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rs1800849 in UCP3 were significantly associated with prediabetes in a rural Chinese population. Overweight modified the effect of rs660339 of UCP2 on type 2 diabetes. These findings suggested that rs1800849 in UCP3 and rs660339 in UCP2 might play an important role in the incidence and development of type 2 diabetes.
Results here presented suggest that UCP variability has different pleiotropic effects, by affecting both telomere length and glucose homeostasis, likely through an influence on energy metabolism and stress response
Cellular feedback regulation may occur between UCP2/UCP3 and ACE. Cellular UCP regulation of sACE suggests a novel means of crosstalk between (and mutual regulation of) cellular and endocrine metabolism.
findings indicate that polymorphisms rs3813929 and rs1800849 from 5-HT2C and UCP3 genes were related to type 2 diabetes mellitus prevalence among the Brazilian obese women candidates for bariatric surgery.
In type 2 diabetics the combination of UCP3-55 CC and PPARgamma2 Pro12Ala genotypes is associated with significantly higher BMI than other PPARgamma2-UCP3 genotype combinations, partly due to a reduced ability in lipids oxidation.
genetic association studies in population in Spain: Data suggest that responses among obese patients (weight loss and changes in insulin resistance/cardiovascular risk factors) to high protein/low carbohydrate reducing diet varies according to a genetic polymorphism in the promoter region of UCP3 (-55CT, rs1800849).
Combined, our data suggest functional significance of UCP-3 for H/R resistance
UCP1 and UCP3 expression is associated with lipid and carbohydrate oxidation in patients submitted to bariatric surgery.
UCP3 overexpression limits keratinocyte proliferation and tumorigenesis through inhibition of Akt.
Children with UCP-3 -55 T/T genotype had a significantly lower adjusted metabolic rate than the C allele carriers.
A newly identified functional variant (rs1626521) in UCP-3 affects postprandial gastric functions and satiety and may contribute to weight gain and alter human mitochondrial function
Genotype and allele distributions of UCP1, UCP2 and UCP3 polymorphisms did not differ significantly between obese and non-obese Type 2 Diabetes Mellitus patients.[Meta-analysis]
The meta-analysis detected a significant association between the UCP2-866G/A, Ins/Del, Ala55Val and UCP3-55C/T polymorphisms and BMI mean differences.
UCP3 genotype prevailed in the women of besieged Leningrad compared to relevant control groups of the persons of the same age who did not suffered hungry disaster.
Studied the impact of SNPs in/near UCP3 and RPTOR on obesity-related traits.
BMI and TBF were significantly different among UCPI -3826A/G and UCP3 -55C/T genotype combinations, suggesting the existence of a gene interaction between UCP1 and UCP3 in influencing obesity and adiposity in multiethnic Malaysians.
The study replicates in two independent populations the association between the -55CT polymorphism of UCP3 and a lower BMI.
In patients with -55CC UCP3 genotype, a high mono-unsaturated hypocaloric diet reduced BMI, weight, waist circumference, waist to hip ratio, fat mass, LDL-cholesterol, total cholesterol and leptin levels.
A higher prevalence of UCP3 rs11235972 GG genotype was observed in Chinese children with nonalcoholic fatty liver disease.
T allele of the UCP3 gene was favourable in obtaining higher VOmax (maximum oxygen uptake)level and might be considered as endurance-related allele
Our findings, focusing on energy balance, provide a mechanistic understanding of the promising effect of early insulin initiation on lipotoxicity. Insulin, by recovering UCP3 activity, alleviated energy surfeit and potentiated AMPK-mediated lipid homeostasis in skeletal muscle cells following exposure to PA and in gastrocnemius of mice fed HFD.
Findings indicate that while heat-induced reduction in uncoupling proteins-3 improves mitochondrial efficiency in vitro, this is not translated to in vivo improvement of exercise economy at 1600 m or 4350 m.
UCP3 can be fully inhibited by all adenine nucleotides tested and IC50 increases with a decrease in PN-phosphorylation. Conserved arginines in the PN-binding pocket are involved in the inhibition of UCP1 and UCP3 to different extents. Fatty acids compete only with ATP bound to UCP3. UCP3 has adapted to fulfill a different role and possibly another transport function in brown adipose tissue, vs highly homologous UCP1.
our study provides evidence that the genetic risk factors for healthy aging differ in males and females, as expected from the differences in the phenotypes associated with healthy aging between the two sexes. It also has implications for how mitochondrial function changes during aging.
Together the data show that both UCP1 and UCP3 play essential and complementary roles in thermogenic responses in the mouse and suggest that UCP3-dependent thermogenesis is an under-appreciated mode of thermogenic energy dissipation.
The results indicate that mitochondrial UCP3 activity affects metabolism well beyond fatty acid oxidation, regulating biochemical pathways associated with amino acid metabolism and redox status.
Gene expression data revealed that 1, 4 or 8h of hypoxia results in temporal changes in various transcriptional genes regulating mitochondrial function and a time-dependent progressive increase in the expression of the mitochondrial uncoupling protein 3 (UCP-3) with concomitant changes in genes encoding sarcoplasmic reticulum calcium release proteins.
our study supports an essential role for UCP3 in modulating cardiac mCa2+ uptake via regulation of mCa1 single-channel activity.
Intriguingly, ectopic expression of constitutively active estrogen receptor alpha decreased UCP3 level and increased cellular ATP content in differentiated myoblastic C2C12 cells. Overall, the present study suggests that estrogen plays a critical role in the regulation of energy expenditure and exercise endurance in female.
We found increased mRNA expression of PDK4 and UCP3, which are known to be upregulated after exercise and regulated by PGC-1alpha after lactate administration.
suggest that VD3/VDR inhibits weight gain by activating UCP3 in the muscles.
the protective effect of PPARalpha activation against cardiac ischemia-reperfusion injury in terms of the expression of uncoupling protein (UCP), was investigated.
low 4-Hydroxy-2-nonenal (HNE) doses activate Nrf2 in cardiomyocytes and provide the first evidence of Nrf2 binding to the Ucp3 promoter in response to HNE, leading to increased protein expression
The hydrophilic sequences within loop 2, and the matrix-localized hydrophilic domain of UCP3, were necessary for binding to Hax-1 at the C-terminal domain, adjacent to the mitochondrial inner membrane.
abundance decreased even more in cold-acclimated UCP1 knockout mice
regulatory mechanism by which insulin inhibits cardiac UCP3 expression through activation of the lipogenic factor SREBP-1.
Ischemia/reperfusion also increased UCP3 transcription, indicating potential for greater uncoupling.
Nrf2 promotes survival by enhancing the expression of uncoupling protein 3 under conditions of oxidative stress.
Data indicated that Trim30 and Ucp3 play pivotal roles in energy balance and glucose homeostasis and might be used as genetic markers to represent the stage of obesity during the early and late stages of adipose tissue development, respectively.
The objective of this study was to estimate the allele and genotype frequencies of the IGF-IR/TaqI, m-calpain/HhaI, and UCP-3/BglI polymorphisms and to determine association between these polymorphisms and growth traits in Chinese indigenous cattle breed.
A study evaluating the relationships of uncoupling protein 2 and 3 expression, SNP of mitochondrial DNA, and residual feed intake (RFI) in Angus steers selected to have high or low RFI is presented.
The effect of single nucleotide polymorphisms in 6 genes and their associations with production factors in beef cattle are reported.
Association of pig UCP3 gene mutations and back fat thickness in the sixth and seventh rib.
Seven deletion polymorphisms were covered in introns of linkage genes of UCP2 and UCP3, showing that UCPs have conservation and genetic reliability.
The in vivo data indicate that beta-adrenergic agonists may function in regulating UCP2 and UCP3 expression in selected muscles.
Mitochondrial uncoupling proteins (UCP) are members of the larger 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. The different UCPs have tissue-specific expression\; this gene is primarily expressed in skeletal muscle. This gene's protein product is postulated to protect mitochondria against lipid-induced oxidative stress. Expression levels of this gene increase when fatty acid supplies to mitochondria exceed their oxidation capacity and the protein enables the export of fatty acids from mitochondria. UCPs contain the three solcar protein domains typically found in MACPs. Two splice variants have been found for this gene.
, mitochondrial uncoupling protein
, mitochondrial uncoupling protein 3
, uncoupling protein
, uncoupling protein 3 (mitochondrial, proton carrier)
, uncoupling protein UCP
, mitochondrial uncoupling protein 3-like
, solute carrier family 25 member 9
, UCP 3
, uncoupling protein 3, mitochondrial
, Uncoupling protein 3, mitochondrial