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Metabolic and chemical properties of low-density lipoproteins (LDLs) were studied in a strain of pigs carrying a specific apo-B allele associated with hypercholesterolemia and premature atherosclerosis. LDL mass was significantly greater in mutant than in control pigs (400 +/- 55 mg/dL vs 103 +/- 26 mg/dL), as was LDL cholesterol. When normal and mutant LDLs were injected into the bloodstream of normal pigs, the fractional catabolic rate (FCR) of mutant LDL was about 30% lower than that of control LDL. In mutant pigs, the mean FCRs of mutant and control LDL were similar, although they were much lower than the corresponding FCRs observed in normal pigs. The density profile of LDL particles differed in control and mutant pigs; the peak LDL flotation rate was shifted from S0f = 5.3 +/- 1.9 in controls to a more buoyant 7.4 +/- 0.5 in mutants. The elevation of LDL in the mutants was restricted to the most buoyant LDL subspecies. This subpopulation of mutant LDL was enriched with cholesteryl ester (47% vs 37%) and depleted of triglyceride, relative to LDL of similar density and size in controls. The lipid compositions of the denser LDL subpopulations (rho greater than 1.043 g/mL) were similar in mutants and controls. We conclude that the hypercholesterolemia of these mutant pigs is accounted for by defective catabolism of LDL. The buoyant cholesterol ester enriched LDL subspecies that accumulate in plasma may contribute to the accelerated atherogenesis that occurs in these animals.

Test meals providing two levels of dietary protein (13% or 26% of the energy) were fed to eight pregnant (P), nine nonpregnant (NP), and two gestational diabetic (GDM) women. Plasma levels of amino acids were measured at 0 h and 2 h. Glucose and insulin were measured at 0, 1/2, and 2 h after the meals. In the fasting state, P women had significantly lower fasting concentrations of most of the amino acids. After the high-protein meal, rises of arginine, ornithine, and branched-chain amino acids (BCAAs: leucine, isoleucine, and valine), were significantly smaller in P women. Changes in BCAAs were normal in GDM women. P women had greater rises of insulin in response to both test meals than did NP women. This may facilitate increased BCAA uptake from the circulation. Rises in plasma glucose tended to be higher in P than NP women, suggesting that insulin's effects on glucose and BCAA uptake may be mediated separately.

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