Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Uncoupling protein-3 (UCP3) is selectively expressed in skeletal muscle of rodents and humans, and in brown adipose tissue (BAT) of rodents. C2C12 myoblast transfection with UCP3 induced a decrease in mitochondrial membrane potential suggesting that UCP3 behaves as an uncoupler of oxidative phosphorylations. Cold-exposure, food restriction and fasting affect UCP3 mRNA expression differently in BAT, compared to muscle. The effects induced by cold-exposure and fasting in BAT, and by fasting in muscle, might be explained by changes in intracellular free fatty acids (FFA). A single bout of exercise or endurance training, respectively, increases or decreases muscle UCP3 expression. The effects of PPARgamma agonists and leptin on BAT and muscle UCP3 mRNA expression are also discussed. Hypotheses to explain the effects of these modulations are presented.
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PMID:Effects of dietary deprivation, obesity and exercise on UCP3 mRNA levels. 1045 27

Uncoupling protein-3 (UCP3) is a mitochondrial protein that can diminish the mitochondrial membrane potential. Levels of muscle Ucp3 mRNA are increased by thyroid hormone and fasting. Ucp3 has been proposed to influence metabolic efficiency and is a candidate obesity gene. We have produced a Ucp3 knockout mouse to test these hypotheses. The Ucp3 (-/-) mice had no detectable immunoreactive UCP3 by Western blotting. In mitochondria from the knockout mice, proton leak was greatly reduced in muscle, minimally reduced in brown fat, and not reduced at all in liver. These data suggest that UCP3 accounts for much of the proton leak in skeletal muscle. Despite the lack of UCP3, no consistent phenotypic abnormality was observed. The knockout mice were not obese and had normal serum insulin, triglyceride, and leptin levels, with a tendency toward reduced free fatty acids and glucose. Knockout mice showed a normal circadian rhythm in body temperature and motor activity and had normal body temperature responses to fasting, stress, thyroid hormone, and cold exposure. The base-line metabolic rate and respiratory exchange ratio were the same in knockout and control mice, as were the effects of fasting, a beta3-adrenergic agonist (CL316243), and thyroid hormone on these parameters. The phenotype of Ucp1/Ucp3 double knockout mice was indistinguishable from Ucp1 single knockout mice. These data suggest that Ucp3 is not a major determinant of metabolic rate but, rather, has other functions.
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PMID:Lack of obesity and normal response to fasting and thyroid hormone in mice lacking uncoupling protein-3. 1074 95