Plasma triglycerides increase two-to-three-fold in normal pregnancy. If mechanistically similar to the atherosclerosis-associated hypertriglyceridemias, hypertrigiyceridemia in pregnancy should be exaggerated by diabetes, obesity, and high carbohydrate feeding. A failure to exaggerate would point to a different physiologic mechanism. To study this matter, we measured fasting plasma triglyceride and cholesterol in 38 normal, 22 gestational-diabetic, and 27 overtly diabetic women in the third trimester, measuring the concomitant effects of age and body weight and, in four subjects, high carbohydrate feeding.
Compared with controls, fasting plasma triglyceride and cholesterol were unchanged in gestational diabetics and in 10 of the 27 overtly diabetic pregnant women treated with insulin and diet. However, 17 of 27 diabetic women treated with an estrogen-progestin supplement during gestation had a 36 per cent higher triglyceride and a 15 per cent higher cholesterol than control. Body weight, age, duration of diabetes, or length of gestation could not account for the observations. In non-hormone-treated subjects, regression analysis showed a positive correlation of triglycerides with age but not with body weight. High carbohydrate feeding in pregnancy produced a triglyceride increase (mean±S.D.) of 9±19 per cent in whole plasma and 17±13 per cent in very-low-density Upoprotein. Respective postpartum increases were 41 and 68 per cent, similar to the responses reported in nonpregnant individuals.
Conclusion: Lack of a major effect of diabetes, body weight, and high carbohydrate feeding on blood lipids in gestation distinguishes pregnancy from the atherosclerosis-associated hypertriglyceridemias and points to a different physiologic control mechanism.