Dietary Carbohydrates in Hyperlipemia (Hyperglyceridemia); Hepatic and Adipose Tissue Lipogenic Activities

Abstract

1. Controlled metabolic studies including periods of intersubstitution of sugar (mainly sucrose) and starch in the diet were made in a series of patients with carbohydrate-induced hyperglyceridemia. 2. Sugar feeding markedly exaggerated the hyperglyceridemia in all of the patients studied. Equicaloric substitution of starch for sugar in the diet resulted in lowering of the elevated serum lipids toward normal. 3. It was necessary to raise the daily carbohydrate intake to 85-90% of the total daily caloric intake in order to induce hyperglyceridemia in normolipemic subjects. 4. Hepatic and adipose tissues were obtained from normal subjects and hyperlipemic patients for lipogenesis and lipolytic activity studies. 5. The mean hepatic and adipose tissue lipogenic activities of hyperglyceridemic patients on relatively high carbohydrate ad libitum diet were found to be several times higher than those of normal controls on a similar diet. The tissue activities of patients maintained on sugar-restrictive carbohydrate moderation diet were normal. 6. The lipolytic activity of the hyperlipemic adipose tissue was many times more active than that of the normal controls and the diet-treated hyperglyceridemic patients. 7. Almost all radioactive ¹⁴C from the labeled precursors was incorporated into phospholipid by the liver tissues of both normal controls and lipemic patients. 8. The adipose tissue of normal controls incorporated the major proportion of the labeled precursors to water soluble fractions of the lipid molecule, and the adipose tissue of hyperglyceridemic patients incorporated ¹⁴C from isotopic acetate, fructose, and glucose predominantly into the fatty acid moiety of the newly synthesized lipid. 9. It is suggested that the adipose tissue of hyperglyceridemic patients on a high carbohydrate diet is highly active in lipid synthesis and also in the release of free fatty acids. The high fatty acid flux to the liver is esterified into triglyceride, incorporated into low density lipoproteins, and transported into the circulation with the aid of phospholipid to produce hyperglyceridemia. 10. Apparently healthy subjects with covert glyceride and carbohydrate metabolism are prone to the development of hyperglyceridemia when dietary sucrose content is increased. The association between dietary carbohydrate, hyperglyceridemia, and coronary artery disease is discussed.