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Department of Endocrinology M and Medical Research Laboratories (C.H.G., N.M., J.S.C., O.S.), Århus University Hospital, DK-8000 Århus C, Denmark; and Endocrine Research Unit (M.D.J.), Mayo Clinic, Rochester, Minnesota 55905
Address all correspondence and requests for reprints to: Claus Højbjerg Gravholt, M.D., Department of Endocrinology M, Århus Kommunehospital, Århus University Hospital, DK-8000 Århus C, Denmark. E-mail: ch.gravholt{at}dadlnet.dk
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 HG (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 (2040 ng/L); whereas, during HG, it increased (110130 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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