title: Relationship between insulin-mediated glucose disposal by muscle and adipose tissue lipolysis in healthy volunteers.
abstract: The present study was performed in 17 nondiabetic subjects and was initiated to determine whether enhanced adipose tissue lipolysis, either basal or catecholamine induced (isoproterenol), and/or resistance to insulin inhibition of isoproterenol-stimulated lipolysis were correlated with resistance to insulin-mediated glucose disposal by muscle. Insulin-mediated glucose disposal was assessed by determining the steady state plasma glucose (SSPG) concentration during the insulin suppression test [180 min infusion of somatostatin (350 micrograms/h), insulin (25 mU/m2min), and glucose (240 mg/m2.min)]. On another occasion, plasma FFA and glycerol concentrations were determined at the end of 3 sequential infusion periods (IP): IP1, somatostatin (350 micrograms/h) plus basal insulin replacement (5 mU/m2.min); IP2, somatostatin (350 micrograms/h), insulin (5 mU/m2.min), and isoproterenol (270 ng/m2.min); and IP3, somatostatin (350 micrograms/h), isoproterenol (270 ng/m2.min), and insulin (10 mU/m2.min). SSPG concentrations correlated with FFA concentrations during all 3 infusion periods after adjustment for age, gender, body mass index, insulin concentration, and ratio of waist to hip girth (IP1:r = 0.61; P < 0.03; IP2: r = 0.70; P < 0.01; IP3: r = 0.65; P < 0.02). Correlations between SSPG and glycerol concentrations were also highly statistically significant (IP1: r = 0.62; P < 0.03; IP2: r = 0.65; P < 0.02; IP3: r = 0.70; P < 0.01). These results demonstrate for the first time that plasma FFA and glycerol concentrations are increased commensurate with the degree of resistance to insulin-mediated glucose disposal at a basal insulin level, in response to isoproterenol stimulation, and after insulin inhibition of isoproterenol-stimulated lipolysis.
authors.affiliation: Department of Medicine, Stanford University School of Medicine, California, USA.
authors.forename: D
authors.initials: D
authors.lastname: Pei
authors.forename: Y D
authors.initials: YD
authors.lastname: Chen
authors.forename: C B
authors.initials: CB
authors.lastname: Hollenbeck
authors.forename: R
authors.initials: R
authors.lastname: Bhargava
authors.forename: G M
authors.initials: GM
authors.lastname: Reaven
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005947:Glucose / Q000378:metabolism*; D005990:Glycerol / Q000097:blood; D006801:Humans; D007328:Insulin / Q000502:physiology*; D007545:Isoproterenol / Q000037:antagonists & inhibitors / Q000494:pharmacology; D008066:Lipolysis / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D009132:Muscles / Q000378:metabolism*; D009994:Osmolar Concentration; D012016:Reference Values; D013004:Somatostatin / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D013004:Somatostatin; D005947:Glucose; D007545:Isoproterenol; D005990:Glycerol