Abstract
Weanling Sprague-Dawley rats received lesions in the dorsomedial hypothalamic nuclei or sham operations. Analysis of variance revealed a significant lesion-induced depression of body weight (BW) and food intake (FI). After sexual maturity, bilateral ovariectomy (OVX) and/or sham-ovariectomy (S-OVX) were performed in each of the above groups. OVX produced a significant increase in BW in both lesioned and non-lesioned rats without changes in food intake. Following DMN lesions efficiency of food utilization (EFU) was greater than normal and OVX caused a further significant increase, irrespective of hypothalamic manipulation. DMN lesions, as previously shown, were followed by a reduction in linear growth; subsequent OVX exerted a growth-promoting effect in both DMN-lesioned and sham-lesioned rats. However, OVX did not alter plasma growth hormone or insulin levels. When calculated on the basis of per gram tissue protein, DMN lesions significantly diminshed the incorporation of glucose into lipids of diaphragm and fat pad, but not of liver. DMN lesions had no effect on the incorporation of glucose into glycogen of diaphragm, fat pad or liver. OVX did not produce significant changes in lipogenesis from glucose or incorporation of glucose into glycogen in either sham-lesioned OVX or DMN-lesioned OVX rats. The data support the concept that increased weight gain following OVX can be attributed to factors other than increased food intake. They also support previous findings that DMN lesions lower the BW “settling point” (i.e., both lean body mass and fat commensurately). The data also suggest that the DMNL rat is responsive to various manipulations—in this case OVX—of the adipose tissue mass “settling point”.
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