scholarly journals Uncoupling protein-3 gene expression: reduced skeletal muscle mRNA in obese humans during pronounced weight loss

Diabetologia ◽  
1999 ◽  
Vol 42 (3) ◽  
pp. 302-309 ◽  
Author(s):  
H. Esterbauer ◽  
H. Oberkofler ◽  
G. Dallinger ◽  
D. Breban ◽  
E. Hell ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Weight Loss ◽  
Uncoupling Protein ◽  
Uncoupling Protein 3

scholarly journals Thyroid hormones directly activate the expression of the human and mouse uncoupling protein-3 genes through a thyroid response element in the proximal promoter region

2005 ◽  
Vol 386 (3) ◽  
pp. 505-513 ◽  
Author(s):  
Gemma SOLANES ◽  
Neus PEDRAZA ◽  
Verónica CALVO ◽  
Antonio VIDAL-PUIG ◽  
Bradford B. LOWELL ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Uncoupling Protein ◽  
Gene Promoter ◽  
Proximal Promoter ◽  
Ucp3 Gene ◽  
Uncoupling Protein 3

The transcription of the human UCP3 (uncoupling protein-3) gene in skeletal muscle is tightly regulated by metabolic signals related to fatty acid availability. However, changes in thyroid status also modulate UCP3 gene expression, albeit by unknown mechanisms. We created transgenic mice bearing the entire human UCP3 gene to investigate the effect of thyroid hormones on human UCP3 gene expression. Treatment of human UCP3 transgenic mice with thyroid hormones induced the expression of the human gene in skeletal muscle. In addition, transient transfection experiments demonstrate that thyroid hormones activate the transcription of the human UCP3 gene promoter when MyoD and the TR (thyroid hormone receptor) were co-transfected. The action of thyroid hormones on UCP3 gene transcription is mediated by the binding of the TR to a proximal region in the UCP3 gene promoter that contains a direct repeat structure. An intact DNA sequence of this site is required for thyroid hormone responsiveness and TR binding. Chromatin immunoprecipitation assays revealed that the TR binds this element in vivo. The murine Ucp3 gene promoter was also dependent on MyoD and responsive to thyroid hormone in transient transfection assays. However, it was much less sensitive to thyroid hormone than the human UCP3 promoter. In summary, UCP3 gene transcription is activated by thyroid hormone treatment in vivo, and this activation is mediated by a TRE (thyroid hormone response element) in the proximal promoter region. Such regulation suggests a link between UCP3 gene expression and the effects of thyroid hormone on mitochondrial function in skeletal muscle.

scholarly journals Developmental and Tissue-Specific Involvement of Peroxisome Proliferator-Activated Receptor-α in the Control of Mouse Uncoupling Protein-3 Gene Expression

Endocrinology ◽  
2006 ◽  
Vol 147 (10) ◽  
pp. 4695-4704 ◽  
Author(s):  
Neus Pedraza ◽  
Meritxell Rosell ◽  
Joan Villarroya ◽  
Roser Iglesias ◽  
Frank J. Gonzalez ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Mrna Expression ◽  
Uncoupling Protein ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ucp3 Gene ◽  
Uncoupling Protein 3

Uncoupling protein-3 (UCP3) is a member of the mitochondrial carrier family expressed preferentially in skeletal muscle and heart. It appears to be involved in metabolic handling of fatty acids in a way that minimizes excessive production of reactive oxygen species. Fatty acids are powerful regulators of UCP3 gene transcription. We have found that the role of peroxisome proliferator-activated receptor-α (PPARα) on the control of UCP3 gene expression depends on the tissue and developmental stage. In adults, UCP3 mRNA expression is unaltered in skeletal muscle from PPARα-null mice both in basal conditions and under the stimulus of starvation. In contrast, UCP3 mRNA is down-regulated in adult heart both in fed and fasted PPARα-null mice. This occurs despite the increased levels of free fatty acids caused by fasting in PPARα-null mice. In neonates, PPARα-null mice show impaired UCP3 mRNA expression in skeletal muscle in response to milk intake, and this is not a result of reduced free fatty acid levels. The murine UCP3 promoter is activated by fatty acids through either PPARα or PPARδ but not by PPARγ or retinoid X receptor alone. PPARδ-dependent activation could be a potential compensatory mechanism to ensure appropriate expression of UCP3 gene in adult skeletal muscle in the absence of PPARα. However, among transcripts from other PPARα and PPARδ target genes, only those acutely induced by milk intake in wild-type neonates were altered in muscle or heart from PPARα-null neonates. Thus, PPARα-dependent regulation is required for appropriate gene regulation of UCP3 as part of the subset of fatty-acid-responsive genes in neonatal muscle and heart.

scholarly journals Induction of Uncoupling Protein 3 Gene Expression in Skeletal Muscle of Preterm Newborns

2003 ◽  
Vol 53 (4) ◽  
pp. 691-697 ◽  
Author(s):  
Petr Brauner ◽  
Pavel Kopecký ◽  
Pavel Flachs ◽  
Josef Ruffer ◽  
Václav Sebroň ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Uncoupling Protein ◽  
Uncoupling Protein 3 ◽  
Preterm Newborns

Acute endurance exercise increases skeletal muscle uncoupling protein-3 gene expression in untrained but not trained humans

Metabolism ◽  
2003 ◽  
Vol 52 (2) ◽  
pp. 152-158 ◽  
Author(s):  
Robert C. Noland ◽  
Robert C. Hickner ◽  
Mercedes Jimenez-Linan ◽  
Antonio Vidal-Puig ◽  
Donghai Zheng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Uncoupling Protein ◽  
Uncoupling Protein 3

scholarly journals Expression of Uncoupling Protein 3 and GLUT4 Gene in Skeletal Muscle of Preterm Newborns: Possible Control by AMP-Activated Protein Kinase

2006 ◽  
Vol 60 (5) ◽  
pp. 569-575 ◽  
Author(s):  
Petr Brauner ◽  
Pavel Kopecky ◽  
Pavel Flachs ◽  
Ondrej Kuda ◽  
Jaroslav Vorlicek ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Uncoupling Protein ◽  
Uncoupling Protein 3 ◽  
Amp Activated Protein Kinase ◽  
Preterm Newborns
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