Submitted to: American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/10/2005
Publication Date: 5/1/2005
Citation: Badaloo, A., Reid, M., Soares, D., Forrester, T., Jahoor, F. 2005. Relationship between liver fat content and the rate of VLDL apolipoprptein B-100 synthesis in children with protein-energy malnutrition. American Journal for Clinical Nutrition. 81:1126-1132. Interpretive Summary: Some children with severe protein-energy malnutrition (PEM) develop fat in their livers. Usually these children are sicker, more difficult to treat and have a higher mortality rate than well nurished children. The reason why this subset of children with PEM develop a fatty liver is still not known. Although it is generally accepted that impaired synthesis of the protein VLDL apolipoprotein B-100 (VLDL-apo B-100), that is responsible for fetching triglycerides out of the liver is the cause, the rate of synthesis of this protein has not been measured in children with PEM. The objective of this study was to determine the relationship between the amount of fat deposited in the liver and the rate of VLDL-apo B-100 synthesis in children with PEM. The rate of VLDL-apo B-100 synthesis was measured by infusing [2H3]leucine in 13 children with PEM. Hepatic fat content was estimated by computerized tomography scanning. There were significant relations between liver fat content, VLDL-apo B-100 concentration and synthesis rate. Thus children with PEM synthesize VLDL-apo B-100 at a faster rate as the amount of liver fat increases. We conclude that fatty infiltration of the liver in PEM is not due to a reduction in the synthesis of VLDL-apo B-100.
Technical Abstract: Fatty infiltration of the liver is associated with an increased morbidity and mortality in children with severe protein-energy malnutrition (PEM), but its pathogenesis remains unclear. Although impaired synthesis of VLDL apolipoprotein B-100 (VLDL-apo B-100) is generally accepted as the pathogenetic mechanism, the rate of it's synthesis has not been measured in children with PEM. The objective of the study was to ascertain the relation between the degree of hepatic steatosis and the rate of VLDL-apo B-100 synthesis in children with PEM. The fractional and absolute rates of VLDL-apo B-100 synthesis were measured with a prime-constant intravenous infusion of [2H3]leucine in 13 severely malnourished children (8 boys and 5 girls) aged 7-18 mo. Hepatic fat content was estimated by computerized tomography scanning by using the ratio of liver to spleen (L:S) attenuation. The ratio is inversely related to hepatic fat content such that the lower the L:S, the greater the amount of fat in the liver. There were significant inverse relations between L:S attenuation and VLDL-apo B-100 concentration (P < 0.02), the absolute rate of VLDL-apo B-100 synthesis (P < 0.02), and plasma triacylglycerol (P < 0.02) and serum cholesterol (P < 0.05) concentrations. These results suggest that children with PEM synthesize VLDL-apo B-100 at a faster rate as the degree of hepatic fat infiltration increases. Thus, fatty infiltration of the liver in PEM is not due to a reduction in the synthesis of VLDL-apo B-100.