Mixed function oxidation and intermediary metabolism: metabolic interdependencies in the liver.

Abstract:

:Both hepatic lipogenesis from glucose and gluconeogenesis from lactate are inhibited by substrates for mixed function oxidation such as aminopyrine. These effects are inducible with phenobarbital pretreatment and absent with a demethylated product of aminopyrine metabolism, aminophenylpyrazolone. The data indicate that an interaction between biosynthesis and drug metabolism occurs in the intact liver cell. In the case of lipogenesis, direct competition for cytosolic NADPH occurs, whereas in the case of gluconeogenesisi, enhanced drug metabolism diverts key intermediates, e.g., malate from glucose synthesis toward NADPH generation. Furthermore, rates of mixed function oxidation were modified following perturbations of intermediary metabolism, e.g., fasting, addition of substrates for glucose synthesis, inhibition of energy metabolism, etc. The data support the hypothesis that in the presence of sufficiently high concentrations of substrate and oxygen, the rate-limiting step for mixed function oxidation in the intact cell is supply of NADPH.

journal_name

Adv Exp Med Biol

authors

Thurman RG,Marazzo DP

doi

10.1007/978-1-4615-9026-2_25

subject

Has Abstract

pub_date

1975-01-01 00:00:00

pages

355-67

issue

00

eissn

0065-2598

issn

2214-8019

journal_volume

58

pub_type

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