RELATIONSHIP BETWEEN INSULIN-MEDIATED GLUCOSE DISPOSAL BY MUSCLE AND ADIPOSE-TISSUE LIPOLYSIS IN HEALTHY-VOLUNTEERS

Citation
D. Pei et al., RELATIONSHIP BETWEEN INSULIN-MEDIATED GLUCOSE DISPOSAL BY MUSCLE AND ADIPOSE-TISSUE LIPOLYSIS IN HEALTHY-VOLUNTEERS, The Journal of clinical endocrinology and metabolism, 80(11), 1995, pp. 3368-3372
Citations number
34
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
80
Issue
11
Year of publication
1995
Pages
3368 - 3372
Database
ISI
SICI code
0021-972X(1995)80:11<3368:RBIGDB>2.0.ZU;2-S
Abstract
The present study was performed in 17 nondiabetic subjects and was ini tiated to determine whether enhanced adipose tissue lipolysis, either basal or catecholamine induced (isoproterenol), and/or resistance to i nsulin inhibition of isoproterenol-stimulated lipolysis were correlate d with resistance to insulin-mediated glucose disposal by muscle. Insu lin-mediated glucose disposal was assessed by determining the steady s tate plasma glucose (SSPG) concentration during the insulin suppressio n test 180 min infusion of somatostatin (350 (mu)g/h), insulin (25 mU /m(2).min), and glucose (240 mg/m(2).min). On another occasion, plasm a FFA and glycerol concentrations were determined at the end of 3 sequ ential infusion periods (IP): IP1, somatostatin (350 (mu)g/h), insulin (5 mUm(2).min), and isoproterenol (270 ng/m(2).min); and IP3, somatos tatin (350 (mu)g/h), isoproterenol (270 ng/m(2).min), and insulin (10 mUm(2).min). SSPG concentrations correlated with FFA concentrationd du ring all 3 infusion periods after adjustment for age, gender, body mas s index, insulin concentration, and ratio of waist to hip girth (IP1: r=0.61; P,0.03; IP2: r=0.07; P<0.01; IP3: r=0.65; P<0.02). Correlation s between SPG and glycerol concentrations were also highly statistical ly significant (IP1: r=0.62; P<0.03; IP2: r=0.65; P<0.02; IP3: r=0.07; P<0.01). These results demonstrate for the first time that plasma FFA and glycerol concentrations are increased commensurate with the degre e of resistance to insulin-mediated glucose disposal at a basal insuli n level, in response to isoproterenol stimulation, and after insulin i nhibition of isoproterenol-stimulated lipolysis.