Uncoupling protein‐3: a new member of the mitochondrial carrier family with tissue‐specific expression

Boss, Olivier; Samec, Sonia; Paoloni-Giacobino, Ariane; Rossier, Colette; Dulloo, Abdul G.; Seydoux, Josiane; Muzzin, Patrick; Giacobino, Jean‐Paul

doi:10.1016/s0014-5793(97)00384-0

Cited by 1,023 publications

(818 citation statements)

References 17 publications

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“…In all experiments n=6, *p<0.05 vs. wo ▲ and participates in adaptive thermogenesis [29]. UCP-2 [30] and UCP-3 [31] have been identified more recently and are expressed in different tissues than UCP-1. UCP-2 is the homologue with the widest distribution and the only one reported to be expressed in pancreatic islets [32].…”

Section: Discussionmentioning

confidence: 93%

Peroxisome proliferator-activated receptor γ coactivator-1-dependent uncoupling protein-2 expression in pancreatic islets of rats: a novel pathway for neural control of insulin secretion

et al. 2003

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Aims/hypothesis. Sympathetic inputs inhibit insulin secretion through α2-adrenergic receptors coupled with Gi protein. High adrenergic tonus generated by exposure of homeothermic animals to cold reduces insulin secretion. In this study we evaluate the participation of UCP-2 in cold-induced regulation of insulin secretion. Methods. Static insulin secretion studies, western blotting and immunohistochemistry were used in this investigation. Results. Exposure of rats to cold during 8 days promoted 60% (n=15, p<0.05) reduction of basal serum insulin levels concentration accompanied by reduction of the area under insulin curve during i.p. GTT (50%, n=15, p<0.05). Isolated islets from cold-exposed rats secreted 57% (n=6, p<0.05) less insulin following a glucose challenge. Previous sympathectomy, partially prevented the effect of cold exposure upon insulin secretion. Islets isolated from cold-exposed rats expressed 51% (n=6, p<0.5) more UCP-2 than islets from control rats, while the inhibition of UCP-2 expression by antisense oligonucleotide treatment partially restored insulin secretion of islets obtained from cold-exposed rats. Cold exposure also induced an increase of 69% (n=6, p<0.05) in PGC-1 protein content in pancreatic islets. Inhibition of islet PGC-1 expression by antisense oligonucleotide abrogated cold-induced UCP-2 expression and partially restored insulin secretion in islets exposed to cold. Conclusion/interpreatation. Our data indicate that sympathetic tonus generated by exposure of rats to cold induces the expression of PGC-1, which participates in the control of UCP-2 expression in pancreatic islets. Increased UCP-2 expression under these conditions could reduce the beta-cell ATP/ADP ratio and negatively regulate insulin secretion. [Diabetologia (2003[Diabetologia ( ) 46:1522[Diabetologia ( -1531 Keywords Insulin, uncoupling protein, PGC-1, islet, sympathetic. Acetylcholine (Ach) mediates parasympathetic signals and acts upon pancreatic beta cells activating muscarinic M3 receptor subtype [4,5], which in turn promotes phospholipase β (PLCβ) stimulation with subsequent diacylglycerol (DAG) and inositol 1,4,5 triphosphate (IP3) accumulation [6]. The net result is the elevation of cytosolic Ca 2+ and increased insulin secretion. In contrast, norepinephrine (NE) released by sympathetic terminals stimulates beta-cell α2 adrenergic receptors that acting through G i or G 0 proThe role played by neural inputs on beta-cell function has been a matter of intense investigation over the latest forty years [1]. The highest effect is believed to be exerted by parasympathetic fibres originated at the

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Section: Discussionmentioning

confidence: 93%

Peroxisome proliferator-activated receptor γ coactivator-1-dependent uncoupling protein-2 expression in pancreatic islets of rats: a novel pathway for neural control of insulin secretion

et al. 2003

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“…16 Uncoupling protein 1 (UCP1), 2 (UCP2) and 3 (UCP3) are mitochondria membrane transporters that are involved in dissipating the proton electrochemical gradient, thereby releasing stored energy as heat. [103][104][105] This implies a role for UCPs in energy expenditure and adiposity. UCP1 mRNA has been detected at low levels in human white adipose tissue and reported to be decreased in intra-abdominal adipose tissue of obese subjects.…”

Section: Pathways Controlling Lipid Storage In Adipocytesmentioning

confidence: 99%

Obesity and polymorphisms in genes regulating human adipose tissue

Dahlman

Arner

2007

Int J Obes

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Obesity is the result of an imbalance between food intake and energy expenditure resulting in the storing of energy as fat. Adipose tissue contains the largest store of energy in the body and plays important roles in regulating energy partitioning. Developments in genomics, in particular microarray-based expression profiling, have provided scientists with a number of new candidate genes whose expression in adipose tissue is regulated by obesity. Integrating expression profiles with genome-wide linkage and/or association analyses is a promising strategy to identify new genes underlying susceptibility to obesity. This article provides a comprehensive review of adipose-tissue-expressed genes implicated in predisposition to human obesity. The authors consider the following genes of particular interest: peroxisome proliferator-activated receptor gamma and, potentially, INSIG2 acting in adipogenesis; the adrenoreceptors beta 2 and 3, as well as hormone-sensitive lipase acting on lipolysis; uncoupling protein 2 acting in mitochondria energy expenditure; and among secreted molecules the cytokine tumor necrosis factor alpha and the hormone leptin. With the rapid development in genome research, we predict that additional alleles in genes regulating adipose tissue function will be established as risk factors for common obesity in the coming years. This has important implications for the prevention of obesity and may also offer new therapeutic targets.

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“…There is also an inhibition of proton conductance in yeast mitochondria by ATP [28]. UCP3 is a UCP1 homologue that is highly skeletal-muscle-specific [29,30]. Its uncoupling activity is a matter of debate [4][5][6]10,12].…”

Section: Effects Of Nucleotides On the Proton Conductance Of Mitochonmentioning

confidence: 99%

Effects of magnesium and nucleotides on the proton conductance of rat skeletal-muscle mitochondria

Cadenas

Brand

2000

Biochemical Journal

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During oxidative phosphorylation most of the protons pumped out to the cytosol across the mitochondrial inner membrane return to the matrix through the ATP synthase, driving ATP synthesis. However, some of them leak back to the matrix through a proton-conductance pathway in the membrane. When the ATP synthase is inhibited with oligomycin and ATP is not being synthesized, all of the respiration is used to drive the proton leak. We report here that Mg# + inhibits the proton conductance in rat skeletal-muscle mitochondria. Addition of Mg# + inhibited both oligomycin-inhibited respiration and the proton conductance, while removal of Mg# + using EDTA activated these processes. The proton conductance was inhibited by more than 80 % as free Mg# + was raised from 25 nM to 220 µM. Half-maximal inhibition occurred at about 1 µM free Mg# + ,

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Uncoupling protein‐3: a new member of the mitochondrial carrier family with tissue‐specific expression

Cited by 1,023 publications

References 17 publications

Peroxisome proliferator-activated receptor γ coactivator-1-dependent uncoupling protein-2 expression in pancreatic islets of rats: a novel pathway for neural control of insulin secretion

Peroxisome proliferator-activated receptor γ coactivator-1-dependent uncoupling protein-2 expression in pancreatic islets of rats: a novel pathway for neural control of insulin secretion

Obesity and polymorphisms in genes regulating human adipose tissue

Effects of magnesium and nucleotides on the proton conductance of rat skeletal-muscle mitochondria

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