Alterations of hepatic microsomal drug metabolism by glucagon

J. V. Aranda; K. W. Renton

doi:10.1139/y75-120

Alterations of hepatic microsomal drug metabolism by glucagon

J. V. Aranda, K. W. Renton

Research output: Contribution to journal › Article › peer-review

2 Citations (Scopus)

Abstract

The effect of glucagon on the components of the hepatic microsomal electron transport chain (NADPH oxidase, NADPH cytochrome c reductase (EC 1.6.2.4), cytochrome P 450, and NADPH cytochrome P 450 reductase), and on two representative oxidative pathways (aminopyrine N demethylation, a type I substrate oxidation; and aniline p hydroxylation, a type II substrate oxidation) was determined. Microsomes from rats pretreated with glucagon (300 μg/kg per day for 3 days) showed a significant decrease in NADPH oxidase and aminopyrine N demethylation with a prolonged hexobarbital sleeping time, and a significant increase in aniline p hydroxylation. Microsomes from rats pretreated with a lower dose of glucagon (30 μg/kg per day for 3 days) showed a significant decrease in the microsomal N demethylation of aminopyrine. Glucagon had no effect when added in vitro to microsomes, suggesting that the in vivo effects of glucagon are mediated indirectly in the intact animal.

Original language	English
Pages (from-to)	873-879
Number of pages	7
Journal	Canadian Journal of Physiology and Pharmacology
Volume	53
Issue number	5
DOIs	https://doi.org/10.1139/y75-120
Publication status	Published - 1975
Externally published	Yes

ASJC Scopus Subject Areas

Physiology
Pharmacology
Physiology (medical)

PubMed: MeSH publication types

Journal Article

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10.1139/y75-120

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title = "Alterations of hepatic microsomal drug metabolism by glucagon",

abstract = "The effect of glucagon on the components of the hepatic microsomal electron transport chain (NADPH oxidase, NADPH cytochrome c reductase (EC 1.6.2.4), cytochrome P 450, and NADPH cytochrome P 450 reductase), and on two representative oxidative pathways (aminopyrine N demethylation, a type I substrate oxidation; and aniline p hydroxylation, a type II substrate oxidation) was determined. Microsomes from rats pretreated with glucagon (300 μg/kg per day for 3 days) showed a significant decrease in NADPH oxidase and aminopyrine N demethylation with a prolonged hexobarbital sleeping time, and a significant increase in aniline p hydroxylation. Microsomes from rats pretreated with a lower dose of glucagon (30 μg/kg per day for 3 days) showed a significant decrease in the microsomal N demethylation of aminopyrine. Glucagon had no effect when added in vitro to microsomes, suggesting that the in vivo effects of glucagon are mediated indirectly in the intact animal.",

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T1 - Alterations of hepatic microsomal drug metabolism by glucagon

AU - Aranda, J. V.

AU - Renton, K. W.

PY - 1975

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N2 - The effect of glucagon on the components of the hepatic microsomal electron transport chain (NADPH oxidase, NADPH cytochrome c reductase (EC 1.6.2.4), cytochrome P 450, and NADPH cytochrome P 450 reductase), and on two representative oxidative pathways (aminopyrine N demethylation, a type I substrate oxidation; and aniline p hydroxylation, a type II substrate oxidation) was determined. Microsomes from rats pretreated with glucagon (300 μg/kg per day for 3 days) showed a significant decrease in NADPH oxidase and aminopyrine N demethylation with a prolonged hexobarbital sleeping time, and a significant increase in aniline p hydroxylation. Microsomes from rats pretreated with a lower dose of glucagon (30 μg/kg per day for 3 days) showed a significant decrease in the microsomal N demethylation of aminopyrine. Glucagon had no effect when added in vitro to microsomes, suggesting that the in vivo effects of glucagon are mediated indirectly in the intact animal.

AB - The effect of glucagon on the components of the hepatic microsomal electron transport chain (NADPH oxidase, NADPH cytochrome c reductase (EC 1.6.2.4), cytochrome P 450, and NADPH cytochrome P 450 reductase), and on two representative oxidative pathways (aminopyrine N demethylation, a type I substrate oxidation; and aniline p hydroxylation, a type II substrate oxidation) was determined. Microsomes from rats pretreated with glucagon (300 μg/kg per day for 3 days) showed a significant decrease in NADPH oxidase and aminopyrine N demethylation with a prolonged hexobarbital sleeping time, and a significant increase in aniline p hydroxylation. Microsomes from rats pretreated with a lower dose of glucagon (30 μg/kg per day for 3 days) showed a significant decrease in the microsomal N demethylation of aminopyrine. Glucagon had no effect when added in vitro to microsomes, suggesting that the in vivo effects of glucagon are mediated indirectly in the intact animal.

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Alterations of hepatic microsomal drug metabolism by glucagon

Abstract

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