Effects of unbalanced diets on cerebral glucose metabolism in the adult rat
Effects of unbalanced diets on cerebral glucose metabolism in the adult rat
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DOI：
10.1212/wnl.45.12.2261
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发表时间：
1995-12-01
期刊：
影响因子：
9.9
通讯作者：
Harik, SI
中科院分区：
文献类型：
--
作者：
AlMudallal, AS;Levin, BE;Harik, SI
在6 ~ 7周的时间里，我们测量了大鼠的葡萄糖区域脑代谢率和选定的脑代谢物：(1)常规实验室饲料；(2)高脂肪、无碳水化合物的生酮饮食，其热量值的10%来自蛋白质，90%来自脂肪；(3)高碳水化合物饮食，热量值的10%来自蛋白质，78%来自碳水化合物，12%来自脂肪。在初步实验中，我们发现，如果饮食中脂肪的热量值低于90%，中度酮症是无法实现的。维持生酮饮食的大鼠血液中β -羟基丁酸盐（0.4 mM）和乙酰乙酸盐（0.2 mM）中度升高，大脑中β -羟基丁酸盐水平增加5至10倍。各组脑内葡萄糖、糖原、乳酸和柠檬酸水平相似。2-脱氧葡萄糖研究表明，生酮饮食并没有显著改变脑区域葡萄糖利用。然而，维持高碳水化合物饮食的大鼠脑葡萄糖利用率明显下降，脑葡萄糖6-磷酸浓度增加。这些发现表明，长期中度酮血症不会显著改变脑葡萄糖磷酸化。然而，即使是边际蛋白质饮食缺乏，当加上富含碳水化合物的饮食时，也会在一定程度上抑制脑葡萄糖的利用，这在代谢性脑病中很常见。我们的研究结果支持临床观点，即蛋白质饮食缺乏加上碳水化合物摄入增加可导致中枢神经系统功能障碍。
We measured regional cerebral metabolic rates for glucose and selected cerebral metabolites in rats fed one of the following diets for 6 to 7 weeks: (1) regular laboratory chow; (2) high-fat, carbohydrate-free ketogenic diet deriving 10% of its caloric value from proteins and 90% from fat; and (3) high-carbohydrate diet deriving 10% of its caloric value from proteins, 78% from carbohydrates, and 12% from fat. In preliminary experiments, we found that moderate ketosis could not be achieved by diets deriving less than about 90% of their caloric value from fat. Rats maintained on the ketogenic diet had moderately elevated blood beta-hydroxybutyrate (0.4 mM) and acetoacetate (0.2 mM), and a five- to 10-fold increase in their cerebral beta-hydroxybutyrate level. Cerebral levels of glucose, glycogen, lactate, and citrate were similar in all groups. 2-Deoxyglucose studies showed that the ketogenic diet did not significantly alter regional brain glucose utilization. However, rats maintained on the high-carbohydrate diet had a marked decrease in their brain glucose utilization and increased cerebral concentrations of glucose 6-phosphate. These findings indicate that long-term moderate ketonemia does not significantly alter brain glucose phosphorylation. However, even marginal protein dietary deficiency, when coupled with a carbohydrate-rich diet, depresses cerebral glucose utilization to a degree often seen in metabolic encephalopathies. Our results support the clinical contention that protein dietary deficiency coupled with increased carbohydrate intake can lead to CNS dysfunction.