alexa Aberrant Activation Of Aldose Reductase Promotes Insulin Insensitivity, Hepatosteatosis And Obesity In Mice In Part Through Modulating Hepatic PPARα, LKB1/AMPKα And IRS-1
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)

Share This Page

Additional Info

Loading Please wait..

5th World Congress on Diabetes & Metabolism
November 03-05, 2014 Embassy Suites Las Vegas, USA

James Y Yang
ScientificTracks Abstracts: J Diabetes Metab
DOI: 10.4172/2155-6156.S1.026
It is well established that aldose reductase (AR) is a critical mediator for a variety of diabetic complications. Recent studies, however, indicate that aberrant activation of AR or overproduction of the polyol pathway-derived endogenous hepatic fructose might contribute to the development of fatty liver diseases as well as the metabolic syndrome. However, the mechanisms underlying AR/the polyol pathway-induced pathogenesis of related metabolic disorders were not clear. In this investigation, we aimed to investigate how the activity change of AR might affect insulin signaling, hepatosteatosis and obesity. We found that in mouse AML12 hepatocytes, overexpression of AR significantly reduced the abundance of phosphorylated LKB1, AMPKα and ACC. Conversely, lentivirus-mediated AR knockdown greatly elevated the levels of phosphorylated LKB1, AMPKα and ACC. Additionally, overexpression of AR reduced the mRNA and protein expression of IRS-1, whereas knockdown of AR greatly elevated IRS-1 mRNA and protein expression. In the Agouti yellow obese mice, loss of AR (Ay/a::AR-/-) significantly ameliorated the Agouti signaling peptide-induced insulin insensitivity, hepatosteatosis and obesity, as compared with that of the Ay/a::AR+/+ control mice. In contrast, liver-specific transgenic overexpression of AR appeared to promote the development of glucose-induced hepatosteatosis and obesity. Together with our previous demonstrations that AR is capable of regulating the activity of PPARα to impact lipid homeostasis, our findings suggest that aberrant activation of AR might promote metabolic remodeling, insulin resistance, hepatosteatosis and obesity in part through modulating the expression or the activity of hepatic PPARα, IRS-1 and LKB1/AMPKα.
James Y Yang earned his PhD from the University of Houston, Houston, Texas, USA. He pursued his Postdoctoral studies at the Columbia University under the guidance of Dr. Abraham Spector. He worked as a Research Assistant Professor/Research Officer at the University of Hong Kong for 7 years. He is currently a Professor in the State Key Laboratory of Cellular Stress Biology and the School of Life Sciences, Xiamen University, Xiamen, China. He has published more than 30 papers in reputed journals including Hepatology, Gut, FRBM, JBC and Diabetologia.
image PDF   |   image HTML

Relevant Topics

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

Agri, Food, Aqua and Veterinary Science Journals

Dr. Krish

1-702-714-7001 Extn: 9040

Clinical and Biochemistry Journals

Datta A

1-702-714-7001Extn: 9037

Business & Management Journals


1-702-714-7001Extn: 9042

Chemical Engineering and Chemistry Journals

Gabriel Shaw

1-702-714-7001 Extn: 9040

Earth & Environmental Sciences

Katie Wilson

1-702-714-7001Extn: 9042

Engineering Journals

James Franklin

1-702-714-7001Extn: 9042

General Science and Health care Journals

Andrea Jason

1-702-714-7001Extn: 9043

Genetics and Molecular Biology Journals

Anna Melissa

1-702-714-7001 Extn: 9006

Immunology & Microbiology Journals

David Gorantl

1-702-714-7001Extn: 9014

Informatics Journals

Stephanie Skinner

1-702-714-7001Extn: 9039

Material Sciences Journals

Rachle Green

1-702-714-7001Extn: 9039

Mathematics and Physics Journals

Jim Willison

1-702-714-7001 Extn: 9042

Medical Journals

Nimmi Anna

1-702-714-7001 Extn: 9038

Neuroscience & Psychology Journals

Nathan T

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

John Behannon

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

1-702-714-7001 Extn: 9042

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