Chronic Administration of β-Adrenergic Agonists Can Mimic the Stimulative Effect of Cold Exposure on Protein Synthesis in Rat Brown Adipose Tissue

1995 ◽  
Vol 117 (1) ◽  
pp. 96-100 ◽  
Author(s):  
Katsumi Tsukazaki ◽  
Hideki Nikami ◽  
Yasutake Shimizu ◽  
Teruo Kawada ◽  
Toshihide Yoshida ◽  
...  
1988 ◽  
Vol 8 (5) ◽  
pp. 465-469 ◽  
Author(s):  
Gérard Mory ◽  
Myriam Gawer ◽  
Jean-Claude Kader

Chronic cold exposure of rats (9 days at 5°C) induces an alteration of the fatty acid composition of phospholipids in brown adipose tissue. The alteration is due to an increase of the unsaturation degree of these lipids. The phenomenon can be reproduced by 10−7 mole. h−1 administration of noradrenaline for 9 days in rats kept at 25°C. Thus, phospholipid alteration in brown fat of cold exposed rats is most probably a consequence of the increase of sympathetic tone which occurs in this tissue during exposure to cold.


1979 ◽  
Vol 57 (6) ◽  
pp. 968-976 ◽  
Author(s):  
Michel Desautels ◽  
Jean Himms-Hagen

Exposure of a rat to cold (4 °C) is known to induce a biphasic change in brown adipose tissue mitochondria, believed to reflect alterations in the thermogenic, purine nucleotide sensitive proton conductance pathway; an initial rapid and large increase in purine nucleotide binding, unaccompanied by any marked change in the 32 000 polypeptide which is the binding site for these nucleotides, is followed by a slower increase in concentration of the 32 000 polypeptide accompanied by a further increase in purine nucleotide binding. The initial rapid effect of cold stress was mimicked by intravenous infusion of noradrenaline; neither the effect of cold exposure for 24 h nor the effect of intravenous infusion of noradrenaline was prevented by cycloheximide. In contrast, the slow adaptive changes in the mitochondria did not occur in response to prolonged (2 weeks) treatment with noradrenaline, although such treatment did induce the expected tissue hypertrophy accompanied by mitochondrial proliferation. Cold-induced (1 week) increases in purine nucleotide binding and 32 000 polypeptide were not prevented by oxytetracycline. The increase in purine nucleotide binding during the 2nd day of cold exposure was prevented by cycloheximide. The effect of cycloheximide on the increase in the 32 000 polypeptide could not be assessed because sufficiently long-term experiments could not be done with this compound. Thus, the initial response to cold stress appears to involve unmasking of mitochondrial proton conductance pathway sites, most probably mediated by noradrenaline. The slower adaptive response occurs in parallel with tissue hypertrophy, which itself may be mediated by noradrenaline, and appears to require cytosolic but not mitochondrial protein synthesis. However, the changes in mitochondrial composition which result in an increased concentration of proton conductance pathway sites are not mediated by noradrenaline.


1996 ◽  
Vol 90 (s34) ◽  
pp. 16P-17P
Author(s):  
C Bing ◽  
L Pickavance ◽  
J S Keith ◽  
H M Frankish ◽  
Q Wang ◽  
...  

iScience ◽  
2021 ◽  
pp. 102434
Author(s):  
Winifred W. Yau ◽  
Kiraely Adam Wong ◽  
Jin Zhou ◽  
Nivetha Kanakaram Thimmukonda ◽  
Yajun Wu ◽  
...  

Metabolism ◽  
2021 ◽  
Vol 117 ◽  
pp. 154709 ◽  
Author(s):  
Tim Hollstein ◽  
Karyne Vinales ◽  
Kong Y. Chen ◽  
Aaron M. Cypess ◽  
Alessio Basolo ◽  
...  

2018 ◽  
Vol 120 (6) ◽  
pp. 9138-9146 ◽  
Author(s):  
Ziye Xu ◽  
Jiaqi Liu ◽  
Wenjing You ◽  
Yizhen Wang ◽  
Tizhong Shan

1995 ◽  
Vol 269 (1) ◽  
pp. R38-R47 ◽  
Author(s):  
J. M. Matz ◽  
M. J. Blake ◽  
H. M. Tatelman ◽  
K. P. Lavoi ◽  
N. J. Holbrook

The accumulation of heat shock proteins (HSPs) after the exposure of cells or organisms to elevated temperatures is well established. It is also known that a variety of other environmental and cellular metabolic stressors can induce HSP synthesis. However, few studies have investigated the effect of cold temperature on HSP expression. Here we report that exposure of Institute of Cancer Research (ICR) mice to cold ambient temperatures results in a tissue-selective induction of HSPs in brown adipose tissue (BAT) coincident with the induction of mitochondrial uncoupling protein synthesis. Cold-induced HSP expression is associated with enhanced binding of heat shock transcription factors to DNA, similar to that which occurs after exposure of cells or tissues to heat and other metabolic stresses. Adrenergic receptor antagonists were found to block cold-induced HSP70 expression in BAT, whereas adrenergic agonists induced BAT HSP expression in the absence of cold exposure. These findings suggest that norepinephrine, released in response to cold exposure, induces HSP expression in BAT. Norepinephrine appears to initiate transcription of HSP genes after binding to BAT adrenergic receptors through, as yet, undetermined signal transduction pathways. Thermogenesis results from an increase in activity and synthesis of several metabolic enzymes in BAT of animals exposed to cold challenge. The concomitant increase in HSPs may function to facilitate the translocation and activity of the enzymes involved in this process.


1987 ◽  
Vol 243 (2) ◽  
pp. 437-442 ◽  
Author(s):  
M G Buckley ◽  
E A Rath

1. The effect of nutritional status on fatty acid synthesis in brown adipose tissue was compared with the effect of cold-exposure. Fatty acid synthesis was measured in vivo by 3H2O incorporation into tissue lipids. The activities of acetyl-CoA carboxylase and fatty acid synthetase and the tissue concentrations of malonyl-CoA and citrate were assayed. 2. In brown adipose tissue of control mice, the tissue content of malonyl-CoA was 13 nmol/g wet wt., higher than values reported in other tissues. From the total tissue water content, the minimum possible concentration was estimated to be 30 microM 3. There were parallel changes in fatty acid synthesis, malonyl-CoA content and acetyl-CoA carboxylase activity in response to starvation and re-feeding. 4. There was no correlation between measured rates of fatty acid synthesis and malonyl-CoA content and acetyl-CoA carboxylase activity in acute cold-exposure. The results suggest there is simultaneous fatty acid synthesis and oxidation in brown adipose tissue of cold-exposed mice. This is probably effected not by decreases in the malonyl-CoA content, but by increases in the concentration of free long-chain fatty acyl-CoA or enhanced peroxisomal oxidation, allowing shorter-chain fatty acids to enter the mitochondria independent of carnitine acyltransferase (overt form) activity.


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