Masaru Maebashi

LIPID-LOWERING EFFECT OF CARNITINE IN PATIENTS WITH TYPE-IV HYPERLIPOPROTEINÆMIA

Serum-lipid concentrations were determined in patients with type-IV hyperlipoproteinaemia treated with 900 mg/day oral DL-carnitine chloride. Serum-triglyceride was significantly reduced and concentrations continued to decline as carnitine administration continued. Total and esterified cholesterol concentrations did not change. Intravenous infusion of carnitine produced the same effects. The results suggest that carnitine is of value in the therapy of type-IV hyperliproteinaemia. Increased oxidation of free fatty acids in the tissues seems to account for the effects of carnitine on serum-lipid concentrations.

Biotin enhances glucose-stimulated insulin secretion in the isolated perfused pancreas of the rat

The effects of biotin on insulin secretion in pair-fed control rats and biotin-deficient rats were investigated using the method of isolated pancreas perfusion. Isolated pancreas perfusion was performed using 20 mM glucose, 10 mM arginine, and 20 mM glucose plus various concentrations of biotin (20 mM glucose + biotin solution) as stimulants of insulin secretion. The insulin response to 20 mM glucose in biotin-deficient rats was approximately 22% of that seen in control rats. The level of the insulin response to 10 mM arginine was also significantly lower in biotin-deficient rats than in control rats. These results indicate that insulin release from the pancreas was disturbed in biotin-deficient rats. The insulin responses to 20 mM glucose + 1 mM biotin in biotin-deficient and control rats increased to 165% and 185%, respectively, of that to 20 mM glucose. These biotin-induced increases in glucose-stimulated insulin release were evident within the first few minutes of the infusion. An enhancement of the arginine-induced insulin response in control rats was not found when arginine and biotin was administered. These results suggest that biotin may play an important role in the mechanism by which glucose stimulates insulin secretion from the beta cells of the pancreatic islets.

Assay of Renin in Peripheral Blood

Long time has elapsed since the discovery of renin-angiotensin system as a possible cause of renal hypertension. But the role of this system in. the pathogenesis of renal or essential hypertension has been entirely unknown. Skeggs et al.1) found increased angiotensin in arterial blood not only in renal and malignant hypertension but also in benign essential hypertension, and concluded that this increase in circulating angiotensin is the principal cause of these hypertensions. Dexter et al.2) and Scornik et al.3) reported that release of renin from the kidney increases only in the initial stage of experimental renal hyperten sion, but it decreases to normal level in the chronic phase in spite of sustained hypertension. Peart4) discussed that the renin-angiotensin system has no relationship to the causation or maintenance of all kinds of hypertension , either renal or malignant. What is the reason of this discrepancy? It has been stressed in answer to this question that there was no reliable method for the estimation of renin or angiotensin in low concentrations as expected in renal or peripheral blood , and that development of such a method is urgently demanded to elucidate this conflic ting problem. New methods were introduced in 1961 by Scornik et al .3) and Boucher et al.5) for the determination of angiotensin in arterial blood , but they are not easily applicable because of the complexity in procedures and the need of large amounts of blood. Recently Helmer6) proposed a simple technique for the detection of renin in renal or peripheral blood. It consisted of dialysis of plasma to remove active substances of low molecular weight and direct assay of the dialyzed plasma on an isolated rabbit aortic strip. He further described that heat-stable and

RENIN INHIBITOR IN PLASMA OF URÆMIC PATIENTS

Abstract Addition of small amounts of plasma of uraemic patients with chronic glomerulonephritis to a mixture of renin and renin-free plasma decreased the rate of angiotensin formation to 66-89% of the value when saline solution was added. However, in the terminal stage of malignant hypertension inhibitory effect of plasma on angiotensin formation could not be observed, although plasma-renin activity was within normal range. This finding suggests that plasma of patients with uraemia contains a substance which inhibits the reaction of renin upon its substrate. This accords with the notion that the incubation method for the assay of plasma-renin does not estimate the absolute level of circulating renin, but rather estimates its activity in plasma as a whole.