scholarly journals Heat production in the new-born rabbit and the fat content of the brown adipose tissue.

1965 ◽  
Vol 181 (3) ◽  
pp. 468-477 ◽  
Author(s):  
D Hull ◽  
M M Segall
Nature ◽  
1965 ◽  
Vol 206 (4980) ◽  
pp. 201-202 ◽  
Author(s):  
M. J. R. DAWKINS ◽  
J. W. SCOPES

Author(s):  
Soren Z. Coulson ◽  
Cayleih E. Robertson ◽  
Sajeni Mahalingam ◽  
Grant B. McClelland

High altitude environments challenge small mammals with persistent low ambient temperatures that require high rates of aerobic heat production in face of low O2 availability. An important component of thermogenic capacity in rodents is non-shivering thermogenesis (NST) mediated by uncoupled mitochondrial respiration in brown adipose tissue (BAT). NST is plastic, and capacity for heat production increases with cold acclimation. However, in lowland native rodents, hypoxia inhibits NST in BAT. We hypothesize that highland deer mice (Peromyscus maniculatus) overcome the hypoxic inhibition of NST through changes in BAT mitochondrial function. We tested this hypothesis using lab born and raised highland and lowland deer mice, and a lowland congeneric (P. leucopus), acclimated to either warm normoxia (25°C, 760 mmHg) or cold hypoxia (5°C, 430 mmHg). We determined the effects of acclimation and ancestry on whole-animal rates of NST, the mass of interscapular BAT (iBAT), and uncoupling protein (UCP)-1 protein expression. To identify changes in mitochondrial function, we conducted high-resolution respirometry on isolated iBAT mitochondria using substrates and inhibitors targeted to UCP-1. We found that rates of NST increased with cold hypoxia acclimation but only in highland deer mice. There was no effect of cold hypoxia acclimation on iBAT mass in any group, but highland deer mice showed increases in UCP-1 expression and UCP-1 stimulated mitochondrial respiration in response to these stressors. Our results suggest that highland deer mice have evolved to increase the capacity for NST in response to chronic cold hypoxia, driven in part by changes in iBAT mitochondrial function.


1985 ◽  
Vol 248 (5) ◽  
pp. E607-E617 ◽  
Author(s):  
J. G. Vander Tuig ◽  
J. Kerner ◽  
D. R. Romsos

Obesity-producing, hypothalamic knife cuts and ventromedial hypothalamic (VMH) lesions in ad libitum-fed adult rats increased intake of a high-fat diet (123 and 130%) and energy retention (880 and 1,099%) during the 4-wk period postsurgery; even when pair fed to control rats, energy retention of the knife-cut and lesioned rats was still elevated (105 and 155%). Thermogenic capacity of brown adipose tissue (BAT), estimated from guanosine diphosphate (GDP) binding to BAT mitochondria, was unchanged in hyperphagic knife-cut and VMH-lesioned rats and was reduced approximately 50% when these rats were pair fed to controls. Urinary excretion of norepinephrine (NE) was approximately twofold higher in ad libitum-fed, knife-cut, and lesioned rats than in control rats; restriction of energy intake decreased NE excretion to control values. Rates of NE turnover in heart paralleled urinary NE excretion, whereas NE turnover in BAT was generally not increased in the hyperphagic rats. Urinary epinephrine excretion, an index of adrenal medullary activity, was depressed in all knife-cut and VMH-lesioned rats. Hyperphagia coupled with a lack of increased heat production in BAT causes gross obesity in ad libitum-fed, knife-cut, and VMH-lesioned rats, whereas obesity in pair-fed rats develops in part at least as a result of reduced heat production by BAT.


1976 ◽  
Vol 231 (1) ◽  
pp. 153-160 ◽  
Author(s):  
T Rabi ◽  
Y Cassuto

Cold acclimation caused the following changes in the brown adipose tissue (BAT) of the hamster: the relative weight of the tissue increased, it color darkened, the multilocular structure predominated, and tissue protein content increased while fat content decreased. There was also an increase in the mitochondrial protein content. Heat acclimation had the opposite effects, i.e., the color became lighter, total and mitochondrial protein decreased, fat content increased, and tissue structure was mostly unilocular. Accordingly, cold acclimation was accompanied by increased tissue respiration in the presence of chi-glycerophosphate (chi-GP) and succinate, whereas heat acclimation reduced the respiratory activity of the tissue with these substrates. Isolated BAT mitochondria from cold-acclimated animals increased activities of chi-GP and NADH oxidase, whereas the activities of succinic and cytochrome oxidases and the amount of mitochondrial cytochromes were unchanged. The effects of heat acclimation were more pronounced: there was a decrease in the activities of chi-GP, succinic, NADH, and cytochrome oxidases, as well as in the cytochrome a and a3 content. When respiration of tissue slices on succinate was compared to the maximal potential respiration, as measured with mitochondria disrupted by freezing and thawing, it was found that the relative activity (slices vs. disrupted mitochondria) was highest in cold-acclimated animals and decreased progressively with increasing acclimation temperatures. It is suggested that the differences in the apparent activity of the mitochondria were due to changes in the conformation of the mitochondria as a result of acclimation.


2004 ◽  
Vol 84 (1) ◽  
pp. 277-359 ◽  
Author(s):  
BARBARA CANNON ◽  
JAN NEDERGAARD

Cannon, Barbara, and Jan Nedergaard. Brown Adipose Tissue: Function and Physiological Significance. Physiol Rev 84: 277–359, 2004; 10.1152/physrev.00015.2003.—The function of brown adipose tissue is to transfer energy from food into heat; physiologically, both the heat produced and the resulting decrease in metabolic efficiency can be of significance. Both the acute activity of the tissue, i.e., the heat production, and the recruitment process in the tissue (that results in a higher thermogenic capacity) are under the control of norepinephrine released from sympathetic nerves. In thermoregulatory thermogenesis, brown adipose tissue is essential for classical nonshivering thermogen-esis (this phenomenon does not exist in the absence of functional brown adipose tissue), as well as for the cold acclimation-recruited norepinephrine-induced thermogenesis. Heat production from brown adipose tissue is activated whenever the organism is in need of extra heat, e.g., postnatally, during entry into a febrile state, and during arousal from hibernation, and the rate of thermogenesis is centrally controlled via a pathway initiated in the hypothalamus. Feeding as such also results in activation of brown adipose tissue; a series of diets, apparently all characterized by being low in protein, result in a leptin-dependent recruitment of the tissue; this metaboloregulatory thermogenesis is also under hypothalamic control. When the tissue is active, high amounts of lipids and glucose are combusted in the tissue. The development of brown adipose tissue with its characteristic protein, uncoupling protein-1 (UCP1), was probably determinative for the evolutionary success of mammals, as its thermogenesis enhances neonatal survival and allows for active life even in cold surroundings.


2011 ◽  
Vol 52 (10) ◽  
pp. 1616-1620 ◽  
Author(s):  
E. A. Carter ◽  
A. A. Bonab ◽  
K. Paul ◽  
J. Yerxa ◽  
R. G. Tompkins ◽  
...  

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