Mice overexpressing human uncoupling protein-3 in skeletal muscle are hyperphagic and lean

By J. Clapham, J. R. Arch, H. Chapman, A. Haynes, C. Lister, G. Moore, V. Piercy, Sabrina A. Carter, I. Lehner, Stephen A. Smith and 17 more. Nature, 2000

629 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/b201830cd6787a90cba3681008807e7c625e666d

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In Physiology

1. J. Silva
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Citations in the corpus

• Regulation of Muscle Fiber Type and Running Endurance by PPARδ (2004, background): “In agreement with the previous characterization of this promoter (Brennan and Hardeman 1993; Clapham et al. 2000), the VP16-PPARd transgene was selectively expressed in skeletal muscle, with 10-fold less in the heart (Figure 1C).”
• Thermogenic mechanisms and their hormonal regulation. (2006, background): “While mice overexpressing UCP3 at very high levels are hyperphagic, yet leaner than controls (58), the expression of UCP2 in yeast mitochondria in amounts similar to those normally found in tissues failed to produce a detectable proton leak, suggesting the uncoupling originally observed in forced ex”
• Myocardial substrate metabolism in the normal and failing heart. (2005, background): “While this clearly occurs, it may not play a major role in the energywasting effects of fatty acid observed in vivo, as many studies show no effect of UCP3 content on the P/O in isolated mitochondria (60, 62, 222, 408, 478).”