Diet-dependent hyperplastic growth of adipose tissue in hypothalamic obese rats.

Accelerated production of fat cells is often seen in dietary obesity in rats but not in obesity occurring in response to damage to the medial area of the hypothalamus (MH). The basis for this difference was examined. MH damage (MHD) was produced in rats by either electric current or small knife cuts. Rats were then fed either chow or a high-fat high-sugar diet (HFS) for up to 6 mo. Fat cell production did not accelerate during the 1st 16 wk after MHD in rats fed only chow, but acceleration clearly occurred in rats fed HFS during only 4 wk. At 18 wk after MHD rats fed only chow showed evidence of accelerated fat cell production. However, there was greater acceleration after MHD in HFS-fed rats held to the same weight gain as chow-fed rats. Rats allowed to freely eat HFS for 6 mo after MHD showed extremely large increases in body weight and fat cell number. The plateau in body weight often seen in rats fed only chow after MHD did not occur. Because HFS-feeding promoted unimpeded production of fat cells, accelerated weight gain induced by MHD could continue indefinitely. These findings suggest that enlargement of fat cells and components of the diet act synergistically in the promotion of adipocyte hyperplasia in adult rats and also suggest that accelerated weight gain after MHD is not due to elevation of a set point for body weight or body fat.