Defective thermoregulatory thermogenesis in monosodium glutamate-induced obesity in mice.

We have studied thermoregulatory thermogenesis in mice rendered obese by neonatal administration of monosodium glutamate (MSG) and in saline treated controls. At 12 weeks of age MSG-treated mice maintained on a chow diet and housed at 24 degrees C, exhibited hypertrophy of brown adipose tissue (BAT) compared to controls (65% increase in wet weight and lipid content, no difference in DNA content). Acute cold exposure (4 degrees C for two hours) resulted in a significantly greater fall in core temperature in MSG-treated than control mice. After cold exposure to 4 degrees C for six hours, control animals mobilized BAT lipid whereas MSG-treated animals did not. Both groups showed comparable increments in oxygen consumption in response to exogenous norepinephrine. The above changes were qualitatively the same for both male and female animals. The following conclusions were reached: (1) MSG-treated mice have defective cold induced thermogenesis, indirect evidence suggests this results from impaired activation of thermogenic mechanisms in BAT; (2) the defect responsible for this lies extrinsic to BAT; and (3) the quantitative significance of defective thermoregulatory thermogenesis for the development of obesity in these mice is uncertain.