TY - JOUR
T1 - Physiological levels of glucagon do not influence lipolysis in abdominal adipose tissue as assessed by microdialysis
AU - Højbjerg Gravholt, Claus
AU - Møller, Niels
AU - Jensen, Michael D.
AU - Christiansen, Jens Sandahl
AU - Schmitz, Ole
PY - 2001/6/5
Y1 - 2001/6/5
N2 - To determine whether glucagon stimulates lipolysis in adipose tissue, seven healthy young male volunteers were studied, with indwelling microdialysis catheters placed sc in abdominal adipose tissue. Subjects were studied three times: 1) during euglucagonemia (EG; glucagon infusion rate, 0.5 ng/kg·min); 2) during hyperglucagonemia (HG; (glucagon infusion rate, 1.5 ng/kg·min); and 3) during EG and a concomitant glucose infusion mimicking the glucose profile from the day of riG (EG+G). Somatostatin (450 μg/h) was infused to suppress hormonal secretion, and replacement doses of insulin and GH were administered. Sampling was done every 30 min for 420 min. Baseline circulating values of insulin, C-peptide, glucagon, GH, glycerol, and free fatty acids were comparable in all three conditions. During EG and EG+G, plasma glucagon was maintained at fasting level (20-40 ng/L); whereas, during HG, it increased (110-130 ng/L). Interstitial concentrations of glycerol were similar in the three conditions [30,870 ± 5,946 (EG) vs. 31,074 ± 7,092 (HG) vs. 29,451 ± 6,217 (EG+G) μmol/L·120 min, P = 0.98]. Plasma glycerol (ANOVA, P = 0.5) and free fatty acids (ANOVA, P = 0.3) were comparable during the different glucagon challenges. We conclude that HG per se does not increase interstitial glycerol (and thus lipolysis) in abdominal sc adipose tissue; nor does modest hyperglycemia, during basal insulinemia and glucagonemia, influence indices of abdominal sc lipolysis.
AB - To determine whether glucagon stimulates lipolysis in adipose tissue, seven healthy young male volunteers were studied, with indwelling microdialysis catheters placed sc in abdominal adipose tissue. Subjects were studied three times: 1) during euglucagonemia (EG; glucagon infusion rate, 0.5 ng/kg·min); 2) during hyperglucagonemia (HG; (glucagon infusion rate, 1.5 ng/kg·min); and 3) during EG and a concomitant glucose infusion mimicking the glucose profile from the day of riG (EG+G). Somatostatin (450 μg/h) was infused to suppress hormonal secretion, and replacement doses of insulin and GH were administered. Sampling was done every 30 min for 420 min. Baseline circulating values of insulin, C-peptide, glucagon, GH, glycerol, and free fatty acids were comparable in all three conditions. During EG and EG+G, plasma glucagon was maintained at fasting level (20-40 ng/L); whereas, during HG, it increased (110-130 ng/L). Interstitial concentrations of glycerol were similar in the three conditions [30,870 ± 5,946 (EG) vs. 31,074 ± 7,092 (HG) vs. 29,451 ± 6,217 (EG+G) μmol/L·120 min, P = 0.98]. Plasma glycerol (ANOVA, P = 0.5) and free fatty acids (ANOVA, P = 0.3) were comparable during the different glucagon challenges. We conclude that HG per se does not increase interstitial glycerol (and thus lipolysis) in abdominal sc adipose tissue; nor does modest hyperglycemia, during basal insulinemia and glucagonemia, influence indices of abdominal sc lipolysis.
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U2 - 10.1210/jc.86.5.2085
DO - 10.1210/jc.86.5.2085
M3 - Article
C2 - 11344211
AN - SCOPUS:0010438919
SN - 0021-972X
VL - 86
SP - 2085
EP - 2089
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 5
ER -