Location: Children's Nutrition Research Center
Title: Nutritional repletion of children with severe acute malnutrition does not affect VLDL apolipoprotein B-100 synthesis rate Authors
|Badaloo, Asha -|
|Forrester, Terrence -|
|Reid, Marvin -|
|Jahoor, Farook -|
Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 23, 2012
Publication Date: May 1, 2012
Citation: Badaloo, A.V., Forrester, T., Reid, M., Jahoor, F. 2012. Nutritional repletion of children with severe acute malnutrition does not affect VLDL apolipoprotein B-100 synthesis rate. Journal of Nutrition. 142(5):931-935. Interpretive Summary: Malnourished children who deposit a lot of fat in their livers are usually sicker and more of them die during hospitalization compared to those children without fat deposits in their livers. Usually, it is the malnourished children who also have a lot of water retention "edema" in their body that develop fat deposits in their livers. It has been proposed that these children deposit fat in their livers because they are not making sufficient quantities of a protein called "VLDL apo B-100" that is responsible for transporting fat out of the liver. However, this proposal has never been tested. We therefore measured the amount of VLDL apo B-100 that malnourished children with edema were making and compared it with the amount that malnourished children without edema were making. We also compared it to how much they were making when they were fully recovered from malnutrition. We found that both groups of malnourished children were making the same amounts of VLDL apo B-100 and the amounts they made when they were malnourished were not less than the amount they made when they got better. These findings suggest that the long-held belief that malnourished children develop fat in their livers because they cannot make sufficient quantities VLDL apo B-100 is incorrect. From another study we now have evidence that the children who deposit fat in their liver cannot use fat efficiently to make energy, suggesting that the unused fat gets deposited in their livers. This is an important finding because a lot of treatment centers treat malnourished children with high-fat diets which will increase the amount of fat deposited in the liver. We have recommended that malnourished children with fat in their livers should not be treated with a high-fat diet until the liver fat starts to disappear.
Technical Abstract: VLDL apo B-100 is essential for the secretion of liver fat. It is thought that synthesis of this lipoprotein is impaired in childhood severe acute malnutrition (SAM), especially in the edematous syndromes, and that this contributes to the common occurrence of hepatic steatosis in this condition. However, to our knowledge, it has not been confirmed that VLDL apo B-100 synthesis is slower in edematous compared with nonedematous SAM and that it is impaired in the malnourished compared with the well-nourished state. Therefore, VLDL apo B-100 kinetics were measured in 2 groups of children with SAM (15 edematous and 7 nonedematous), aged 4-20 mo, at 3 stages during treatment. Measurements were done at 4 +/- 1 d postadmission, mid- catch-up growth in weight, and at recovery (normal weight-for-length). VLDL apo B-100 synthesis was determined using stable isotope methodology to measure the rate of incorporation of (2)H(3)-leucine into its apoprotein moiety. The fractional and absolute synthesis of VLDL apo B-100 did not differ between the groups or from the initial malnourished stage to the recovery stage. Concentrations of VLDL apo B-100 were greater in the edematous than in the nonedematous group (P < 0.04) and did not differ from the initial stage to recovery. The data indicate that VLDL apo B-100 synthesis is not reduced when children develop either edematous or nonedematous SAM.