Fabregat I, Revilla E, Machado A
Biochem Biophys Res Commun. 1987 Jul 31;146(2):920-5. doi: 10.1016/0006-291x(87)90618-8.
The short-term activation of the pentose phosphate cycle by insulin in rat adipocytes and hepatocytes has been studied. This NADPH-producing pathway is regulated by the activation or inhibition of different NADPH-consuming pathways. The stimulation of the fatty acid synthesis by insulin produced an increase in the flux through the pentose phosphate cycle. Kynurenate produced a decrease in the fatty acid synthesis and, consequently a diminution in the flux through the pentose phosphate cycle. Incubation of adipocytes and hepatocytes in presence of kynurenate (10 mM and 3 mM respectively) and insulin (5 nM), prevents both insulin activation on fatty acid synthesis and pentose phosphate cycle. These results suggest that insulin activates the pentose phosphate cycle through the activation of fatty acid synthesis.
对胰岛素在大鼠脂肪细胞和肝细胞中对磷酸戊糖途径的短期激活作用进行了研究。这条产生NADPH的途径是由不同的消耗NADPH途径的激活或抑制来调节的。胰岛素对脂肪酸合成的刺激导致磷酸戊糖途径通量增加。犬尿烯酸使脂肪酸合成减少,从而使磷酸戊糖途径通量降低。在分别存在10 mM犬尿烯酸和3 mM犬尿烯酸以及5 nM胰岛素的情况下培养脂肪细胞和肝细胞,可阻止胰岛素对脂肪酸合成和磷酸戊糖途径的激活。这些结果表明,胰岛素通过激活脂肪酸合成来激活磷酸戊糖途径。