Concordant mRNA Expression of UCP-3, but Not UCP-2, with Mitochondrial Thioesterase-1 in Brown Adipose Tissue and Skeletal Muscle in db/db Diabetic Mice

2001 ◽  
Vol 287 (5) ◽  
pp. 1058-1062 ◽  
Author(s):  
John C. Clapham ◽  
Victoria H. Coulthard ◽  
Gary B.T. Moore
2011 ◽  
Vol 120 (03) ◽  
pp. 139-144 ◽  
Author(s):  
N. Mizutani ◽  
N. Ozaki ◽  
Y. Seino ◽  
A. Fukami ◽  
E. Sakamoto ◽  
...  

AbstractAngiopoietin-like protein 4 (Angptl4) is thought to cause an increase in serum triglyceride levels. In the present study, we elucidated Angptl4 expression in the mouse models of type 1 and type 2 diabetes mellitus, and investigated the possible mechanisms involved.Type 1 diabetes was induced in C57BL/6 J mice by treating them with streptozotocin (STZ). Type 2 diabetes was induced by feeding the mice a high-fat diet (HFD) for 18 weeks.The levels of Angptl4 mRNA expression in liver, white adipose tissue (WAT), and brown adipose tissue (BAT) were found to increase in the STZ diabetic mice relative to control mice. This effect was attenuated by insulin administration. In the HFD diabetic mice, the Angptl4 mRNA expression levels were increased in liver, WAT, and BAT. Treatment with metformin for 4 weeks attenuated the increased levels of Angptl4 mRNA. Fatty acids (FAs) such as palmitate and linoleate induced Angptl4 mRNA expression in H4IIE hepatoma cells and 3T3-L1 adipocytes. Treatment with insulin but not metformin attenuated FA-induced Angptl4 mRNA expression in H4IIE. Both insulin and metformin did not influence the effect of FAs in 3T3-L1 cells.These observations demonstrated that Angptl4 mRNA expression was increased through the elevated free FAs in diabetic mice.


2008 ◽  
Vol 19 (12) ◽  
pp. 840-847 ◽  
Author(s):  
Sachiko Nomura ◽  
Takashi Ichinose ◽  
Manabu Jinde ◽  
Yu Kawashima ◽  
Kaoru Tachiyashiki ◽  
...  

2002 ◽  
Vol 283 (5) ◽  
pp. E980-E987 ◽  
Author(s):  
Philippe Cettour-Rose ◽  
Albert G. Burger ◽  
Christoph A. Meier ◽  
Theo J. Visser ◽  
Françoise Rohner-Jeanrenaud

To assess whether intracerebroventricular leptin administration affects monodeiodinase type II (D2) activity in the tissues where it is expressed [cerebral cortex, hypothalamus, pituitary, and brown adipose tissue (BAT)], hepatic monodeiodinase type I (D1) activity was inhibited with propylthiouracil (PTU), and small doses of thyroxine (T4; 0.6 nmol · 100 g body wt−1 · day−1) were supplemented to compensate for the PTU-induced hypothyroidism. Two groups of rats were infused with leptin for 6 days, one of them being additionally treated with reverse triiodothyronine (rT3), an inhibitor of D2. Control rats were infused with vehicle and pair-fed the amount of food consumed by leptin-infused animals. Central leptin administration produced marked increases in D2 mRNA expression and activity in BAT, changes that were likely responsible for increased plasma T3 and decreased plasma T4 levels. Indeed, plasma T3 and T4 concentrations were unaltered by central leptin administration in the presence of rT3. The additional observation of a leptin-induced increased mRNA expression of BAT uncoupling protein-1 suggested that the effect on BAT D2 may be mediated by the sympathetic nervous system.


1971 ◽  
Vol 49 (6) ◽  
pp. 545-553 ◽  
Author(s):  
Jean Himms–Hagen

The aim of these experiments was to depress the increased metabolic activity of the brown adipose tissue in the intact rat during acclimation to cold in order to elucidate further the possible thermogenic and endocrine functions of this tissue. The antibiotic oxytetracycline was administered twice daily for 2 weeks to rats living at 4 °C in an attempt to inhibit the proliferation of mitochondria and of mitochondrial inner membrane known to occur in the brown adipose tissue in response to cold; control rats received saline during the same period. Total cytochrome oxidase activity served as an index of the amount of mitochondrial inner membrane in brown adipose tissue, liver, and skeletal muscle. The development of an enhanced calorigenic response to intravenously infused noradrenaline served as an index of the extent of acclimation to cold.Treatment with oxytetracycline inhibited both the cold-induced increase in cytochrome oxidase activity in brown adipose tissue and the cold-induced development of an enhanced calorigenic response to noradrenaline in the intact rats; a direct correlation was noted between the amount of cytochrome oxidase in brown adipose tissue and the size of the metabolic response to noradrenaline of the intact animals. However, the amount of oxygen that could be consumed by the total cytochrome oxidase in the brown adipose tissue was itself too small to account for the increase in oxygen consumption by the rat. Treatment of the rats with oxytetracycline did not alter the cold-induced growth of brown adipose tissue (as judged by the increase in wet weight and the increase in total protein); it also did not alter the cytochrome oxidase activities of liver or skeletal muscle. The effect of oxytetracycline seems, therefore, to be fairly specific for the mitochondria of the most rapidly dividing tissue, the brown adipose tissue. The conclusion is drawn that a protein synthesized in the mitochondria of the brown adipose tissue in response to cold is essential for adaptation to cold.


2017 ◽  
Vol 102 (12) ◽  
pp. 1584-1595 ◽  
Author(s):  
Sofía Moran-Ramos ◽  
Natali N. Guerrero-Vargas ◽  
Rebeca Mendez-Hernandez ◽  
Maria del Carmen Basualdo ◽  
Carolina Escobar ◽  
...  

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