Increased purine nucleotide binding, altered polypeptide composition, and thermogenesis in brown adipose tissue mitochondria of cold-acclimated rats

1978 ◽  
Vol 56 (6) ◽  
pp. 378-383 ◽  
Author(s):  
M. Desautels ◽  
G. Zaror-Behrens ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Nucleotide Binding ◽  
Proton Conductance ◽  
Purine Nucleotide ◽  
Polypeptide Composition ◽  
Purine Nucleotides ◽  
Brown Adipose ◽  
Simultaneous Decrease ◽  
Thermogenic Capacity

Rapid increases in atractyloside-insensitive binding of purine nucleotides (ADP or GDP) and in a polypeptide of 32 000 occur in brown adipose tissue mitochondria of the rat during acclimation to cold. The increased binding is apparent within 1 h and reaches a maximum after 3–7 days of exposure to 4 °C. The increase in the 32 000 peptide occurs more slowly and reaches a maximum after 2–3 weeks. There is a simultaneous decrease in a polypeptide of 96 000, apparent after 1 day and reaching a maximum after 1–2 weeks. Results are interpreted in terms of the appearance of an increased amount of the purine nucleotide-sensitive proton conductance pathway in association with the development of an enhanced thermogenic capacity of brown adipose tissue mitochondria during acclimation of the rat to cold.

Roles of noradrenaline and protein synthesis in the cold-induced increase in purine nucleotide binding by rat brown adipose tissue mitochondria

1979 ◽  
Vol 57 (6) ◽  
pp. 968-976 ◽  
Author(s):  
Michel Desautels ◽  
Jean Himms-Hagen
Keyword(s):  
Protein Synthesis ◽  
Adipose Tissue ◽  
Cold Stress ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Intravenous Infusion ◽  
Nucleotide Binding ◽  
Proton Conductance ◽  
Purine Nucleotide ◽  
Brown Adipose

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.

Fatty acid utilization and purine nucleotide binding in brown adipose tissue of genetically obese (/) mice

Life Sciences ◽  
1983 ◽  
Vol 32 (18) ◽  
pp. 2123-2130 ◽  
Author(s):  
Sylvette Bas ◽  
Elisabeth Imesch ◽  
Daniel Ricquier ◽  
Françoise Assimacopoulos-Jeannet ◽  
Josiane Seydoux ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Nucleotide Binding ◽  
Obese Mice ◽  
Purine Nucleotide ◽  
Fatty Acid Utilization ◽  
Brown Adipose

Growth of interscapular brown adipose tissue in cold-acclimated hypophysectomized rats maintained on thyroxine and corticosterone

1982 ◽  
Vol 60 (8) ◽  
pp. 838-842 ◽  
Author(s):  
Mathias Fellenz ◽  
Joan Triandafillou ◽  
Cynthia Gwilliam ◽  
Jean Himms-Hagen
Keyword(s):  
Molecular Weight ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Relative Proportion ◽  
Pituitary Hormones ◽  
Proton Conductance ◽  
Polypeptide Composition ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Hypophysectomized Rats

Brown adipose tissue (BAT) of rats is known to grow in response to acclimation to cold. The growth is accompanied by changes in mitochondrial polypeptide composition (an increase in the relative proportion of a polypeptide of molecular weight 32 000, known to be associated with the thermogenic proton conductance pathway). The mediator of the change in mitochondrial polypeptide composition is unknown. The objective of these experiments was to find out whether any of the pituitary hormones might be the mediator. Treatment of rats with growth hormone failed to alter BAT size or mitochondrial polypeptide composition. BAT grew and the change in BAT mitochondrial polypeptide composition occurred in cold-acclimated hypophysectomized rats, maintained on thyroxine and corticosterone to ensure their survival in the cold. It is concluded that none of the pituitary hormones is the mediator for the cold-induced change in BAT mitochondrial polypeptide composition or is required to exert a direct effect on BAT for cold-induced BAT growth to occur. It also seems unlikely that more than a maintenance amount of glucocorticoids is required for normal cold-induced growth of BAT; these hormones are thus also unlikely to mediate the change in BAT mitochondrial polypeptide composition. The requirement for no more than a maintenance amount of thyroxine for BAT growth and for the cold-induced change in BAT mitochondrial polypeptide composition confirms previous conclusions drawn from studies on cold-acclimated thyroidectomized rats.

Brown adipose tissue metabolism in ob/ob mice: effects of a high-fat diet and adrenalectomy

1987 ◽  
Vol 253 (2) ◽  
pp. E149-E157
Author(s):  
H. K. Kim ◽  
D. R. Romsos
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
High Fat ◽  
Adipose Tissue Metabolism ◽  
High Carbohydrate ◽  
Bat Mitochondria ◽  
Norepinephrine Turnover ◽  
Brown Adipose ◽  
Thermogenic Capacity

Adrenalectomy prevents development of obesity in ob/ob mice fed high-carbohydrate stock diets partly by stimulating the low thermogenic capacity of their brown adipose tissue (BAT). Adrenalectomy, however, fails to prevent development of obesity in ob/ob mice fed a high-fat diet. Effects of adrenalectomy on BAT metabolism in ob/ob mice fed a high-fat diet were thus examined. ob/ob mice fed the high-fat diet developed gross obesity despite normal BAT metabolism, as assessed by rates of norepinephrine turnover in BAT, GDP binding to BAT mitochondria, and GDP-inhibitable, chloride-induced mitochondrial swelling. Adrenalectomy failed to arrest the development of obesity or to influence BAT metabolism in ob/ob mice fed the high-fat diet. Development of obesity in ob/ob mice fed a high-fat diet is not associated with low thermogenic capacity of BAT or with adrenal secretions, as it is in ob/ob mice fed high-carbohydrate stock diets.

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