Metabolic Control Mechanisms in Precancerous Liver

Sabine, John R.

doi:10.3109/10408448009032924

Cited by 2 publications

(1 citation statement)

References 62 publications

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“…The absence of a diurnal pattern and the decreased activity of hepatic HMG-CoA reductase activity in the dystrophic hamster, which has been shown to have increased membrane cholesterol (Slack et a!., 1980), is therefore different from that found in some other disease states, e.g. cancer, where feedback control is lacking although diurnal rhythm is retained (Sabine, 1980). The liver is the main source of plasma cholesterol in man and rat (Dietschy & Wilson, 1970), and the rate of cholesterol synthesis (i.e.…”

Section: Discussionmentioning

confidence: 90%

3-Hydroxy-3-methylglutaryl-coenzyme A reductase in normal and dystrophic hamsters

Greenough¹,

Boegman²

1982

Biochemical Journal

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The activity and diurnal variation of 3-hydroxy-3-methyglutaryl-CoA reductase (EC 1.1.1.34; HMG-CoA reductase), the rate-limiting enzyme in the cholesterol-biosynthetic pathway, of normal and dystrophic hamsters was determined. Liver enzyme activity showed a diurnal pattern in the normal male, but not in the dystrophic male. Enzyme values in normal males at the midpoint of the 12 h dark period were 10 times those in dystrophic males. No evidence for diurnal variation in the HMG-CoA reductase of the brain was observed, and similar activities were found for normal and dystrophic animals. The apparent Km for HMG-CoA reductase from the liver of normal or dystrophic hamsters was approx. 9 microM, and the Vmax. was 5.9 and 21.7 pmol/min per mg of protein for dystrophic and normal hamsters respectively.

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Section: Discussionmentioning

confidence: 90%

3-Hydroxy-3-methylglutaryl-coenzyme A reductase in normal and dystrophic hamsters

Greenough¹,

Boegman²

1982

Biochemical Journal

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Membrane-mediated control of hepatic β-hydroxy-β-methylglutaryl-coenzyme A reductase

Sipat¹,

Sabine²

1981

Biochemical Journal

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Previously we [Sabine & James (1976) Life Sci. 18, 1185--1192] proposed that 'the activity of hepatic beta-hydroxy-beta-methylglutaryl-coenzyme A reductase is critically regulated by the fluidity of its supporting microsomal membrane'. In the present work we examined further this concept of membrane-mediated control, with respect to the specific hypothesis that such control might function as a common mechanism both for the co-ordinated regulation of other enzymes affected by cholesterol feeding and also for the subcellular integration of the several physiological factors known to influence this enzyme's activity. Contrary to earlier expectations, this hypothesis now appears not to hold. We report here that, under those conditions of short-term cholesterol feeding that affected the reductase, a variety of other microsomal enzymes did not display membrane-function interactions, i.e. neither enzymes involved in cholesterol metabolism and also affected by cholesterol feeding (cholesterol 7 alpha-hydroxylase), nor those involved in cholesterol metabolism and not affected by cholesterol feeding (hydroxymethylglutaryl-CoA hydrolase, acyl-CoA:cholesterol acyltransferase), nor those not directly involved in cholesterol metabolism at all (glucose 6-phosphatase). Furthermore, we observed no evidence for the operation of membrane-mediated control of the reductase in other situations known to influence its activity, i.e. starvation, diurnal rhythm, the very early stages of cholesterol feeding and various manipulations in vitro.

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Metabolic Control Mechanisms in Precancerous Liver

Cited by 2 publications

References 62 publications

3-Hydroxy-3-methylglutaryl-coenzyme A reductase in normal and dystrophic hamsters

3-Hydroxy-3-methylglutaryl-coenzyme A reductase in normal and dystrophic hamsters

Membrane-mediated control of hepatic β-hydroxy-β-methylglutaryl-coenzyme A reductase

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