Ohta Y, Kitazaki T, Tsuda M
Central Research Division, Takeda Chemical Industries, Ltd., Osaka, Japan.
Endocrinol Jpn. 1988 Feb;35(1):83-92. doi: 10.1507/endocrj1954.35.83.
Thermogenesis of brown adipose tissue (BAT) of genetically obese mice, KKAY mice, was examined by measuring the BAT mitochondrial guanosine diphosphate (GDP) binding as an index of thermogenesis and comparing it with that of normal C57BL mice. No great difference in GDP binding was observed in KKAY and C57BL mice fed a stock diet. However, when they were given a sucrose solution, the increase in BAT mitochondrial GDP binding of KKAY mice (+22%) was much lower than that of C57BL mice (+106%). A high fat diet increased BAT mitochondrial GDP binding in KKAY mice to the same extent (+82%) as in C57BL mice. When the mice were fasted for 48 h, BAT mitochondrial GDP binding of C57BL mice decreased by 70%, while that of KKAY mice showed no change. Both acute exposure to cold and norepinephrine injections increased GDP binding in KKAY mice by 90% and 131%, respectively. These results indicate that low BAT thermogenesis in response to sucrose intake may be a cause of obesity in KKAY mice, and this may be brought about by defects in the central nervous system.
通过测量棕色脂肪组织（BAT）线粒体鸟苷二磷酸（GDP）结合量作为产热指标，并与正常C57BL小鼠进行比较，研究了遗传性肥胖小鼠KKAY小鼠的BAT产热情况。喂食常规饲料的KKAY小鼠和C57BL小鼠在GDP结合方面未观察到显著差异。然而，当给它们蔗糖溶液时，KKAY小鼠BAT线粒体GDP结合量的增加（+22%）远低于C57BL小鼠（+106%）。高脂饮食使KKAY小鼠BAT线粒体GDP结合量增加的程度（+82%）与C57BL小鼠相同。当小鼠禁食48小时时，C57BL小鼠BAT线粒体GDP结合量下降了70%，而KKAY小鼠则没有变化。急性冷暴露和注射去甲肾上腺素分别使KKAY小鼠的GDP结合量增加了90%和131%。这些结果表明，KKAY小鼠对蔗糖摄入的低BAT产热可能是其肥胖的一个原因，这可能是由中枢神经系统缺陷导致的。
