We examined the relationship among glucose tolerance, efficiency of weight gain, and cellularity of brown adipose tissue (BAT) in rats (initial weight: 362 ± 1 g) made hyperphagic and obese by feeding on a highly palatable “cafeteria” (CAF) diet for 4–8 wk. As compared with chow-fed controls, CAF feeding resulted in a 45–60% increase in caloric intake (P < 0.01), a 40–50% increase in weight gain (P < 0.01), and hyperinsulinemia. Glucose disposal rate (K) on intravenous glucose tolerance test (IVGTT) was ≥ 1.4% in all chow-fed rats, but fell to ≤ 1.3 in 10 of 23 CAF-fed rats. As compared with the chow-fed controls, rats with normal glucose tolerance demonstrated a 12% decline in efficiency of weight gain (g/100 kcal of food consumed) in response to CAF feeding (P < 0.05). In marked contrast, in rats with impaired glucose tolerance, efficiency of weight gain failed to decline in response to overfeeding and was 18% higher than in the overfed group with normal glucose tolerance (P < 0.01). Although CAF feeding increased the mass of interscapular BAT by 110–130% in rats with normal as well as impaired glucose tolerance, DNA content of BAT rose only in the normal-K CAF-fed rats (0.19 ± 0.01 mg DNA/100 mg versus 0.12 ± 0.02 in chow-fed controls and 0.12 ± 0.01 in low-K rats).
We conclude that (1) impaired glucose tolerance accompanying dietary-induced obesity is associated with an increase in efficiency of weight gain and (2) failure of BAT cellularity to increase may contribute to the increase in efficiency. These data suggest that the link between obesity and diabetes may be bidirectional: obesity increases the risk of diabetes while impaired glucose tolerance may accelerate the development of obesity by enhancing efficiency of weight gain.