Save
Email
Print
ShareScienceDaily (Nov. 12, 2005) — The role of mitochondrial dysfunction in the pathogenesis of insulin resistance is a widely debated topic. It has been shown that young, lean, insulin-resistant offspring of parents with type 2 diabetes have reduced mitochondrial function. But the precise role of this decreased function in relation to insulin resistance and type 2 diabetes was not clear.
In a paper appearing online on November 10 in advance of print publication of the December issue of the Journal of Clinical Investigation, Gerald Shulman and colleagues from Yale University take muscle biopsies from these offspring and show that they have reduced mitochondrial content as assessed by electron microscopy. The subjects also have lower insulin-stimulated muscle glucose uptake and increased lipid content in muscle cells. However in contrast to two recent studies, the authors did not find any alterations in PGC-1a or PGC-1b or other downstream regulators of mitochondrial gene expression.
These results provide new insights into the earliest defects that may be responsible for the pathogenesis of type 2 diabetes. Moreover, reduced mitochondrial content could result in reduced mitochondrial function, which predisposes the offspring of type, 2 diabetic parents to muscle cell lipid accumulation, which then leads to defective insulin signaling and action.
TITLE: Reduced mitochondrial density and increased IRS-1 serine phosphorylation in muscle of insulin-resistant offspring of Type 2 diabetic parents.
Recommend this story on Facebook, Twitter,
and Google +1:
Other bookmarking and sharing tools:
Story Source:
The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
more 
