scholarly journals 3′,5′-Cyclic Adenosine Monophosphate-Response Sequences of the Uncoupling Protein Gene Are Sequentially Recruited During Darglitazone-Induced Brown Adipocyte Differentiation*

Endocrinology ◽  
1997 ◽  
Vol 138 (12) ◽  
pp. 5325-5332 ◽  
Author(s):  
Rogério Rabelo ◽  
Anne Camirand ◽  
J. Enrique Silva
Keyword(s):  
Adipocyte Differentiation ◽  
Protein Gene ◽  
Uncoupling Protein ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Brown Adipocyte ◽  
Uncoupling Protein Gene

scholarly journals Triiodothyronine Induces the Transcription of the Uncoupling Protein Gene and Stabilizes Its mRNA in Fetal Rat Brown Adipocyte Primary Cultures

1996 ◽  
Vol 271 (4) ◽  
pp. 2076-2081 ◽  
Author(s):  
Carmen Guerra ◽  
Cesar Roncero ◽  
Almudena Porras ◽  
Margarita Fernández ◽  
Manuel Benito
Keyword(s):  
Protein Gene ◽  
Uncoupling Protein ◽  
Primary Cultures ◽  
Brown Adipocyte ◽  
Fetal Rat ◽  
Uncoupling Protein Gene

Growth factor regulation of uncoupling protein-1 mRNA expression in brown adipocytes

2002 ◽  
Vol 282 (1) ◽  
pp. C105-C112 ◽  
Author(s):  
Bibian García ◽  
Maria-Jesús Obregón
Keyword(s):  
Growth Factor ◽  
Adipocyte Differentiation ◽  
Uncoupling Protein ◽  
Brown Adipocyte ◽  
Mrna Levels ◽  
Uncoupling Protein 1 ◽  
Brown Adipocytes ◽  
Proliferation And Differentiation ◽  
Epidermal Growth ◽  
Continuous Presence

To study the effect of the mitogens epidermal growth factor (EGF), acidic and basic fibroblast growth factors (aFGF and bFGF), and vasopressin on brown adipocyte differentiation, we analyzed the expression of uncoupling protein-1 (UCP-1) mRNA. Quiescent brown preadipocytes express high levels of UCP-1 mRNA in response to triiodothyronine (T3) and norepinephrine (NE). The addition of serum or the mitogenic condition aFGF + vasopressin + NE or EGF + vasopressin + NE decreases UCP-1 mRNA. A second addition of mitogens further decreases UCP-1 mRNA. Treatment with aFGF or bFGF alone increases UCP-1 mRNA, whereas the addition of EGF or vasopressin dramatically reduces UCP-1 mRNA levels. The continuous presence of T3 increases UCP-1 mRNA levels in cells treated with EGF, aFGF, or bFGF. The effect of T3 on the stimulation of DNA synthesis also was tested. T3 inhibits the mitogenic activity of aFGF and bFGF. In conclusion, mitogens like aFGF or bFGF allow brown adipocyte differentiation, whereas EGF and vasopressin inhibit the differentiation process. T3 behaves as an important hormone that regulates both brown adipocyte proliferation and differentiation.

scholarly journals Sirtuin/Uncoupling Protein Gene Variants and Carotid Plaque Area and Morphology

2015 ◽  
Vol 10 (8) ◽  
pp. 1247-1252 ◽  
Author(s):  
Chuanhui Dong ◽  
David Della-Morte ◽  
Digna Cabral ◽  
Liyong Wang ◽  
Susan H. Blanton ◽  
...  
Keyword(s):  
Carotid Plaque ◽  
Protein Gene ◽  
Uncoupling Protein ◽  
Gene Variants ◽  
Plaque Area ◽  
Uncoupling Protein Gene

Expression of an uncoupling protein gene homolog in chickens

2002 ◽  
Vol 133 (2) ◽  
pp. 345-358 ◽  
Author(s):  
Christina M Evock-Clover ◽  
Stephen M Poch ◽  
Mark P Richards ◽  
Christopher M Ashwell ◽  
John P McMurtry
Keyword(s):  
Protein Gene ◽  
Uncoupling Protein ◽  
Uncoupling Protein Gene

scholarly journals SUN-587 IDH1-Dependent Alpha-KG Regulates Brown Fat Differentiation and Function by Modulating Histone Methylation

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Won Kon Kim ◽  
Baek-Soo Han
Keyword(s):  
Histone Methylation ◽  
Molecular Mechanisms ◽  
Adipocyte Differentiation ◽  
Uncoupling Protein ◽  
Ectopic Expression ◽  
Brown Adipocyte ◽  
Brown Adipocytes ◽  
Brown Adipose ◽  
And Function ◽  
Brown Adipogenesis

Abstract Brown adipocytes play important roles in the regulation of energy homeostasis by uncoupling protein 1-mediated non-shivering thermogenesis. Recent studies suggest that brown adipocytes as novel therapeutic targets for combating obesity and associated diseases, such as type II diabetes. However, the molecular mechanisms underlying brown adipocyte differentiation and function are not fully understood. We employed previous findings obtained through proteomic studies performed to assess proteins displaying altered levels during brown adipocyte differentiation. Here, we performed assays to determine the functional significance of their altered levels during brown adipogenesis and development. We identified isocitrate dehydrogenase 1 (IDH1) as upregulated during brown adipocyte differentiation, with subsequent investigations revealing that ectopic expression of IDH1 inhibited brown adipogenesis, whereas suppression of IDH1 levels promoted differentiation of brown adipocytes. Additionally, Idh1 overexpression resulted in increased levels of intracellular α-ketoglutarate (α-KG) and inhibited the expression of genes involved in brown adipogenesis. Exogenous treatment with α-KG reduced brown adipogenesis during the early phase of differentiation, and ChIP analysis revealed that IDH1-mediated α-KG reduced trimethylation of histone H3 lysine 4 in the promoters of genes associated with brown adipogenesis. Furthermore, administration of α-KG decreased adipogenic gene expression by modulating histone methylation in brown adipose tissues of mice. These results suggested that the IDH1–α-KG axis plays an important role in regulating brown adipocyte differentiation and might represent a therapeutic target for treating metabolic diseases.

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