INSULIN SENSITIVITY AND INSULIN-RESPONSE IN WOMEN WITH GESTATIONAL DIABETES-MELLITUS

Citation
B. Persson et al., INSULIN SENSITIVITY AND INSULIN-RESPONSE IN WOMEN WITH GESTATIONAL DIABETES-MELLITUS, Hormone and Metabolic Research, 29(8), 1997, pp. 393-397
Citations number
21
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
00185043
Volume
29
Issue
8
Year of publication
1997
Pages
393 - 397
Database
ISI
SICI code
0018-5043(1997)29:8<393:ISAIIW>2.0.ZU;2-N
Abstract
Gestational diabetes mellitus (GDM) is associated with much increased risk of developing diabetes later on in life. Using the frequently sam pled intravenous glucose tolerance test and the minimal model analyses we have therefore determined the early insulin response to glucose (E IR) and insulin sensitivity (S-i), in women with GDM of different seve rity (n = 14) and in normal women (n = 10), During the last trimester of pregnancy, GDMs compared to controls had significantly lower EIR (p < 0.001) and S-i (p < 0.01). The reduction in EIR was less marked in GDM patients treated with diet alone (n = 6) as compared to GMD patien ts (n = 8) who subsequently during pregnancy needed treatment also wit h insulin. The insulin treated GDM group only had higher fasting gluco se level than controls (5.2 vs 4.2 mmol/l, p < 0.001). Both GDM subgro ups had slightly elevated basal levels of FFA and 3-hydroxybutyrate. S -i and EIR were inversely correlated in control women and their fastin g glucose correlated both to EIR (r = 0.63, p < 0.05) and to S-i (r = 0.59, p < 0.05). In the GDM subgroups S-i and EIR were unrelated and t here were no correlations between fasting glucose and S-i or EIR. Thes e results suggest that glucose intolerance in GDM patients in the last trimester of pregnancy is characterized by both an impaired insulin s ecretion and an increased resistance to insulin. The impairment of ins ulin secretion and action increases with the severity of hyperglycemia , and the relative insulin deficiency characterizing GDM patients is a ssociated with a selected defect in insulin action mainly affecting gl ucoregulation.