Laboratory of Nutritional Biochemistry, Graduate School of Nutritional and Environmental Sciences, University of Shizuoka , Shizuoka, Japan.
Research Fellow of Japan Society for the Promotion of Science , Tokyo, Japan.
Biosci Biotechnol Biochem. 2020 Nov;84(11):2367-2373. doi: 10.1080/09168451.2020.1792268. Epub 2020 Jul 14.
We investigated whether the deletion of glycerol-3-phosphate dehydrogenase (GPD) 1 would affect carbohydrate oxidation, fat oxidation, and body weight by using the GPD1 null mice (BALB/cHeA (HeA)). We found that fat oxidation in HeA mice was significantly high during the early active phase than in BALB/cBy (By) mice used as a control under conditions. Metabolic tracer experiment revealed that fatty acid oxidation in the skeletal muscle of HeA mice tended to be high. The energy expenditure and fat oxidation in HeA mice under fasting conditions were significantly higher than that in the By mice. Moreover, we monitored body weight gain in HeA mice under feeding and found lower body weight gain. These data indicate that GPD1 deficiency induces enhancement of fat oxidation with suppression of weight gain. We propose that GPD1 deletion contributes to the reduction of body weight gain via enhancement of fat oxidation.
我们使用 GPD1 缺失小鼠(BALB/cHeA(HeA))研究了甘油-3-磷酸脱氢酶(GPD)1 的缺失是否会影响碳水化合物氧化、脂肪氧化和体重。我们发现,在早期活动期,HeA 小鼠的脂肪氧化明显高于作为对照的 BALB/cBy(By)小鼠。代谢示踪实验表明,HeA 小鼠骨骼肌中的脂肪酸氧化趋于升高。HeA 小鼠在禁食状态下的能量消耗和脂肪氧化明显高于 By 小鼠。此外,我们监测了 HeA 小鼠在喂养状态下的体重增加情况,发现体重增加较低。这些数据表明,GPD1 缺乏会诱导脂肪氧化增强,同时抑制体重增加。我们提出,通过增强脂肪氧化,GPD1 缺失有助于降低体重增加。