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Abdominal adiposity, as indexed by the waist to hip girth ratio (WHR), has been associated with increased risk and incidence of coronary heart disease (CHD). The purpose of this study was to determine if this enhanced risk is related to alterations in the structure of low density lipoproteins (LDL). LDL were isolated from nine nonobese men with an average WHR of 1.046 and nine nonobese men with a WHR of 0.94, who were matched on age (45.6 +/- 2.7 v 47.7 +/- 2.3 mean +/- SEM) percent body fat (26.5 +/- 0.5 v 26.1 +/- 0.9), and body mass index (27.3 +/- 0.6 v 26.3 +/- 0.6). The average molecular weight of LDL from the subjects with a high WHR was lower than that of subjects with low WHR (2.70 v 3.02 x 10(6) d), the average hydrated density higher (1.050 v 1.040 g/mL), and the mobility (Rf) on 2% to 16% polyacrylamide gradient gel electrophoresis higher. Subfractionation by equilibrium density ultracentrifugation showed that the LDL of subjects with a high WHR was predominantly in the heavy density range (1.038 to 1.048 g/mL) compared with the LDL of subjects with low WHR, which was in the lighter density range (1.030 to 1.040 g/mL). Chemical analysis of the subfractions showed that the peak density fractions of LDL of subjects with a high WHR had a lower cholesterol to protein ratio than the peak density fractions of LDL of subjects with low WHR. Electron microscopy of these peak density fractions showed that LDL of subjects with high WHR was smaller than that of subjects with low WHR. These characteristics of LDL of subjects with abdominal adiposity closely resemble the properties of LDL of patients with documented CHD. It is concluded that the increased risk of CHD associated with abdominal adiposity may be due in part to the alterations in LDL characteristics, and that these alterations in LDL are independent of the degree of obesity.

Microscopic and analytical studies of the lipids in the heart and muscle of the BIO 82.62 myopathic hamsters and age-matched normal animals at the average ages of 33, 67, and 108 days were performed. Microscopic examinations did not show increased lipid depositions in the hearts of the diseased animals as was found in the BIO 14.6 strain. No consistent differences in the lipid content of the cardiomyopathic hamsters (BIO 82.62) and age-matched controls were observed in the three age groups except in the cholesterol content of muscle. Cholesterol increased significantly (P less than 0.01) in the 67 and 108 day old animals. This increase elevated the cholesterol/phospholipid ratio. Analysis of the fatty acid composition of triglycerides showed that the cardiomyopathic hamsters store more saturated fatty acids in both heart and muscle than do their normal counterparts. The abundance of more saturated fatty acids may imply that either the desaturation mechanism is altered in the diseased animals or that unsaturated fatty acids are preferentially utilized in other processes.

After reviewing all the available results from our laboratory and numerous reports in the literature concerning changes that have occurred in various aspects of protein metabolism during exercise, a number of conclusions can be drawn with some degree of confidence. During exercise, protein synthesis is depressed and this change leaves amino acids available for catabolic processes. The rate of leucine oxidation appears to be increased during exercise, and there is a movement of amino acids, mostly in the form of alanine, from muscle to liver where the rate of gluconeogenesis is increased as a result of exercise. These changes in protein metabolism are probably physiologically significant in at least three ways: amino acid conversion to citric acid cycle intermediates enhances the rate of oxidation of acetyl-CoA generated from glucose and fatty acid oxidation; increased conversion of amino acids to glucose helps to prevent hypoglycemia; oxidation of some amino acids may provide energy for muscular contraction.

The purpose of this study was to determine if there was a relationship between plasma beta-VLDL concentrations and atherosclerosis severity in cholesterol-fed pigeons, and if so, whether this correlated with cholesterol accumulation in tissues rich in cells of the monocyte-macrophage system (liver, spleen, peritoneal macrophages). Among individual birds consuming a cholesterol-containing diet, plasma beta-VLDL concentrations ranged from 14 to 1979 mg/dl. In these animals the cholesterol content of peritoneal macrophages, liver, and spleen was positively correlated with plasma concentrations of beta-VLDL and LDL, but not with HDL. When added in vitro to peritoneal macrophages from control pigeons, beta-VLDL stimulated a nearly 200-fold increase in cholesterol accumulation, but there was no relationship between the ability of beta-VLDL to stimulate macrophage cholesterol accumulation and the extent of atherosclerosis in the animal from which the beta-VLDL was obtained. Cholesterol feeding for up to 6 months increased the severity of atherosclerosis in both atherosclerosis-susceptible White Carneau and resistant Show Racer pigeons, but there was no correlation of atherosclerosis severity with beta-VLDL or HDL concentrations, and only a weak relationship with LDL concentrations. The results are consistent with the conclusion that atherosclerosis susceptibility in pigeons cannot be explained by quantitative or qualitative differences in plasma beta-VLDL. Instead, differences in susceptibility are probably mediated at the level of the arterial wall, perhaps by genetic differences that influence the way an individual animals' arterial cells (endothelial, smooth muscle, macrophages) interact with specific plasma lipoproteins.