STUDIES IN LIPOPROTEIN LIPASES (HEPATIC AND ENTRAHEPATIC) IN PROTEIN CALORIE MALNUTRITION

Abstract

Protein-calorie malnutrition (PCM) is a common paediatric problem in Nigeria and the two main types, kwashiorkor and marasmus show differences in serum lipid profiles. The role of lipoprotein lipase (LPL.) in lipid metabolism in protein- malnutrition has hitherto received scant attention. It was suggested that an altered LPL activity could be a factor responsible for the abnormal lipid metabolism in kwashiorkor. Studies of serum lipids and post heparin serum lipolytic activities (PHLA) were carried out in kwashiorkor and marasmus children before and after treatment and also in control children. These parameters, as well as tissue LPL activities were also measured in young rats fed with 3 percent and 20 percent protein diets respectively. In marasmus, the normal levels of scrum hepatic and extra hepatic PHLA seemed consistent with normal levels of circulating FFA and triglyceride in that condition. In kwashiorkor, the reduction in total scrum PHLA was mostly in the hepatic HO with no significant reduction in extrahepatic PHLA. The pattern in scrum hepatic PHLA showed a lower activity in kwashiorkor patients with high concentration of triglycerides. After treatment, serum PHLA rose significantly and the mean levels were within normal range. The results suggested that a defect in metabolism of blood lipids caused by a low hepatic PHLA might cause hypertriglyceridemia in kwashiorkor. After feeding young rats on a 3 percent protein diet for 4 weeks, adipose tissue and heart LPL activities did not show any significant rise, as in rats on 20 percent protein. During this period, liver LPL activities in protein malnourished, pairfed and adequately fed rats were reduced when compared with the baseline level, but the difference between the baseline activity and that in the pairfed rats was not significant. The results suggested that the normal changes in adipose tissue and heart LPL activities during growth were impaired by prolonged protein deficiency. On the other hand liver LPL depended on the nutritional status of the animal, but the effect of protein deficiency was minimal. In conclusion, the accumulation of excess liver fat in protein- malnutrition might not be due to an abnormal liver LPL activity, but due to an impairment of the normal changes with age in activities of LPL on extrahepatic tissues. This could be a major factor contributing to the derange lipid metabolism in kwashiorkor.