribute to impaired glucose tolerance (IGT) among HIV‐infected patients on highly active antiretroviral therapy (HAART). Methods Eighteen HIV‐infected male patients (six lipodystrophic and 12 nonlipodystrophic) with normal glucose tolerance (NGT) were compared with 10 HIV‐infected male patients (eight lipodystrophic and two nonlipodystrophic) with IGT. Plasma concentrations of GLP‐1 and GIP were determined frequently during a 3‐h, 75‐g glucose tolerance test. Insulin secretion rates (ISRs) were calculated by deconvolution of C‐peptide concentrations. Results The incremental area under the curve (incrAUC) for GLP‐1 was increased by 250% in IGT patients compared with NGT patients (1455±422 vs. 409±254 pmol/L/180 min, respectively; P <0.05), whereas the incrAUC for GIP did not differ between the study groups (7689±1097 vs. 8041±998 pmol/L/180 min, respectively; not significant). In pooled study groups, the GIP incrAUC correlated positively with the ISR incrAUC without adjustment ( r =0.38, P <0.05) and following adjustment for glucose incrAUC ( r =0.49, P <0.01). Conclusions Our data suggest: (1) that glucose‐intolerant, HIV‐infected male patients may display enhanced GLP‐1 responses to oral glucose compared with normal glucose‐tolerant HIV‐infected male patients, which may represent a compensatory mechanism rather than explain the IGT; (2) that the GIP response may be associated with ISR independently of plasma glucose in nondiabetic HIV‐infected males on HAART.