PLASMA LEPTIN CONCENTRATIONS DO NOT APPEAR TO DECREASE INSULIN-MEDIATED GLUCOSE DISPOSAL OR GLUCOSE-STIMULATED INSULIN-SECRETION IN WOMEN WITH NORMAL GLUCOSE-TOLERANCE

Citation
M. Carantoni et al., PLASMA LEPTIN CONCENTRATIONS DO NOT APPEAR TO DECREASE INSULIN-MEDIATED GLUCOSE DISPOSAL OR GLUCOSE-STIMULATED INSULIN-SECRETION IN WOMEN WITH NORMAL GLUCOSE-TOLERANCE, Diabetes, 47(2), 1998, pp. 244-247
Citations number
22
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00121797
Volume
47
Issue
2
Year of publication
1998
Pages
244 - 247
Database
ISI
SICI code
0012-1797(1998)47:2<244:PLCDNA>2.0.ZU;2-I
Abstract
The aim of this study was to test the hypothesis that plasma leptin co ncentrations contributed to the pathophysiology of NIDDM by decreasing both insulin-mediated glucose disposal and glucose-stimulated insulin secretion, The study was performed ire 60 women with normal oral gluc ose tolerance, Differences in insulin-mediated glucose disposal were d etermined by comparing the steady-state plasma glucose (SSPG) concentr ations attained at the end of a 180-min constant infusion of somatosta tin, glucose, and insulin, while comparisons of glucose-stimulated ins ulin secretion were based on the incremental increase ire insulin conc entration 30 min after an oral glucose challenge (Delta Ins) as compar ed with the fasting value, The results showed that the higher the fast ing plasma leptin concentration, the greater the degree of insulin res istance (r = 0.47, P < 0.01), Furthermore, multiple regression analysi s indicated that the relationship between leptin and SSPG was independ ent of age and degree of obesity as estimated by BMI. However, since t he total integrated plasma insulin response was highly correlated with both SSPG (r = 0.80, P < 0.001) and leptin (r = 0.55, P < 0.01), mult iple regression analysis was repeated, adding total insulin response t o the model, When this was done, the significant relationship between leptin and SSPG disappeared, whereas both BMI (P < 0.03) and insulin r esponse (P < 0.001) were correlated with SSPG. A significant relations hip between leptin and Delta Ins was seen, but it was a positive one ( r = 0.31, P < 0.02), not a negative one as would be expected if circul ating levels: of leptin inhibited glucose-stimulated insulin secret-io n, Furthermore, multiple: regression analysis could only confirm an in dependent relationship between Delta Ins and SSPG, but not between Del ta Ins and lep. tin, The results of these studies do not support the v iew that circulating leptin has a primary effect on either insulin act ion or secretion in normal female volunteers. It seems more likely tha t chronic hyperinsulinemia in insulin-resistant individuals acts to in crease adipose tissue leptin synthesis and secretion, leading to highe r ambient leptin concentrations.