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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Rao G S, George R, Ramasarma T

Biochem J. 1976 Mar 15;154(3):639-45. doi: 10.1042/bj1540639.

Re-feeding starved rats increased the biogenesis of sterols in livers, with highest activity at 6h after the start of food intake. 2. Complete deficiency of protein or fat and partial deficiency of carbohydrate in the diet had no effect on sterol biogenesis. 3. Glucose, citrate or pyruvate, when administered intraperitoneally to starved rats, stimulated the biogenesis of sterols only at high concentrations. 4. ATP given intraperitoneally at low concentrations (10mg/rat) stimulated biogenesis of sterols, but not of fatty acids, from [1-14C]acetate. This effect was also obtained with other adenosine compounds, but not with adenine or guanosine. 5. Administration of adenosine compounds to starved rats also increased the incorporation of [1-14C]acetate into sterols in liver slices and also the activity of microsomal 3-hydroxy-3-methylglutaryl-CoA reductase. The results suggest a regulatory role for adenosine compounds in the hepatic biogenesis of isoprenoid compounds.

重新喂食饥饿的大鼠会增加肝脏中甾醇的生物合成，在开始进食后6小时活性最高。2. 饮食中完全缺乏蛋白质或脂肪以及部分缺乏碳水化合物对甾醇生物合成没有影响。3. 当向饥饿的大鼠腹腔注射葡萄糖、柠檬酸盐或丙酮酸时，只有在高浓度下才会刺激甾醇的生物合成。4. 以低浓度（10毫克/只大鼠）腹腔注射ATP可刺激[1-14C]乙酸盐生成甾醇，但不刺激脂肪酸生成。其他腺苷化合物也有此作用，但腺嘌呤或鸟苷则无此作用。5. 给饥饿的大鼠施用腺苷化合物还会增加[1-14C]乙酸盐在肝切片中掺入甾醇的量，以及微粒体3-羟基-3-甲基戊二酰辅酶A还原酶的活性。结果表明腺苷化合物在类异戊二烯化合物的肝脏生物合成中起调节作用。

Rao G S, George R, Ramasarma T

Biochem J. 1976 Mar 15;154(3):639-45. doi: 10.1042/bj1540639.

Re-feeding starved rats increased the biogenesis of sterols in livers, with highest activity at 6h after the start of food intake. 2. Complete deficiency of protein or fat and partial deficiency of carbohydrate in the diet had no effect on sterol biogenesis. 3. Glucose, citrate or pyruvate, when administered intraperitoneally to starved rats, stimulated the biogenesis of sterols only at high concentrations. 4. ATP given intraperitoneally at low concentrations (10mg/rat) stimulated biogenesis of sterols, but not of fatty acids, from [1-14C]acetate. This effect was also obtained with other adenosine compounds, but not with adenine or guanosine. 5. Administration of adenosine compounds to starved rats also increased the incorporation of [1-14C]acetate into sterols in liver slices and also the activity of microsomal 3-hydroxy-3-methylglutaryl-CoA reductase. The results suggest a regulatory role for adenosine compounds in the hepatic biogenesis of isoprenoid compounds.

重新喂食饥饿的大鼠会增加肝脏中甾醇的生物合成，在开始进食后6小时活性最高。2. 饮食中完全缺乏蛋白质或脂肪以及部分缺乏碳水化合物对甾醇生物合成没有影响。3. 当向饥饿的大鼠腹腔注射葡萄糖、柠檬酸盐或丙酮酸时，只有在高浓度下才会刺激甾醇的生物合成。4. 以低浓度（10毫克/只大鼠）腹腔注射ATP可刺激[1-14C]乙酸盐生成甾醇，但不刺激脂肪酸生成。其他腺苷化合物也有此作用，但腺嘌呤或鸟苷则无此作用。5. 给饥饿的大鼠施用腺苷化合物还会增加[1-14C]乙酸盐在肝切片中掺入甾醇的量，以及微粒体3-羟基-3-甲基戊二酰辅酶A还原酶的活性。结果表明腺苷化合物在类异戊二烯化合物的肝脏生物合成中起调节作用。