| First Author | Skilling H | Year | 2010 |
| Journal | Biochem Biophys Res Commun | Volume | 400 |
| Issue | 3 | Pages | 318-22 |
| PubMed ID | 20727852 | Mgi Jnum | J:165594 |
| Mgi Id | MGI:4837795 | Doi | 10.1016/j.bbrc.2010.08.053 |
| Citation | Skilling H, et al. (2010) Brown adipose tissue function in short-chain acyl-CoA dehydrogenase deficient mice. Biochem Biophys Res Commun 400(3):318-22 |
| abstractText | Brown adipose tissue is a highly specialized organ that uses mitochondrial fatty acid oxidation to fuel non-shivering thermogenesis. In mice, mutations in the acyl-CoA dehydrogenase family of fatty acid oxidation genes are associated with sensitivity to cold. Brown adipose tissue function has not previously been characterized in these knockout strains. Short-chain acyl-CoA dehydrogenase (SCAD) deficient mice were found to have increased brown adipose tissue mass as well as modest cardiac hypertrophy. Uncoupling protein-1 was reduced by 70% in brown adipose tissue and this was not due to a change in mitochondrial number, nor was it due to decreased signal transduction through protein kinase A which is known to be a major regulator of uncoupling protein-1 expression. PKA activity and in vitro lipolysis were normal in brown adipose tissue, although in white adipose tissue a modest increase in basal lipolysis was seen in SCAD-/- mice. Finally, an in vivo norepinephrine challenge of brown adipose tissue thermogenesis revealed normal heat production in SCAD-/- mice. These results suggest that reduced brown adipose tissue function is not the major factor causing cold sensitivity in acyl-CoA dehydrogenase knockout strains. We speculate that other mechanisms such as shivering capacity, cardiac function, and reduced hepatic glycogen stores are involved. |
