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The direct effect of incretin hormones on glucose metabolism
Author(s) -
Karstoft Kristian,
Mortensen Stefan Peter,
Knudsen Sine Haugaard,
Solomon Thomas Phillip James
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb748
Subject(s) - medicine , endocrinology , insulin , glucagon , incretin , glucose clamp technique , somatostatin , carbohydrate metabolism , basal (medicine) , glucagon like peptide 1 , c peptide , glucose uptake , diabetes mellitus , pancreatic hormone , type 2 diabetes , insulin resistance
Objective To assess if glucagon‐like peptide (GLP‐1) and glucose‐dependent insulinotropic polypeptide (GIP) have a direct effect on glucose metabolism independent of their effect on the endocrine pancreas. Methods Five healthy males (22+/−1 years, BMI 21+/−1) with normal glucose metabolism (fasting glucose = 5.0+/−0.1 mM, HbA1c = 5.2+/−0.1%) were studied using the pancreatic clamp technique (100 ng/kg/min somatostatin infusion with basal replacement of insulin, glucagon and growth hormone) in 3 different trials (GLP‐1 [0.5 pmol/kg/min], GIP [1.5 pmol/kg/min] or saline infusion). A 2‐step clamp was performed at euglycemic (90 min) and hyperglycemic (90 min; euglycemic + 5.4 mM) levels. Peripheral blood flow and vascular function (forearm flow‐mediated dilation; FMD) were determined by ultrasound Doppler. Results Insulin was maintained at basal levels during euglycemia in all 3 trials, with equal decreases in C‐peptide levels. During hyperglycemia, insulin and C‐peptide levels increased in all trials (P<0.05). Glucose infusion rates were higher during euglycemia in the GLP‐1 trial as compared to the saline trial (P<0.05), also when adjusted for insulin values (P=0.10). Peripheral blood flow and vascular function did not differ between trials. Conclusion These data suggest a direct insulin/glucagon‐independent effect of GLP‐1 on glucose metabolism during euglycemia.