Ayala A, Fabregat I, Machado A
Departamento de Bioquimica, Facultad de Farmacia, Universidad de Sevilla, Spain.
Mol Cell Biochem. 1991 Jun 26;105(1):1-5. doi: 10.1007/BF00230368.
Previous studies examining the regulation of the synthesis of G6PDH and 6PGDH in rat liver and adipose tissue have focused on the induction of these enzymes by different diets and some hormones. In rat liver these enzymatic activities seem to be regulated by a mechanism involving changes in the NADPH requirements. In this paper we have studied the effect of changes in the flux through different NADPH-consuming pathways on G6PDH and 6PGDH levels in adipose tissue and on the NADPH/NADP ratio. The results show that: I) an increase in the consumption of NADPH, caused by the activation of either fatty acid synthesis or detoxification systems which consume NADPH, is paralleled by an increase in the levels of these enzymes; II) when the increase in consumption of NADPH is prevented, the G6PDH and 6PGDH levels do not change.
以往关于大鼠肝脏和脂肪组织中葡萄糖-6-磷酸脱氢酶(G6PDH)和6-磷酸葡萄糖酸脱氢酶(6PGDH)合成调节的研究,主要集中在不同饮食和某些激素对这些酶的诱导作用上。在大鼠肝脏中,这些酶的活性似乎受一种涉及NADPH需求变化的机制调控。在本文中,我们研究了通过不同消耗NADPH途径的通量变化对脂肪组织中G6PDH和6PGDH水平以及NADPH/NADP比值的影响。结果表明:I)脂肪酸合成或消耗NADPH的解毒系统激活导致的NADPH消耗增加,与这些酶水平的增加平行;II)当NADPH消耗的增加被阻止时,G6PDH和6PGDH水平不变。