Abstract
This experiment examined both the short-term and the long-term effects of ovariectomy on brown adipose tissue growth and function in rats to determine if reduced brown adipose tissue thermogenesis might contribute to the weight gain and adiposity. Brown adipose tissue function was assessed by measuring sympathetic nervous system activity (estimated by the rate of norepinephrine turnover) and mitochondrial proton conductance (estimated by specific GDP binding) in interscapular brown adipose tissue. Rats ( n=12 per group) were killed 0 (sham), 1, 2, 4, and 12 weeks after ovariectomy. During the first five weeks after ovariectomy rats overate and rapidly gained weight. The weight gain was due to increases in all carcass components. Five weeks after ovariectomy food intake returned to control levels, and body weights stabilized 12–16% above sham-operated control weights for the duration of the experiment. Between week 4 and week 12 after surgery there was a redistribution of carcass composition, with decreases in carcass water and fat-free dry weights offset by a further increase in total carcass lipid. Brown adipose tissue pads were heavier in the 1-, 2-, and 4-week ovariectomy groups, but only in the 4-week group was the increase statistically significant. Brown adipose tissue protein, DNA, and norepinephrine content was unchanged 1-, 2-, 4-, or 12-weeks after ovariectomy. There was no difference in either the rate of norepinephrine turnover or specific mitochondrial GDP binding between sham-operated and 1-, 2-, 4-, or 12-week ovariectomized rats. These results indicate that the dynamic phase of ovariectomy-induced weight gain in rats cannot, even in part, be explained by a reduction in brown adipose tissue thermogenesis.
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