| Literature DB >> 20802160 |
Misato Kobayashi1, Tamio Ohno, Natsuko Hada, Masato Fujiyoshi, Masako Kuga, Masahiko Nishimura, Atsushi Murai, Fumihiko Horio.
Abstract
Each abdominal fat depot, such as mesenteric or epididymal, differently contributes to the development of insulin resistance. The aim of this study was to identify the genetic regions that contribute to fat accumulation in epididymal/mesenteric fat and to examine whether or not the genetic regions that affect glucose metabolism and body fat distribution are coincident. We previously mapped a major quantitative trait locus (QTL) (T2dm2sa) for impaired glucose tolerance on chromosome 2 and revealed that SM.A-T2dm2sa congenic mice showed not only glucose tolerance but also fat accumulation. In the present study, to identify the loci/genes that control the accumulation of abdominal fat, we performed QTL analyses of epididymal/mesenteric fat weight by using (A/J x SM.A-T2dm2sa)F2 mice in which the effect of T2dm2sa was excluded. As a result, two highly significant QTLs for mesenteric fat, as well as three significant QTLs for epididymal/mesenteric fat, were mapped on the different chromosomal regions. This suggests that the fat accumulations in individual fat depots are controlled by distinct genomic regions. Our comparison of these QTLs for abdominal fat distribution with those for glucose metabolism revealed that the major genetic factors affecting body fat distribution do not coincide with genetic factors affecting glucose metabolism in (A/J x SM.A-T2dm2sa)F2.Entities:
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Year: 2010 PMID: 20802160 PMCID: PMC2975718 DOI: 10.1194/jlr.M009563
Source DB: PubMed Journal: J Lipid Res ISSN: 0022-2275 Impact factor: 5.922