%0 Journal Article
%T Alteration of Major Insulin Signaling Molecules by Chronic Ethanol in Hypertensive Vascular  Smooth Muscle Cells of Rats
%A Sparkle D. Williams
%A Benny Washington
%J CellBio
%P 186-191
%@ 2325-7792
%D 2013
%I Scientific Research Publishing
%R 10.4236/cellbio.2013.24021
%X <p class=\"MsoNormal\">
	<span lang=\"EN-US\">Insulin resistance is an important risk factor in the
development of cardiovascular diseases such as hypertension and
atherosclerosis. However, despite its importance</span><span lang=\"EN-US\">,</span><span lang=\"EN-US\"> the specific role
of insulin resistance in the etiology of these diseases is poorly understood.
At the same time, ethanol (ETOH) is a potent vasoconstrictor that primarily
induces down</span><span lang=\"EN-US\"> </span><span lang=\"EN-US\">regulation of mitogen activated protein kinases (MAPKs) which could
exacerbate insulin resistance and possibly lead to cardiovascular diseases. This
article describes how chronic ETOH exposure interferes with insulin signaling
in hypertensive vascular smooth muscle cells (HVSMCs) which leads to the
alteration of MAPKs, the major signaling molecules. Elevated (50</span><span lang=\"EN-US\"> </span><span lang=\"EN-US\">-</span><span lang=\"EN-US\"> </span><span lang=\"EN-US\">800 mM)
chronic exposure (24 hr) of HVSMCS to ETOH prior to insulin stimulation
decreased insulin-induced ERK 1/2 (MAPKs) and AKT expression. Similar
experiments were conducted using normotensive cells from rat. These cells
showed reductions in insulin-induced ERK 1/2 phosphorylation as well, but only
at higher concentrations of ETOH (400</span><span lang=\"EN-US\"> </span><span lang=\"EN-US\">-</span><span lang=\"EN-US\"> </span><span lang=\"EN-US\">800 mM). These alterations in insulin signaling
could provide an alternative molecular mechanism that may increase the risk of
insulin resistance, thus increasing the possibility of cardiovascular diseases.</span><span lang=\"EN-US\"><o:p></o:p></span>
</p>
%K HVSMCs
%K Ethanol
%K Insulin
%K ERK 1/2
%K AKT
%U http://www.scirp.org/journal/PaperInformation.aspx?PaperID=40433