GH directly stimulates UCP3 expression

2018 ◽  
Vol 40 ◽  
pp. 44-54 ◽  
Author(s):  
Misa Hayashi ◽  
Kumi Futawaka ◽  
Midori Matsushita ◽  
Rie Koyama ◽  
Yue Fun ◽  
...  
Keyword(s):  
2016 ◽  
Vol 62 (1) ◽  
pp. 32-39 ◽  
Author(s):  
Tomoki ABE ◽  
Katsuya HIRASAKA ◽  
Shohei KOHNO ◽  
Chisato TOMIDA ◽  
Marie HARUNA ◽  
...  

2006 ◽  
Vol 101 (1) ◽  
pp. 339-347 ◽  
Author(s):  
Jamie L. Barger ◽  
Brian M. Barnes ◽  
Bert B. Boyer

Uncoupling protein (UCP) 1 (UCP1) catalyzes a proton leak in brown adipose tissue (BAT) mitochondria that results in nonshivering thermogenesis (NST), but the extent to which UCP homologs mediate NST in other tissues is controversial. To clarify the role of UCP3 in mediating NST in a hibernating species, we measured Ucp3 expression in skeletal muscle of arctic ground squirrels in one of three activity states (not hibernating, not hibernating and fasted for 48 h, or hibernating) and housed at 5°C or −10°C. We then compared Ucp3 mRNA levels in skeletal muscle with Ucp1 mRNA and UCP1 protein levels in BAT in the same animals. Ucp1 mRNA and UCP1 protein levels were increased on cold exposure and decreased with fasting, with the highest UCP1 levels in thermogenic hibernators. In contrast, Ucp3 mRNA levels were not affected by temperature but were increased 10-fold during fasting and >3-fold during hibernation. UCP3 protein levels were increased nearly fivefold in skeletal muscle mitochondria isolated from fasted squirrels compared with nonhibernators, but proton leak kinetics in the presence of BSA were unchanged. Proton leak in BAT mitochondria also did not differ between fed and fasted animals but did show classical inhibition by the purine nucleotide GDP. Levels of nonesterified fatty acids were highest during hibernation, and tissue temperatures during hibernation were related to Ucp1, but not Ucp3, expression. Taken together, these results do not support a role for UCP3 as a physiologically relevant mediator of NST in muscle.


2017 ◽  
Vol 14 (4) ◽  
pp. 396 ◽  
Author(s):  
Giatromanolaki Alexandra ◽  
Balaska Konstantina ◽  
Kalamida Dimitra ◽  
Kakouratos Christos ◽  
Sivridis Efthimios ◽  
...  

2001 ◽  
Vol 29 (5) ◽  
pp. A98-A98
Author(s):  
M-E Harper ◽  
R. Dent ◽  
V. Bezaire ◽  
A. Antoniou ◽  
A. Gauthier ◽  
...  

2001 ◽  
Vol 29 (5) ◽  
pp. A120-A120
Author(s):  
J.A. Harper ◽  
J.A. Stuart ◽  
K.M. Brindle ◽  
M.B. Jekabsons ◽  
S. Cadenas ◽  
...  

2003 ◽  
Vol 284 (2) ◽  
pp. E449-E451 ◽  
Author(s):  
Matthijs K. C. Hesselink ◽  
Patrick Schrauwen

2009 ◽  
Vol 38 (1) ◽  
pp. 54-62 ◽  
Author(s):  
Tobias Fromme ◽  
Christoph Hoffmann ◽  
Kerstin Nau ◽  
Jan Rozman ◽  
Kathrin Reichwald ◽  
...  

Uncoupling protein 3 (Ucp3) is a transport protein of the inner mitochondrial membrane and presumably is implicated in the maintenance or tolerance of high lipid oxidation rates. Ucp3 is predominantly expressed in skeletal muscle and brown adipose tissue and is regulated by a transcription factor complex involving peroxisome proliferator-activated receptor-α, MyoD, and COUP transcription factor II. By analysis of a mutant Djungarian hamster model lacking Ucp3 transcription specifically in brown adipose tissue, we identified a putative transcription factor-binding site that confers tissue specificity. A naturally occurring intronic point mutation disrupting this site leads to brown adipose tissue-specific loss of Ucp3 expression and an altered body weight trajectory. Our findings provide insight into tissue-specific Ucp3 regulation and, for the first time, unambiguously demonstrate that changes in Ucp3 expression can interfere with body weight regulation.


2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Jong Wook Song ◽  
Hyo Jung Kim ◽  
Hyelin Lee ◽  
Jae-woo Kim ◽  
Young-Lan Kwak

Activation of peroxisome proliferator-activated receptorα(PPARα) confers cardioprotection, while its mechanism remains elusive. We investigated the protective effect of PPARαactivation against cardiac ischemia-reperfusion injury in terms of the expression of uncoupling protein (UCP). Myocardial infarct size and UCP expression were measured in rats treated with WY-14643 20 mg/kg, a PPARαligand, or vehicle. WY-14643 increased UCP3 expressionin vivo. Myocardial infarct size was decreased in the WY-14643 group (76 ± 8% versus 42 ± 12%,P<0.05). During reperfusion, the incidence of arrhythmia was higher in the control group compared with the WY-14643 group (9/10 versus 3/10,P<0.05). H9c2 cells were incubated for 24 h with WY-14643 or vehicle. WY-14643 increased UCP3 expression in H9c2 cells. WY-14643 decreased hypoxia-stimulated ROS production. Cells treated with WY-14643 were more resistant to hypoxia-reoxygenation than the untreated cells. Knocking-down UCP3 by siRNA prevented WY-14643 from attenuating the production of ROS. UCP3 siRNA abolished the effect of WY-14643 on cell viability against hypoxia-reoxygenation. In summary, administration of PPARαagonist WY-14643 mitigated the extent of myocardial infarction and incidence of reperfusion-induced arrhythmia. PPARαactivation conferred cytoprotective effect against hypoxia-reoxygenation. Associated mechanisms involved increased UCP3 expression and resultant attenuation of ROS production.


2021 ◽  
Vol 9 (1) ◽  
pp. 139-146
Author(s):  
Walaa M Sarhan ◽  
Safaa El-Hussien Tawfik ◽  
Amal S El-Shal ◽  
Vishruti Makani ◽  
Hanim M. Abdel-Nour

Increased consumption of Trans Fats is associated with increased risk of Coronary Heart Disease. Uncoupling proteins (UCPs) are mitochondrial proteins that disperse the inter-membrane electrochemical potential as heat. We aimed to detect the relation of high Trans-fat intake in diet on the expression of UCP2&3 m-RNA in children. A specific questionnaire to parents of sixty-eight children (4-15 years) was conducted. Accordingly, the subjects were sub-grouped into; High Trans-fat consuming group (37 subjects) and a Medium Trans-fat consuming one (31 subjects). Samples collected from Peripheral blood to analyze UCP2&3 mRNA expression by Real Time Polymerase Chain Reaction (RT-PCR). Levels of UCP2 expression was reduced in children consuming High Trans-fat (2.5 ±0.7) in comparison with Medium Trans-fat consuming ones (1.5± 0.2) with (p<0.001). However, not much significance was showed in UCP3 expression with values (2.1±0.5) in the High consuming group and (1.9±0.2) in Medium consuming group with (p=0.08). In Delta relationship the diet-induced changes in UCP2 (r=0.66, P=0.002) and UCP3 (r=0.61, P=0.06) mRNA expression was negatively correlated with percentage of Trans-fat in diet. The correlation of UCP2&3 mRNA expression and high Trans-fat intake suggests a mechanism by which high Trans-fat diet plays a role in childhood obesity.


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