alexa Mechanisms of Fatty Acid-Induced Insulin Resistance in
ISSN: 2155-6156

Journal of Diabetes & Metabolism
Open Access

Like us on:
OMICS International organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Open Access Journals gaining more Readers and Citations

700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers

This Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)

Review Article

Mechanisms of Fatty Acid-Induced Insulin Resistance in Muscle and Liver

Rafik Ragheb1,2,3,4,5* and Amina M. Medhat1

1University of Ain Shams – Department of Biochemistry – Faculty of Science, Cairo – Egypt

2University Health Network, Canada

3Hospital for Sick Children, Canada

4Mount Sinai Hospital, Canada

5University of Toronto, Toronto, Canada

Corresponding Author:
Rafik Ragheb
University of Toronto, Toronto – Canada
Tel/Fax: 1-905-2099660
E-mail: [email protected]

Received Date: April 06, 2011; Accepted Date: May 13, 2011; Published Date: May 16, 2011

Citation: Ragheb R, Medhat AM (2011) Mechanisms of Fatty Acid-Induced Insulin Resistance in Muscle and Liver. J Diabetes Metab 2:127. doi:10.4172/2155-6156.1000127

Copyright: © 2011 Ragheb R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Insulin Resistance occurs as a result of disturbances in lipid metabolism and increased levels of circulating fatty acids that accumulate within the insulin sensitive tissues such as muscle, liver and adipose tissues. Increased fatty acid flux has been suggested to be strongly associated with insulin resistant states such as obesity and type 2-diabetes. Fatty acids appear to cause this defect in glucose transport by inhibiting insulin -stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and reducing IRS-1 associated phosphatidyl-inositol 3-kinase activity that implicate other insulin signaling components downstream of the insulin signaling cascade. A number of different metabolic abnormalities may increase intramyocellular or intrahepatic fatty acid metabolites that induce the disease state of insulin resistance through a number of different cellular mechanisms. The current review point out the link between enhanced FFA flux and activation of PKC and how it impacts on both the insulin signaling in muscle and liver.


Share This Page

Additional Info

Loading Please wait..
Peer Reviewed Journals
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version