Evidence that fasting can induce a selective loss of uncoupling protein from brown adipose tissue mitochondria of mice

1986 ◽  
Vol 6 (9) ◽  
pp. 805-810 ◽  
Author(s):  
P. Trayhurn ◽  
G. Jennings
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cytochrome Oxidase ◽  
Oxidase Activity ◽  
Uncoupling Protein ◽  
Cytochrome Oxidase Activity ◽  
Selective Loss ◽  
Brown Adipose ◽  
Fasting And Refeeding ◽  
Total Tissue

The effects of fasting and refeeding on the concentration of uncoupling protein in brown adipose tissue mitochondria have been investigated in mice. Fasting mice for 48 h led to a large decrease in the total cytochrome oxidase activity of the interscapular brown fat pad. Mitochondrial GDP binding and the specific mitochondrial concentration of uncoupling protein also fell on fasting. After 24 h refeeding both GDP binding and the mitochondrial concentration of uncoupling protein were normalized, but there was no alteration in the total tissue cytochrome oxidase activity. Fasting appears to induce a selective loss of uncoupling protein from brown adipose tissue mitochondria, which is rapidly reversible on refeeding.

Nonshivering thermogenesis and the thermogenic capacity of brown fat in fasted and/or refed mice

1988 ◽  
Vol 254 (1) ◽  
pp. R11-R16 ◽  
Author(s):  
P. Trayhurn ◽  
G. Jennings
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cytochrome Oxidase ◽  
Oxidase Activity ◽  
Uncoupling Protein ◽  
Nonshivering Thermogenesis ◽  
Interscapular Brown Adipose Tissue ◽  
Cytochrome Oxidase Activity ◽  
Brown Adipose ◽  
Thermogenic Capacity

The effects of fasting and refeeding on nonshivering thermogenesis and the properties of brown adipose tissue have been investigated in mice. Fasting for 48 h led to a substantial reduction in the capacity for nonshivering thermogenesis, and there was no recovery of thermogenic capacity during the first 5 days of refeeding. A period of 10-15 days of refeeding was required for full restoration of thermogenic capacity. The mice were hyperphagic during the first 6 days of refeeding, but body weight was recovered after 24 h. The amount of interscapular brown adipose tissue decreased substantially on fasting, but it recovered 24 h after the initiation of refeeding. Cytochrome oxidase activity, the level of mitochondrial GDP binding, and the specific mitochondrial concentration of uncoupling protein in brown adipose tissue were each reduced by fasting. Although both GDP binding and the specific concentration of uncoupling protein rapidly returned to normal on refeeding, the activity of cytochrome oxidase was not normalized until 10 days after the end of the fast. These results indicate that a prolonged period of refeeding is required for the recovery in the capacity for nonshivering thermogenesis following a fast, a similar time course being evident for the recovery of cytochrome oxidase activity in brown adipose tissue. It is suggested that the fasting-induced reduction in the capacity for nonshivering thermogenesis is linked primarily to a loss of mitochondria from brown adipose tissue and that the normalization of thermogenic capacity is dependent on the restoration of mitochondrial mass.

scholarly journals GDP binding to brown-adipose-tissue mitochondria of mice treated chronically with corticosterone

1983 ◽  
Vol 214 (1) ◽  
pp. 265-268 ◽  
Author(s):  
K S Galpin ◽  
R G Henderson ◽  
W P T James ◽  
P Trayhurn
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cytochrome Oxidase ◽  
Oxidase Activity ◽  
Cytochrome Oxidase Activity ◽  
Acute Response ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Ad Libitum ◽  
Stimulation Of

Cytochrome oxidase activity and mitochondrial GDP binding were decreased in brown adipose tissue of mice treated chronically with corticosterone. These changes occurred both in corticosterone-treated mice fed ad libitum and in treated mice pair-fed to control animals. Although the dietary stimulation of brown-adipose-tissue thermogenesis was suppressed by corticosterone, the acute response to cold was not affected.

Inhibition by Oxytetracycline of the Development of the Enhanced Response to Noradrenaline in Cold-Acclimated Rats: A New Approach to the Study of Nonshivering Thermogenesis

1971 ◽  
Vol 49 (6) ◽  
pp. 545-553 ◽  
Author(s):  
Jean Himms–Hagen
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cytochrome Oxidase ◽  
Oxidase Activity ◽  
Metabolic Response ◽  
Inner Membrane ◽  
Cytochrome Oxidase Activity ◽  
Mitochondrial Inner Membrane ◽  
Brown Adipose

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.

Changes in cytochrome oxidase activity in brown adipose tissue during oestrous cycle in the rat

1998 ◽  
Vol 139 (4) ◽  
pp. 433-437 ◽  
Author(s):  
M Puerta ◽  
M Rocha ◽  
S Gonzalez-Covaleda ◽  
S. McBennett ◽  
J. Andrews
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cytochrome Oxidase ◽  
Oxidase Activity ◽  
Oestrous Cycle ◽  
Cytochrome Oxidase Activity ◽  
Brown Adipose

Effect of warm or cold exposure on GDP binding and uncoupling protein in rat brown fat

1987 ◽  
Vol 252 (2) ◽  
pp. E237-E243 ◽  
Author(s):  
P. Trayhurn ◽  
M. Ashwell ◽  
G. Jennings ◽  
D. Richard ◽  
D. M. Stirling
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cytochrome Oxidase ◽  
Uncoupling Protein ◽  
Activity Level ◽  
Brown Adipose ◽  
Different Temperatures ◽  
Acute And Chronic Exposure ◽  
Environmental Temperatures ◽  
Total Tissue

The effects of acute and chronic exposure to different environmental temperatures on the total tissue cytochrome oxidase activity, level of mitochondrial GDP binding, and specific mitochondrial concentration of uncoupling protein have been investigated in rat brown adipose tissue, a radioimmunoassay being used to measure uncoupling protein. Acclimation at different temperatures for 3 wk produced parallel changes in GDP binding, the concentration of uncoupling protein, and the activity of cytochrome oxidase, each parameter rising with decreasing temperature between thermoneutrality (29 degrees C) and 4 degrees C. Acute exposure of warm-acclimated (29 degrees C) rats to the cold (4 degrees C) led to a rapid increase in GDP binding without any alteration in the amount of uncoupling protein. The increase in binding was accompanied by an increase in the rate of acetate-induced swelling of the mitochondria. The concentration of uncoupling protein in warm-acclimated rats was significantly raised only after 48 h exposure to cold. When cold-acclimated rats were exposed acutely to the warm, there was a rapid decrease in GDP binding without any alteration in the amount of uncoupling protein. It is concluded that after alterations in environmental temperature the concentration of uncoupling protein in brown adipose tissue mitochondria changes much more slowly than GDP binding and that binding can therefore be dissociated from the amount of the protein.

Reduction of dietary obesity in aP2-Ucp transgenic mice: mechanism and adipose tissue morphology

1996 ◽  
Vol 270 (5) ◽  
pp. E776-E786 ◽  
Author(s):  
J. Kopecky ◽  
M. Rossmeisl ◽  
Z. Hodny ◽  
I. Syrovy ◽  
M. Horakova ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Transgenic Mice ◽  
Cytochrome Oxidase ◽  
Oxidase Activity ◽  
Brown Fat ◽  
Small Cells ◽  
Cytochrome Oxidase Activity ◽  
Tissue Morphology ◽  
Brown Adipose ◽  
White Fat

C57BL6/J mice with the expression of the mitochondrial uncoupling protein (UCP) gene from the fat-specific aP2 gene promoter were used to study the mechanism by which the aP2-Ucp transgene affects adiposity and reduces high-fat diet induced obesity. In the transgenic mice, UCP synthesized in white fat was inserted into mitochondria, and oxygen uptake by epididymal fat fragments indicated UCP-induced thermogenesis. The respirometry data, UCP content, cytochrome oxidase activity, and tissue morphology suggested functional involution of brown fat. Despite 25- to 50-fold lower mitochondrial cytochrome oxidase activity in white than in brown fat cells, total oxidative capacity in white and brown adipose tissue is comparable. Appearance of novel small cells in the gonadal fat of the transgenic mice was associated with a higher DNA content than that of the nontransgenic mice. The results prove a potential of transgenically altered mitochondria in white fat to modulate adiposity and energy expenditure and suggest the existence of a yet unidentified site-specific link between energy metabolism in adipocytes and cellularity.

scholarly journals Biogenesis of thermogenic mitochondria in brown adipose tissue of Djungarian hamsters during cold adaptation

1996 ◽  
Vol 316 (2) ◽  
pp. 607-613 ◽  
Author(s):  
Martin KLINGENSPOR ◽  
Marc IVEMEYER ◽  
Herbert WIESINGER ◽  
Kirsten HAAS ◽  
Gerhard HELDMAIER ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Cold Adaptation ◽  
Uncoupling Protein ◽  
Respiratory Chain Complexes ◽  
Mitochondrial Transcription Factor ◽  
Chain Complexes ◽  
Brown Adipose ◽  
Total Tissue

After cold exposure, cytochrome c oxidase (COX) activity increased about 2.5-fold within 2 weeks in the brown adipose tissue (BAT) of Djungarian hamsters. The mRNAs for COX subunits I and III and the 12 S rRNA, encoded on mitochondrial DNA (mtDNA), as well as mRNAs for COX subunits IV, Va and mitochondrial transcription factor A, encoded in the nucleus, were unchanged when expressed per unit of total tissue RNA. However, since total tissue RNA doubled per BAT depot, while total DNA remained unchanged, the actual levels of these transcripts were increased within BAT cells. In contrast, the abundance of mRNA for uncoupling protein was increased 10-fold, indicating specific activation of this gene. In addition, the maximal rate of protein synthesis analysed in a faithful in organello system was increased 2.5-fold in mitochondria isolated from BAT after 7 days of cold exposure. We conclude from these data that the biogenesis of thermogenic mitochondria in BAT following cold adaptation is achieved by increasing the overall capacity for synthesis of mitochondrial proteins in both compartments, by increasing their mRNAs as well as the ribosomes needed for their translation. In addition, the translational rate for COX subunits as well as all other proteins encoded on mtDNA is increased. Thus the pool of subunits encoded on mtDNA required for assembly of respiratory chain complexes is provided. By comparison with other models of increased mitochondrial biogenesis, we propose that thyroid hormone (generated within BAT cells by 5´-deiodinase, and induced upon sympathetic stimulation), which is a well known regulator of the biogenesis of mitochondria in many tissues, is also the major effector of these adaptive changes in BAT.

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