Shambaugh G E, Koehler R A
Metabolism. 1983 May;32(5):421-7. doi: 10.1016/0026-0495(83)90001-x.
The metabolic regulation of alpha-ketoisocaproic acid was studied in fetal brain from rats. Starvation of the mother for days 18-20 did not alter CO2 evolution from alpha-ketoisocaproic acid in fetal brain slices but significantly diminished the incorporation of the branched-chain keto acids into leucine. When fetal brain slices from starved mothers were exposed to graded concentrations of labeled alpha-ketoisocaproic acid (0.05-2.5 mM), over 70% of the labeled products were consistently represented by leucine and less than 30% by CO2. Both beta-hydroxybutyrate and pyruvate, alone and in combination, diminished the amount of 14CO2 that evolved from alpha-ketoisocaproic acid-1-14C, but had no effect on the conversion of the keto acid to labeled leucine. It is concluded that exogenous alpha-ketoisocaproic acid is preferentially converted to leucine by fetal brain slices independent of the nutritional state of the mother. During maternal starvation, beta-hydroxybutyrate, by restraining irreversible decarboxylation of alpha-ketoisocaproic acid, could act to salvage the keto acid for conversion to leucine. Thus alpha-ketoisocaproic acid metabolism in the fetal brain may be regulated in part by altered metabolic functions in this structure and in part by changing components in circulating fuel mixtures reaching the fetus from the starved mother.
对来自大鼠胎儿大脑中α-酮异己酸的代谢调节进行了研究。在第18至20天使母体饥饿，并未改变胎儿脑切片中α-酮异己酸的二氧化碳生成量，但显著减少了支链酮酸掺入亮氨酸的量。当将来自饥饿母体的胎儿脑切片暴露于分级浓度的标记α-酮异己酸（0.05 - 2.5 mM）时，超过70%的标记产物始终由亮氨酸代表，而由二氧化碳代表的不到30%。单独或联合使用β-羟基丁酸和丙酮酸，均可减少α-酮异己酸-1-¹⁴C产生的¹⁴CO₂量，但对酮酸转化为标记亮氨酸没有影响。得出的结论是，外源性α-酮异己酸被胎儿脑切片优先转化为亮氨酸，这与母体的营养状态无关。在母体饥饿期间，β-羟基丁酸通过抑制α-酮异己酸的不可逆脱羧作用，可起到挽救酮酸以转化为亮氨酸的作用。因此，胎儿大脑中α-酮异己酸的代谢可能部分受该结构中代谢功能改变的调节，部分受来自饥饿母体到达胎儿的循环燃料混合物中成分变化的调节。
