During pregnancy or after experimental manipulations of ovarian hormone levels, Syrian hamsters exhibit changes in energy balance and body fat content without modifying their food intake. The present experiments determined whether fluctuations in voluntary exercise play a role in these changes in energy balance, as they appear to do in other species. As expected, pregnant hamsters maintained a constant level of food intake and lost approximately 40% of their body fat. These animals did not show the abrupt decrease in activity after mating that is seen in rats. Instead, they maintained their high, premating level of running wheel activity until the last 3 days of pregnancy. Similarly, ovariectomy and replacement therapy with estradiol or estradiol+progesterone caused substantial changes in energy balance in the absence of significant changes in food intake or running wheel activity. These findings indicate that, unlike rats, Syrian hamsters do not exhibit substantial changes in voluntary exercise during pregnancy or in response to manipulations of ovarian steroid levels. Therefore, neither changes in food intake nor in voluntary exercise play any important role in the pregnancy- or steroid-induced changes in energy balance in Syrian hamsters.
The effects of pregnancy and ovarian steroids on the in vivo distribution of newly synthesized fatty acids (incorporation of tritium from 3H2O into fatty acid) in Syrian hamsters (Mesocricetus auratus) were examined. During late, but not early, gestation hamsters had reduced levels of newly synthesized fatty acids in heart, liver, uterus, and white adipose tissues (parametrial and inguinal fat pads). Treatment of ovariectomized hamsters with estradiol + progesterone significantly decreased fatty acid synthesis-uptake in heart, liver, and inguinal white adipose tissue. Treatment with either estradiol or progesterone alone was without significant effect in any tissue. Pretreatment of hamsters with Triton WR-1339 (tyloxapol), an inhibitor of lipoprotein lipase activity and tissue triglyceride uptake, abolished the effects of estradiol + progesterone in white adipose tissue and heart but not in liver. Thus hamsters lose body fat during pregnancy in part because of decreased de novo lipogenesis. The effect of pregnancy on lipogenesis is mimicked by treatment with estradiol + progesterone but not by either hormone alone. Furthermore, it appears that the liver is the principal site of estradiol + progesterone action on lipogenesis in Syrian hamsters.
This study examined the effect of intragastric force-feeding of a milk diet on body weights of rats with lesions of the area postrema/caudal medial nucleus of the solitary tract (AP/cmNTS). Force-feeding was conducted over the first 10 days after the ablation. Body weight was monitored both during and after force-feeding. Food intake was measured during all ad libitum feeding periods. During force-feeding, rats with AP/cmNTS lesions gained weight at the same rate as force-fed sham-lesioned rats or sham-lesioned rats that voluntarily ingested an equal amount of the milk. When returned to ad libitum feeding, lesioned rats that had been force-fed were not hypophagic and did not lose weight. Body weights of such rats remained above those of lesioned rats that were not force-fed and similar to those of nonlesioned rats throughout this study. Despite their normal weights, preliminary analysis indicated that body fat of the force-fed lesioned rats may have been reduced. These findings suggest that the effects of AP/cmNTS ablation are multiple and that reduction of body weight need not be the primary effect of such lesions.
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