Avtor/Urednik		Jenež, Andrej
Naslov		Mechanism of osmotic shock-induced glucose transport in insulin resistant 3T3-L1 adipocytes
Prevedeni naslov		Mehanizem transporta glukoze v osmotskem šoku v insulinsko rezistentnih 3T3-L1 adipocitih
Tip		monografija
Kraj izdaje		Ljubljana
Založnik		Medicinska fakulteta
Leto izdaje		2000
Obseg		str. 53
Jezik		eng
Abstrakt		Osmotic shock treatment of 3T3-L1 adipocytes causes an increase in glucose transport activity and translocation of GLUT-4 protein similar to that elicited by insulin treatment. Insulin stimulation of GLUT-4 translocation and glucose transport activity was completely inhibited by wortmannin, however, activation by osmotic shock was only partialy blocked. Additionally, we have found that the newly identified insulin rcceptor substrate (IRS) Gab-1 (Grb2-associated binder-1) is tyrosine phosphorylated following sorbitol stimulation. Treatment of cells with the tyrosine kinase inhibitor genestin inhibited osmotic shockstimulated Gab-1 phosphorylation, as well as shock-induced glucose transport. rurthennore, pretreatment with the selective Src family kinase inhibitor PP2 completely inhibited the ability of sorbitol treatment to cause tyrosine phosphorylation of Gab-1. We have also shown that microinjection of anti-Gab-1 antibody inhibits osmotic shock-induced GLUT-4 translocation. Furthermore, phosphorylated Gab-1 binds and activates phosphatidylinositol 3-kinase (PI 3-kinase) in response to osmotic shock. The PI 3-kinase activity associated with Gab-1 was 82% of that associated with antiphosphotyrosine, indicating that Gab-I is the major site for PI 3-kinase recruitment following osmotic shock stimulation. (Abstract truncated at 2000 characters)
Deskriptorji		ADIPOCYTES OSMOTIC PRESSURE INSULIN RESISTANCE MONOSACCHARIDE TRANSPORT PROTEINS DEOXYGLUCOSE SORBITOL TYROSINE PHOSPHATIDYLINOSITOLS INSULIN RECEPTORS, INSULIN CELLS, CULTURED 3T3 CELLS