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A B S T R A C T Heme oxygenase (HO), the enzyme system catalyzing the conversion of heme to bilirubin, was studied in the liver and spleen of fed, fasted, and refed rats. Fasting up to 72 hr resulted in a threefold increase in hepatic HO activity, while starvation beyond this period led to a gradual decline in enzyme activity. Refeeding of rats fasted for 48 hr depressed hepatic HO activity to basal values within 24 hr.Splenic HO was unaffected by fasting and refeeding.Hypoglycemia induced by injections of insulin or mannose was a powerful stimulator of hepatic HO. Glucose given together with the insulin abolished the stimulatory effect of the latter. Parenteral treatment with glucagon led to a twofold, and with epinephrine to a fivefold, increase of hepatic HO activity; arginine, which releases endogenous glucagon, stimulated the enzyme fivefold. These stimulatory effects of glucagon and epinephrine could be duplicated by administration of cyclic adenosine monophosphate (AMP), while thyroxine and hydrocortisone were ineffective. Nicotinic acid, which inhibits lipolysis, failed to modify the stimulatory effect of epinephrine. None of these hormones altered HO activity in the spleen.These findings demonstrate that the enzymatic mechanism involved in the formation of bilirubin from heme in the liver is stimulated by fasting, hypoglycemia, epinephrine, glucagon, and cyclic AMP. They further suggest that the enzyme stimulation produced by fasting

). Plasma total homocysteine levels and prognosis in patients with previous premature myocardial infarction: a 10-year follow-up study. J Intern Med 2003; 253: 284-292.Objectives. To explore plasma total homocysteine (tHcy) as a predictor of long-term prognosis after premature myocardial infarction (MI). Design. Prospective cohort study. Settings. Akershus University Hospital. Subjects. A total of 247 patients (193 men and 54 women) in stable clinical phase after premature MI (males: first MI at age £55; females £60). Main outcome measures. The primary end-point was total mortality and the secondary end-point was cardiac death. The third end-point was major cardiac events: a combination of cardiac death, MI and cardiac arrest.Results. After 10 years, 44 patients had died, 36 from cardiac causes. Major cardiac event occurred in 70 patients. The relative risk for death of all causes increased 1.43 (95% CI, 1.08-1.88) per tHcy quartile (P for trend ¼ 0.01), and was only modestly reduced after adjustment for age, ejection fraction, total cholesterol, C-reactive protein, fibrinogen, smoking and hypertension to 1.37 (95% CI, 1.04-1.80) (P for trend ¼ 0.03). Similar results were observed when cardiac death was used as the end-point, but we observed no association between tHcy and the endpoint major cardiac event. Conclusions. Total homocysteine was an independent predictor of total and cardiac mortality in stable patients following premature MI. tHcy had no effect on major cardiac event in contrast to most other risk factors in this study. Thus, the mechanism(s) underlying the effects of homocysteine on coronary heart disease may differ from other risk factors.

The intestinal lactase activity in six newborn jaundiced light-treated infants with diarrhea and in eight normal controls were compared by lactose tolerance test (LTT). The ability to hydrolyze lactose was minimal in the jaundiced infants during light-treatment compared to the controls which could absorb lactose very well. Peroral intestinal biopsies were taken from the newborn jaundiced infants during light-treatment. By histochemical technique no intestinal lactase activity was found in these intestines. When the jaundiced infants with diarrhea were given lactose-free diet, the stools normalized. The effect was reversed when breast milk was given while the baby was still jaundiced and light-treated. These findings indicate that the increased amounts of unconjugated bilirubin in the intestine of jaundiced infants during light-treatment inhibit the intestinal brush-border lactase. When the icterus fades the lactase is again active. The practical consequence is to give light-treated infants lactose-free diet if they get diarrhea, and to reintroduce breast milk or other lactose containing diet when the baby is no longer icteric.