Author/Editor		Tomažič, M; Janež, A; Sketelj, A; Kocijančič, A; Eckel, J; Sharma, PM
Title		Comparison of altreations in insulin signalling pathway in adipocytes from type II diabetic women and women with gestational diabetes mellitus
Type		članek
Source		Diabetologia
Vol. and No.		Letnik 45
Publication year		2002
Volume		str. 502-8
Language		eng
Abstract		Aims/hypotlhesis. The cellular mechanisms for the insulin resistance in pregnancy and gestational diabetes mellitus are not known. The membrane protein plasma cell glycoprotein PC-l has been identified as an inhibitor of insulin receptor tyrosine kinase activity and could have a role in insulin resistance. This study aimed to examine the effects of insulin on glucose transport and changes in insulin receptor tyrosine phosphorylation, IRS-1 and PC-1. Method,s. Adipocytes were obtained either during electivc cesarean section from three groups of subjects (Type II diabetic pregnant women (n=6) women with gestational diabetes mellitus (n=10) and pregnant women with normal glucose tolerance (n=C) as pregnant control subjects) or during elective gynaecological surgery from non-pregnant (n=6) control subjects. Results. Insulin stimulated glucose transport was reduced by 50% in women with gestational diabetes mellitus and 70% in pregnant women with Type II diabetes, compared to the non-pregnant control subjects. After maximal insulin stimulation of adipocytes, 1RTK phosphorylation was reduced by 29.5% in women with gestational diabetes mellitus and 44.5% in women with Type II diabetes, compared to the nonpregnant control subjects. We also found that IRS-1 phosphorylation was reduced by 32% and 48%, respectively. On the other hand, PC-1 content in adipocytes in women with gestational diabetes rnellitus increased by 320% and 668% in Type II diabetic women, compared to the non-pregnant control subjects. Conclusions/interpretation. Our results indicate that women with gestational diabetes mellitus and Type II diabetes have increased PC-1 content and suggest that this could contribute to lower phosphorylation levels of IRTK and IRS-l. (Abstract truncated at 2000 characters).
Descriptors		DIABETES MELLITUS, NON-INSULIN-DEPENDENT DIABETES, GESTATIONAL ADIPOCYTES INSULIN INSULIN RESISTANCE PREGNANCY INSULIN RECEPTOR PROTEIN-TYROSINE KINASE GLUCOSE PHOSPHORYLATION P-GLYCOPROTEIN