CLINICAL STUDY ON LIPID METABOLISM. EFFECT OF GLUCOSE AND INSULIN ON NEFA METABOLISM.

Abstract

The lipid metabolism, especially Nefa oxidation to expired CO2 and transfer to plasma triglycerides was investigated by using palmitic acid-1 -C14 with reference to glucose metabolism in arteriosclerotic, diabetic, hyperlipemic and control subjects. 1 ) In a fasting state, Nefa oxidation in the cells of an arteriosclerotic subject was twice as much as that in the control subject and transfer of Nefa into plasma triglycerides was 3 times in the arteriosclerotic, 2 or 3 times in the hyperlipemic, 2 times in the diabetic subject as much as that in the control subject. The Nefa oxidation rate in the cells of an arteriosclerotic subject was most increased to reach to 4 times and in the diabetics 2 times as much as that in the control subject. Rate of Nefa transfer to plasma triglycerides increased in both arteriosclerotic and diabetic subjects to 6 or 4 times as much as that in the normal subject. 2) Glucose loading increased the Nefa oxidation in the control, diabetic and male hyperlipemic subject, while decreased in an arteriosclerotic and a female hyperlipemic subject. By glucose loading the transfer of Nefa into plasma triglycerides was only slightly changed in the control, arteriosclerotic and diabetic subject, while was increased in the male hyperlipemic subject. By glucose loading the rate of Nefa oxidation in the cell was increased in the control and diabetic subject, while decreased in the arteriosclerotic subject ; then the rates became to almost same in all cases. The rate of Nefa transfer into plasma triglycerides in the arteriosclerotic and diabetic subject was decreased, while in the control subject was increased a little by glucose loading. 3) The Nefa oxidation was markedly or a little depressed in the control or arteriosclerotic subject respectively and unchanged in a diabetic subject by insulin administration. Insulin de-pressed the Nefa transfer into plasma triglycerides in the control and arteriosclerotic subject. By insulin administration, the rate of Nefa oxidation was unchanged in the arteriosclerotic and depressed in the control and diabetic subject ; especially, in the diabetic subject was most influenced. 4) In an arteriosclerotic subject, the accelerated Nefa oxidation in a fasting state was decreased to half by glucose administration and unchanged by insulin loading. Then, available glucose seems to be insufficient in the cells of arteriosclerosis. In a diabetic subject, Nefa oxidation was not increased in a fasting state and increased by glucose loading and unchanged by insulin loading. Then, insulin seems to be insufficient in the cell of diabetes mellitus. In a control subject, Nefa oxidation was accelerated by glucose loading and depressed by insulin loading. In an arteriosclerotic subject, Nefa transfer into plasma triglycerides was markedly accelerated in a fasting state ; this Nefa transfer was changed a little by glucose and decreased by insulin loading. In arteriosclerotic subjects, it would be suggested that disturbances in lipid metabolism may be partly caused by the deficiency of glucose metabolism. In a diabetic subject, Nefa transfer was moderately accelerated in a fasting state and slightly changed by glucose or insulin loading. In diabetes mellitus, glucose seems to have the direct influence, while insulin, the indirect influence through glucose metabolism, on lipid metabolism. In a control subject, Nefa transfer was slightly increased by glucose and markedly decreased by insulin loading.