Current Metabolic-Genetic Interrelationship in Human Atherosclerosis

SUMMARY

A few simple laboratory methods have been suggested for phenotyping of clinical hyperlipidemias. Proper classification of plasma lipid abnormalities would provide the physician with an insight into the basic metabolic disorder in hyperlipidemia and atherosclerosis.

One of the more important developments has been the demonstration that increased sensitivity to dietary carbohydrate as manifested in hyperpre-beta-lipoproteinemia (rich in both cholesterol and triglycerides) may be quite widespread among apparently healthy persons while the process is exaggerated in the majority of atherosclerotic patients.

Evidence is accumulating rapidly to support the concept for disorder in carbohydrate metabolism as the major etiological factor in human atherosclerosis. Although hyperlipidemia is frequently encountered in diabetes mellitus, patients with abnormal sensitivity to carbohydrate are characterized primarily by increased endogenous lipogenesis. Preliminary data suggest that this disorder is initiated and sustained by an abnormal insulin mechanism with high plasma insulin-like activities, but normal blood sugar response to carbohydrate meals.

The current status of several promising chemotherapeutic agents is reviewed. Their effects upon the control of this special form of disorder in carbohydrate metabolism are being actively investigated. Tentatively, a sugar-restrictive 125-g carbohydrate diet seems to be useful for the control of the metabolic disorder.