Poisson J P, Blond J P, Lemarchal P
Diabete Metab. 1979 Mar;5(1):43-6.
Streptozotocin diabetic rats were administered the same tracer dose of either [1 14C] gamma-linolenic or [1 14C] dihomo-gamma-linolenic acid by stomach tube seven days after streptozotocin injection. They were killed 48 hours later and the radioactivity in individual fatty acids of the liver determined by radio-gas chromatography. Results were compared to those obtained in non diabetic rats similarly prepared. With either radioactive precursor, 14C radioactivity recovered in hepatic dihomo-gamma-linolenic acid was not significantly affected by the diabetic state. On the other hand, 14C radioactivity incorporated into arachidonic acid was considerably decreased in diabetic rats, compared with normal rats, when the weights of hepatic arachidonic acid were the same in the two groups of animals. These results suggest that streptozotocin diabetes causes a partial inhibition of the 5-desaturation of dihomo-gamma-linolenic acid in rat liver in vivo.
链脲佐菌素诱导的糖尿病大鼠在注射链脲佐菌素7天后,通过胃管给予相同示踪剂量的[1,14C]γ-亚麻酸或[1,14C]二高-γ-亚麻酸。48小时后将它们处死,通过放射性气相色谱法测定肝脏中各脂肪酸的放射性。将结果与以类似方式制备的非糖尿病大鼠所获得的结果进行比较。无论使用哪种放射性前体,肝脏中二高-γ-亚麻酸中回收的14C放射性均未受到糖尿病状态的显著影响。另一方面,当两组动物肝脏中花生四烯酸的重量相同时,与正常大鼠相比,糖尿病大鼠中掺入花生四烯酸的14C放射性显著降低。这些结果表明,链脲佐菌素诱导的糖尿病在体内会导致大鼠肝脏中二高-γ-亚麻酸5-去饱和作用的部分抑制。