Uncoupling protein 1 (UCP1, mitochondrial, proton carrier)

Nutrigenomics

See Also

• [INSIG2 (Insulin Induced Gene 2)]?
• Mitochondria?
• Trp64Arg polymorphism of the beta3-adrenergic receptor gene

UCP1 uncoupling protein 1 (mitochondrial, proton carrier) [Homo sapiens]

• Chromosome: 19; Location: 19p11-q11
• Official Symbol: UCP1 and Name: uncoupling protein 1 (mitochondrial, proton carrier)
• Gene type: protein coding
• Gene name: UCP1
• Gene description: uncoupling protein 1 (mitochondrial, proton carrier)
• Gene aliases: UCP; SLC25A7
• Organism: Homo sapiens

Summary

Summary: Mitochondrial uncoupling proteins (UCP) are members of the family of mitochondrial anion carrier proteins (MACP). UCPs separate oxidative phosphorylation from ATP synthesis with energy dissipated as heat, also referred to as the mitochondrial proton leak. UCPs facilitate the transfer of anions from the inner to the outer mitochondrial membrane and the return transfer of protons from the outer to the inner mitochondrial membrane. They also reduce the mitochondrial membrane potential in mammalian cells. Tissue specificity occurs for the different UCPs and the exact methods of how UCPs transfer H+/OH- are not known. UCPs contain the three homologous protein domains of MACPs. This gene is expressed only in brown adipose tissue, a specialized tissue which functions to produce heat.

Abstracts

Additive effect of A-->G (-3826) variant of the uncoupling protein gene and the Trp64Arg mutation of the beta 3-adrenergic receptor gene on weight gain in morbid obesity.

Int J Obes Relat Metab Disord. 1996 Dec;20(12):1062-6. Clement K, Ruiz J, Cassard-Doulcier AM, Bouillaud F, Ricquier D, Basdevant A, Guy-Grand B, Froguel P.

• OBJECTIVE: Obesity results from an imbalance between caloric intake and energy expenditure, which is partly genetically determined. We have investigated, using a PCR-RFLP assay, the effects on weight gain of two genetic variants of the uncoupling proteins and the beta 3-adrenoceptor, two major expressed proteins of the brown adipose tissue (BAT) involved in thermo-genesis. SUBJECTS: 238 morbidly obese and 91 non obese Caucasian subjects. RESULTS: A high prevalence (27%) in French Caucasians of the A-->G change variation located in the 5' flanking domain of the UCP gene was observed with no significant difference between morbidly obese patients and non obese subjects, suggesting that UCP gene is not a major gene for obesity. However, in the population of morbidly obese subjects, the presence of the A-->G allelic variant of the UCP gene showed to be an associated factor of high weight gain during adult life (odd-ratio: 1.4, P = 0.02). Such an association was previously described for the Trp64Arg mutation of the beta 3-AR gene. Furthermore, an additive effect of these two gene variants on weight gain was observed (Odd-Ratio: 4.95, trend test: P = 0.05). The attributable risks for UCP gene and beta 3-AR gene variants were respectively: 25% and 9%. CONCLUSION: These data support the hypothesis of a possible link between energy balance, BAT and weight gain in human.

UCP1 is essential for adaptive adrenergic nonshivering thermogenesis

Am J Physiol Endocrinol Metab. 2006 Apr 4; Golozoubova V, Cannon B, Nedergaard J.

• Participation of brown adipose tissue (through the action of the uncoupling protein UCP1) in adaptive adrenergic nonshivering thermogenesis is recognized, but the existence of a response to adrenergic stimulation in UCP1-ablated mice implies that a mechanism for an alternative adaptive adrenergic thermogenesis may exist. We have here used UCP1-ablated mice to examine the existence of an alternative adaptive adrenergic nonshivering thermogenesis, examined as the oxygen consumption response to systemically injected norepinephrine into anaesthetized or conscious mice, acclimated to different temperatures. While confirming that UCP1-dependent adrenergic nonshivering thermogenesis is adaptive, we demonstrate that the adrenergic UCP1-independent thermogenesis is not recruitable by cold acclimation. Thus, at least in the mouse, no other proteins or enzymatic pathways exist that can participate in or with time take over the UCP1-mediation of adaptive adrenergic nonshivering thermogenesis, even in the total absence of UCP1. UCP1 is thus the only protein capable of mediating cold-acclimation-recruited adaptive adrenergic nonshivering thermogenesis.