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By Rodolfo Paoletti, Dr. David Kritchevsky

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9% NaCl. c Rats were also injected with cortisone or cortisol at either 8 AM, 4 PM, or 11 PM, and killed 5, 8, and 12 hours later. No significant difference in the activity of HMGCoA reductase was noted. d Inferred from text of article. b 38 VICTOR W. RODWELL ET AL. 4. Norepinephrine When norepinephrine is injected into normal rats, incorporation of isotope from acetate into cholesterol doubles by 12 hours (Bortz, 1968). Twelve hours after injection of norepinephrine into adrenalectomized rats, hepatic reductase activity has risen 30% (Edwards, 1973) (Table VI).

Although catecholamines elevate reductase activity (Edwards, 1973; Bortz, 1968), no evidence is available which implicates their involvement in the rhythm. By contrast, glucocorticoids may b e involved in the control of the rhythm by preventing increases in reductase activity. , 1974). The effects of hormones on reductase activity and their possible regulatory roles are further discussed in Section VIII. F. D U A L P E A K I N H M G - C O A R E D U C T A S E A C T I V I T Y Shapiro and Rodwell (1972) observed dual peaks in the diurnal rhythm of rat liver HMG-CoA reductase (Fig.

Rates of [l- 14 C]acetate metabolism to sterols ( · ) , fatty acids (x), and C 0 2 (□), and levels of HMG-CoA reductase activity (O) were determined. Reproduced, with permission, from Kandutsch and Chen (1973). of steroids to suppress reductase activity (Kandutsch and Chen, 1974). Conversion of cholesterol to a more active derivative and subsequent inactivation by further catabolism should thus be considered as possibilities in the steroid regulation of HMG-CoA reductase. 2. Regulation by Cholesteryl Esters Suppression of reductase activity by dietary cholesterol is accompanied by an increase in hepatic cholesterol content due mainly to increased levels of cholesteryl esters (Harry et ah, 1973).

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