DEFECTIVE STIMULATION OF THYROXINE 5'-DEIODINASE ACTIVITY BY COLD-EXPOSURE AND NOREPINEPHRINE IN BROWN ADIPOSE-TISSUE OF MONOSODIUM GLUTAMATE-OBESE MICE

In order to examine the possible change in the thyroid hormone metabol ism in the monosodium glutamate (MSG)-obese mice, we determined the io dothyronine deiodinase activity of brown adipose tissue (BAT), liver a nd kidney of male and female mice. There was no significant difference in the type II thyroxine 5'-deiodinase (T-4 5'DII) activity in BAT be tween MSG-obese and control mice when they were kept at the ambient te mperature of 22 degrees C. T-4 5'DII activity in BAT of control mice i ncreased markedly after exposure to cold (4 degrees C) for 4 h; howeve r, the extent of cold-induced increase in T-4 5'DII activity in BAT of MSG-obese mice was greatly reduced. Injection of norepinephrine (NE) (0.8 mg/kg, s.c.) 4 h previously increased T-4 5'DII activity in BAT o f control mice, but NE-induced increase in T-4 5'DII activity was also markedly reduced in BAT of MSG-obese mice. Both cold-and NE-induced i ncrease in T-4 5'DII activity was greater in female, although similar tendency was obtained in male mice. Type I 3,3',5'-triiodothyronine de iodinase (rT(3) 5'DI) activity of liver and kidney, and serum thyroxin e (T-4) and 3,5,3'-triiodothyronine (T-3) levels in MSG-obese mice wer e essentially the same as those of the control male and female mice ir respective of cold exposure. These results suggest that defective stim ulation of T-4 5'DII activity of BAT by cold in the MSG-obese mice is due to deficient sympathetic input to BAT and/or to diminished respons e of BAT to NE, and may contribute to a possible cause of inability of MSG-obese mice to maintain body temperature under cold exposure.