Biomedical subjects
Publications and source records attributed to P Zee.
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The potential of medium chain triglyceride (MCT) and long chain triglyceride (LCT) as sources of plasma ketones was investigated in suckling rats. Initially high concentrations of plasma ketones in 6-, 10, and 17-day-old rats increased 2- to 3-fold after acute feeding of MCT. This feeding had the same effect in fed or fasted adult rats. Corn oil (as a source of LCT) induced a large increase in the plasma ketone concentration of suckling rats and a relatively small but significant increase in fasted adult rats. The LCT treatment did not affect plasma ketone levels in fed adult rats. The results show clearly that feeding either LCT or MCT will enhance hyperketonemia in suckling rats. In the livers of all animals, regardless of age, the capacity for incorporation of [1(-14C)]octanoate into CO2 and acetoacetate far exceeded that for [1(-14C)]palmitate. The hyperketonemic action of LCT in suckling rats was accompanied by an increased activity of carnitine palmityltransferase and increased level of carnitine.
Approximately 4,000 preschool black children from low-income families in South Memphis participated for three years in a supplementary food program sponsored by the US Department of Agriculture. Part of this group received additional benefit from food stamps, day-care centers, and an infant-feeding program. We evaluated the effects of this participation in 250 children selected randomly from the enrollment list of the supplemetary program. Each child was examined for height, weight, head circumference, and levels of hemoglobin, serum iron, and vitamins A and C. The data were then compared with those from a similar survey in the same area conducted three years before. The results of this comparison indicate considerable improvements in height and weight and a reduction in the incidence of anemia and in the numbers of children with low plasma vitamin A levels. In the absence of other recognizable intervening factors, we conclude that federal food assistance programs were primarily responsible for the observed nutritional improvements.
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The regulation of hepatic ketogenesis, as related to the metabolism of fatty acids through oxidative and synthetic pathways, was studied in developing rats. [1-14C] palmitate was used as a substrate to determine the proportions of free fatty acids utilized for the production of ketone bodies, CO2 and complex lipids. Similar developmental patterns of hepatic ketogenesis were obtained by measuring the production of either [14C] acetoacetate from exogenous [1-14C] palmitate or the sum of unlabeled acetoacetate and beta-hydroxybutyrate from endogenous fatty acids. The production of total ketone bodies was low during the late fetal stage and at birth, but increased rapidly to a miximum value within 24 hr after brith. The maximal ketogenic capacity appeared to be maintained for the first 10 days of life. 14CO2 production from [1-14C] palmitate increased by two- to fourfold during the suckling period, from its initial low rate seen at birth. The capacity for synthesis of total complex lipids was low at birth and had increased by day 3 to a maximal value, which was comparable to that of adult fed rats. The high lipogenic capacity lasted throughout the remaining suckling period. When ketogenesis was inhibited by 4-pentenoic acid, the rate of synthesis of complex lipids did not increase despite an increase in unutilized fatty acids. During the mid-suckling period, approximately equal amounts of [1-14C] palmitate were utilized for the synthesis of ketone plus CO2 and for complex lipid synthesis. By contrast, in adult fed rats, the incorporation of fatty acids into complex lipids was four times higher than that of ketone plus CO2. These observations suggest that stimulated hepatic ketogenesis in suckling rats results from the rapid oxidation of fatty acids and consequent increased production of acetyl CoA, but not from impaired capacity for synthesis of complex lipids.
Medium-chain triglycerides (MCT) induce ketosis in several mammalian species including man. To clarify the regulation of this metabolic alteration, we fed rats either MCT or long-chain triglyceride (corn oil) and then attempted to correlate ketosis with changes in (i) concentrations of selected metabolites in plasma and (ii) the synthetic and oxidative capacities of the liver. By 1 hour after MCT feeding, plasma levels of total ketone bodies had increased 18-fold, with a maximum value reached 1 hour later. By contrast, total plasma ketones in rats fed corn oil were increased only about 2-fold at 2 hours after feeding and did not exceed this value at later intervals. Hepatic concentrations of ketone bodies also increased after MCT or corn oil feeding. Although plasma concentrations of glucose decreased and insulin increased in rats fed MCT, they were not affected by corn oil feeding. MCT-induced ketosis was depressed by glucose administration. Neither MCT nor corn oil feeding impaired utilization of glucose by the liver. Hepatic lipogenesis was suppressed 50% and 90% by MCT and corn oil feeding, respectively. A marked increase of long-chain fatty acids in plasma was observed in rats fed corn oil but not in rats fed MCT. The pronounced increase of ketones in MCT-fed rats was closely related to an elevation of octanoate. In liver slices of MCT-fed rats, ketogenesis from octanoate was 10-fold higher than from palmitate, and octanoate was oxidized 4 times more rapidly than palmitate. The ketosis of MCT-fed rats was depressed by administration of 4-pentenoic acid, a potent inhibitor of fatty acid oxidation. These results support the concept that ketosis induced by MCT stems from rapid oxidation of medium-chain fatty acids. Hyperinsulinemia, hypoglycemia and depressed lipogenesis resulting from MCT feeding appear to potentiate but not initiate ketosis.
A possible regulatory role of insulin in the development of ketosis in newborn and suckling rats was investigated. The average plasma concentration of total ketone bodies measured at birth was 0.414 +/- 0.037 mumol/ml. Within 24 hr after birth the level of ketones had increased to 4 times its initial value. The 3- to 4-fold increase in plasma ketones was maintained during the first 5 days of life but started to decline thereafter. Plasma insulin of newborn rats at birth (62 +/- 8 muU/ml) was comparable to that of fed adult rats (85 +/- 10 muU/ml). The levels decreased to 28 muU/ml on the first day of life and stayed low throughout the suckling period despite a tendency to increase at the time close to weaning. The capacities for ketone production in liver homogenates of suckling rats was inversely related to the levels of insulin. Administration of insulin (0.125 mU/g body weight, im) and glucose (1.75 mg/g body weight, ip) both suppressed plasma ketone bodies in suckling rats. Insulin administration increased plasma insulin but failed to decrease plasma glucose. Injection of glucose increased plasma insulin and glucose. Neither insulin nor glucose treatment changed the plasma levels of free fatty acids. These data suggest that a limited availability of insulin permits a high rate of ketogenesis and hence induced ketosis in newborn and suckling rats.
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