Coleman D L
Proc Natl Acad Sci U S A. 1980 Jan;77(1):290-3. doi: 10.1073/pnas.77.1.290.
Mice were found to convert acetone to lactate at appreciable rates. The conversion of acetone to gluconeogenic precursors could provide additional glycolytic intermediates that would allow the more complete utilization of lipid stores and increase survival time during starvation. In mice that were starved for 3 days or were provided with acetone in the drinking water the acetone-metabolizing pathway was induced to levels severalfold normal. Mice heterozygous for obesity-producing mutations, either obese (ob/+) or diabetes (db/+), showed induction of the activity of this pathway to a significantly higher degree than did homozygous normal (+/+) mice of the same strain. This more effective conversion of acetone to lactate exhibited by heterozygous mice could account for their prolonged survival on a starvation regimen compared to that of normal homozygotes. The rate-limiting step in the pathway appears to be the conversion of acetone to a hydroxylated derivative. The enzyme system effecting this conversion is an NADPH-requiring microsomal oxygenase found in the liver.
研究发现，小鼠能够以可观的速率将丙酮转化为乳酸。丙酮向糖异生前体的转化可以提供额外的糖酵解中间体，从而更充分地利用脂质储备，并延长饥饿期间的存活时间。在饥饿3天或饮用水中添加丙酮的小鼠中，丙酮代谢途径被诱导至正常水平的数倍。携带致肥胖突变的杂合小鼠，无论是肥胖（ob/+）还是糖尿病（db/+），与同品系的纯合正常（+/+）小鼠相比，该途径的活性诱导程度明显更高。杂合小鼠表现出的丙酮向乳酸的更有效转化，可能解释了它们在饥饿状态下比正常纯合子存活时间更长的原因。该途径中的限速步骤似乎是丙酮向羟基化衍生物的转化。催化这种转化的酶系统是一种存在于肝脏中的需要NADPH的微粒体加氧酶。
