Dietary fat and cholesterol induced modification of minipig lipoprotein fluidity and composition.

1. Miniature swine were fed a low (2.7%) fat control stock diet alone or supplemented with either 20% lard plus 1% cholesterol or 20% lard alone for periods of up to 6 months. 2. Cholesterol feeding reduced VLDL fluidity drastically and LDL fluidity minimally but had no effect on HDL fluidity. 3. Lard feeding had no effect on lipoprotein fluidity. 4. The rigid VLDL produced by cholesterol feeding was enriched in cholesterol and phospholipid contents, similar to beta-VLDL. 5. Plasma cholesterol concentrations were increased by 1.5 to 5-fold in pigs fed stock diets supplemented with 20% lard, with or without added cholesterol, but plasma triacylglycerol concentrations were not affected by either diet modification. 6. Diet effects were complete within 4 weeks with no further changes for periods up to 6 months. 7. Regression of the induced hypercholesterolemia was also accomplished within one month of removing cholesterol from the diet.     

Genes, variation of cholesterol and fat intake and serum lipids

Several studies have examined gene-diet interactions in the response of plasma lipid concentrations to changes in dietary fat and/or cholesterol. Among the gene loci examined, APOE has been the most studied, and the current evidence suggests that this locus might be responsible for some of the interindividual variability in dietary response. Other loci, including APOA4, APOA1 and APOB have also been found to account for some of the variability in the fasting and fed states.     

Dietary taurine enhances cholesterol degradation and reduces serum and liver cholesterol concentrations in rats fed a high-cholesterol diet

Summary.  The effect of taurine on hypercholesterolemia induced by feeding a high-cholesterol (HC) diet (10 g/kg) to rats was examined. When taurine was supplemented to HC for 2 wk, serum total cholesterol significantly decreased and serum HDL-cholesterol increased compared with the HC diet group. In the hypercholesterolemic rats fed the HC diet, the excretion of fecal bile acids and hepatic cholesterol 7α-hydroxylase (CYP7A1) activity and its mRNA level increased significantly, and the supplementation of taurine further enhanced these indexes, indicating an increase in cholesterol degradation. Agarose gel electrophoresis revealed that, in hypercholesterolemic rats fed the HC diet, the serum level of the heavier VLDL increased significantly, but taurine repressed this increase and normalized this pattern. Significant correlations were observed between the time-dependent increase of CYP7A1 gene expression and the decrease of blood cholesterol concentration in rats fed the HC diet supplemented with taurine. These results suggest that the hypocholesterolemic effects of taurine observed in the hypocholesterolemic rats fed the HC diet were mainly due to the enhancement of cholesterol degradation and the excretion of bile acid. Received December 4, 2001 Accepted January 2, 2002 Published online September 10, 2002 Acknowledgment This work was supported by a grant of Taisho Pharmaceutical Co., Ltd (Japan). We thank J. I. Gordon for their generous gifts of cDNAs. Authors' address: Dr. Hidehiko Yokogoshi, School of Food and Nutritional Sciences, The University of Shizuoka, Shizuoka 4228526, Japan, E-mail: yokogosi@u-shizuoka-ken.ac.jp     

Dietary cholesterol and atherosclerosis

The perceived relationship between dietary cholesterol, plasma cholesterol and atherosclerosis is based on three lines of evidence: animal feeding studies, epidemiological surveys, and clinical trials. Over the past quarter century studies investigating the relationship between dietary cholesterol and atherosclerosis have raised questions regarding the contribution of dietary cholesterol to heart disease risk and the validity of dietary cholesterol restrictions based on these lines of evidence. Animal feeding studies have shown that for most species large doses of cholesterol are necessary to induce hypercholesterolemia and atherosclerosis, while for other species even small cholesterol intakes induce hypercholesterolemia. The species-to-species variability in the plasma cholesterol response to dietary cholesterol, and the distinctly different plasma lipoprotein profiles of most animal models make extrapolation of the data from animal feeding studies to human health extremely complicated and difficult to interpret. Epidemiological surveys often report positive relationships between cholesterol intakes and cardiovascular disease based on simple regression analyses; however, when multiple regression analyses account for the colinearity of dietary cholesterol and saturated fat calories, there is a null relationship between dietary cholesterol and coronary heart disease morbidity and mortality. An additional complication of epidemiological survey data is that dietary patterns high in animal products are often low in grains, fruits and vegetables which can contribute to increased risk of atherosclerosis. Clinical feeding studies show that a 100 mg/day change in dietary cholesterol will on average change the plasma total cholesterol level by 2.2-2.5 mg/dl, with a 1.9 mg/dl change in low density lipoprotein (LDL) cholesterol and a 0.4 mg/dl change in high density lipoprotein (HDL) cholesterol. Data indicate that dietary cholesterol has little effect on the plasma LDL:HDL ratio. Analysis of the available epidemiological and clinical data indicates that for the general population, dietary cholesterol makes no significant contribution to atherosclerosis and risk of cardiovascular disease.     

Dietary fat and carcinogenesis.

Epidemiologic investigations have suggested a relationship between dietary fat intake and various types of cancer incidences. Furthermore, epidemiologic studies as well as studies with animal models have demonstrated that not only the amount but also the type of fat consumed is important. At present, the mechanism by which dietary fat modulates carcinogenesis has not been elucidated. The effects of dietary fat on the development of tumours have been summarized in the present review with emphasis on colorectal, pancreas, breast and prostate cancer. It is concluded that influence on synthesis of prostaglandins and leukotrienes may be the universal mechanism by which dietary fats modulate carcinogenesis.     

Subcutaneous fat accumulation shows a beneficial correlation with serum cholesterol in postmenopausal Japanese women

This study aimed to investigate whether accumulation of subcutaneous abdominal fat has a beneficial correlation with lipid metabolism in premenopausal and/or postmenopausal Japanese women. The study enrolled 146 premenopausal women, ranging in age from 19 to 54 years, and 82 postmeno-pausal women, ranging in age from 47 to 66 years. Fat distribution, including abdominal visceral fat area (VFA) and abdominal subcutaneous fat area (SFA), were measured in an outpatient clinic by magnetic resonance imaging. Homogeneity of the regression slopes for SFA to total cholesterol (P = 0.030), low-density lipoprotein cholesterol (P = 0.020), apolipoprotein B (apoB) (P = 0.001), and the ratio of apoB to apolipoprotein A-I (apoA-I) (P = 0.003) were not found between premenopausal and postmenopausal women, even after adjustment for both VFA and age. However, the regression slopes for VFA to all measured lipid parameters, as well as apolipoproteins, were homogeneous between the premenopausal and postmeno-pausal groups. Abdominal SFA in postmenopausal women correlated negatively with total cholesterol (P = 0.007), low-density lipoprotein cholesterol (P = 0.002), apoB (P < 0.001), and the ratio of apoB to apoA-I (P = 0.001), after adjustment for age and VFA, but this was not the case in premenopausal women. The mechanisms involved in the beneficial effects of subcutaneous fat accumulation in postmenopausal women remain obscure, but upregulated aromatase expression, derived from adipose tissue, may possibly improve lipid and apolipoprotein metabolism.     

Dietary fat and cancer trends--a critique

Recent speculation concerning the relationship of dietary fat and cancer causation is challenged. Correlations between increase in per capita dietary fat intake and cancer mortality over a 60-year period show significant positive correlations for total fat and vegetable fat, and negative or no correlation for animal fat. The significant positive correlation for vegetable fat could not always be explained by the effects of total unsaturated components; individual unsaturated components, such as oleic or linoleic fatty acids; or the saturated component; but could be explained by the trans fatty acid component.