Abstract

To clarify whether reduced brown adipose tissue (BAT) thermogenesis and resting metabolic rate (RMR) are the cause or the consequence of obesity in monosodium-L-glutamate (MSG)-treated mice, we measured guanosine-5'-diphosphate (GDP) binding, and oxygen consumption in the interscapular BAT (IBAT) mitochondria, and the RMR in pre-obese (3-week-old) and obese (12-week-old) MSG-treated mice. Decreases in IBAT mitochondrial GDP binding and oxygen consumption as well as lowered RMR in MSG-treated mice were found even in the pre-obese stage as well as the obese stage, when compared to those in control mice. These findings suggest that reduced BAT thermogenesis may be one of the contributing factors in the development of obesity.

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