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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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UCP5/BMCP1 transcript isoforms in human skeletal muscle: relationship of the short-insert isoform with lipid oxidation and resting metabolic rates.

Uncoupling protein 5 (UCP5) or brain mitochondrial carrier protein-1 (BMCP1) enhances mitochondrial proton leak in vitro and its hepatic and brain expression profiles are modulated by diet and cold exposure in mice. Alternative splicing generates three isoforms: a long form (UCP5L), a short form (UCP5S), and a short form with a 31 amino acid insert (UCP5SI). We investigated the relationship between skeletal muscle UCP5 expression and in vivo energy metabolism in 36 non-diabetic Pima Indians. We determined the expression levels of total UCP5 (UCP5T), and the isoforms UCP5L, UCP5S, and UCP5SI (66.8, 32.5, and 0.8% of UCP5T, respectively). None correlated with body weight or percent body fat. The transcript level of UCP5SI, but not the others, was positively correlated with resting metabolic rate (r=0.38, P=0.02, adjusted for age, sex, fat mass, and fat-free mass) and lipid oxidation rate (adjusted for age, sex, and percent body fat) during a euglycemic clamp with infusion of insulin at a physiologic concentration (r=0.42, P=0.01).[1]

References

  1. UCP5/BMCP1 transcript isoforms in human skeletal muscle: relationship of the short-insert isoform with lipid oxidation and resting metabolic rates. Yang, X., Pratley, R.E., Tokraks, S., Tataranni, P.A., Permana, P.A. Mol. Genet. Metab. (2002) [Pubmed]
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