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From the Donner Laboratory, Ernest Orlando Lawrence Berkeley National Laboratory, University of California, Berkeley (D.M.D., H.A.F., P.T.W., R.M.K.), and the Children's Hospital, Oakland, Calif (D.M.D., H.A.F.).
Correspondence to Ronald M. Krauss, MD, Donner Laboratory, Room 465, Ernest Orlando Lawrence Berkeley National Laboratory, 1 Cyclotron Rd, Berkeley, CA 94720. E-mail rmkrauss{at}lbl.gov
Abstract A predominance of small, dense LDL particles (subclass pattern B) characterizes a metabolic trait that is associated with higher levels of triglyceride-rich lipoproteins and lower levels of HDL compared with those of individuals with predominantly larger LDL (pattern A). This trait appears to be under the influence of one or more genes, with maximal expression in adult males and reduced expression in premenopausal females. In a previous study, men with LDL subclass pattern B had significantly greater reductions in LDL cholesterol (LDL-C) and apolipoprotein B than men with pattern A. We hypothesized that despite the low prevalence of pattern B in premenopausal women, genetic predisposition to this trait could affect dietary responsiveness. Specifically, we predicted that LDL-C reduction on a low-fat, high-carbohydrate diet would be greatest in daughters of two pattern B parents, intermediate in daughters with one pattern B parent, and least in daughters with no pattern B parents. When 72 premenopausal women were placed on a 20% fat diet for 8 weeks, the changes in LDL-C (mmol/L) compared with levels on basal diets were significantly related to the number of pattern B parents (two B parents: -0.92±0.61, one B parent: -0.23±0.10, no B parents: -0.05±0.06) and could not be explained by diet adherence or baseline characteristics including initial lipoprotein profile or body mass index. The number of pattern B parents was also related to reductions in plasma mass concentrations of IDL, total LDL, and large LDL and to increases in plasma triglycerides. There was a significant inverse correlation between changes in triglyceride and LDL-C induced by the low-fat, high-carbohydrate diet. Thus, genetic and metabolic factors underlying LDL subclass pattern B may result in enhanced LDL and triglyceride responsiveness to substitution of dietary carbohydrate for fat in premenopausal women.
Key Words: LDL pattern women lipoproteins diet
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