CiteULike is a free online bibliography manager. Register and you can start organising your references online.

Increase of insulin sensitivity and reversal of age-dependent glucose intolerance with inhibition of ASIC3. Export

Biochemical and biophysical research communications, Vol. 371, No. 4. (11 July 2008), pp. 729-734.

Citation Format

[Posts]

View FullText article


X Reviews [Write a review of this article]

X Find related articles from these CiteULike users

X Find related articles with these CiteULike tags

X Posting History

X Abstract

Glucose tolerance progressively declines with age in humans and is often accompanied by insulin resistance and a high prevalence of type 2 diabetes. Little is known about the mechanism underlying the age-related changes in glucose metabolism. Here we reported that acid-sensing ion channel 3 (ASIC3) is functionally expressed in adipose cells. ASIC3(-/-) mice were protected against age-dependent glucose intolerance with enhanced insulin sensitivity. Acute administration of ASIC3-selective blocker APETx2 improved the glucose control and increased the insulin sensitivity in older (25-27 weeks) ASIC3(+/+) mice. Moreover, the enhanced glucose control in aging ASIC3(-/-) mice was associated with high baseline levels of Akt phosphorylation and high copy number of mitochondrial DNA in adipose tissues. Taken together, our data suggest that ASIC3 signaling might be involved in the control of age-dependent glucose intolerance and insulin resistance.


X BibTeX record

X RIS record


Privacy Statement | Terms & Conditions
CiteULike organises scholarly (or academic) papers or literature and provides bibliographic (which means it makes bibliographies) for universities and higher education establishments. It helps undergraduates and postgraduates. People studying for PhDs or in postdoctoral (postdoc) positions. The service is similar in scope to EndNote or RefWorks or any other reference manager like BibTeX, but it is a social bookmarking service for scientists and humanities researchers.