Search PubMed⌕ Search

Biomedical subjects

D Kritchevsky

Publications and source records attributed to D Kritchevsky.

At least 37 records · Page 2Linked to original sources
PubMed1998

Early atherosclerotic plaques in the aorta following cytomegalovirus infection of mice.

We show here that BALB/c mice inoculated with murine cytomegalovirus (MCMV) express viral antigens in the endothelial and smooth muscle cells of the aortic wall, and that accumulation of inflammatory cells in the aortic lumen, similar to that seen in early atherosclerotic lesions in humans, colocalizes with the site of virus antigen expression. Immunosuppression of the mice at the time of virus infection increased the expression of viral antigens and the size of early atherosclerotic lesions in the intima. The percentage of the low-density lipoprotein cholesterol (LDL-C), the major lipid contributor to atherosclerotic plaques, was significantly increased in the serum of MCMV-infected mice, whether or not the mice were fed a high cholesterol diet. Human cytomegalovirus (HCMV) significantly increased the esterified cholesterol component of the total cholesterol in a human arterial smooth muscle cell line infected in vitro with HCMV. These results suggest that CMV infection is involved in two of the major mechanisms that lead to development of atherosclerosis, i.e., immune injury and high LDL-C.

Animals↗
PubMed1998

Effects of specific fatty acids (8:0, 14:0, cis-18:1, trans-18:1) on plasma lipoproteins, early atherogenic potential, and LDL oxidative properties in the hamster.

Although comparative studies of the cholesterolemic properties of trans fatty acids relative to cis-unsaturates and saturates have been conducted in humans and animals, there is no recent information relating these lipid responses to susceptibility to atherosclerosis. Therefore, hamsters were fed diets containing equivalent amounts of cholesterol (0.12% wt/wt) and test fats (20% wt/wt) for 8 weeks. Each test fat contained between 50-52% of the-total triacylglycerols as a single fatty acid, i.e., 8:0, 14:0, 18:0, cis-18:1, or trans-18:1 while the balance consisted of 16:0, cis-18:1 and 18:2 that were the same for all groups. Plasma total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), and high density lipoprotein cholesterol (HDL-C) levels were not different for 8:0, cis-18:1, and trans-18:1, whereas 14:0 caused a significant rise in plasma TC, LDL-C, and HDL-C. LDL oxidation measurements showed that the lag phase of conjugated diene formation was longest for the trans-18:1 and cis-18:1 groups while rate of conjugated diene formation was lowest for the trans-18:1 and cis-18:1 groups. The trans-18:1- and cis-18:1-fed animals had significantly higher levels of LDL alpha-tocopherol relative to the 8:0- and 14:0-fed animals. Aortic fatty streak formation was highest for the 14:0- and 8:0-fed animals and lowest for the trans-18:1. In conclusion, the plasma lipid and antioxidant properties of trans-18:1 and cis-18:1 were comparable while the trans-18:1-fed hamsters had the least amount of early atherosclerosis. In addition, 8:0-fed animals unexpectedly had early atherosclerosis formation similar to the 14:0-fed animals.

Animals↗
PubMed1997

Interaction of fiber and energy registration in experimental colon carcinogens.

Male, F344 rats were fed ad libitum diets in which the fiber was either 10% wheat bran or 4% cellulose. The diets contained equivalent amounts of fiber. Other groups were fed wheat bran or cellulose-containing diets which were pair fed to the controls to provide 10, 20, or 30% energy restriction (ER). Colon cancer was induced by five weekly feedings of DMH. After 28 weeks, colon tumor incidence in the ad libitum fed groups was: cellulose 70%, wheat bran 42%. At 10, 20, or 30% ER tumor incidence was 46, 29, and 21% in rats fed cellulose and 17, 17, and 21% in those fed wheat bran, respectively. The data confirm the greater protective action of wheat bran compared to cellulose.

1,2-Dimethylhydrazine↗
PubMed1997

Phytosterols.

Explore the source record for details and available documents.

Absorption↗
PubMed1997

Trans fatty acids and cardiovascular risk.

The major source of trans unsaturated fatty acid bearing fats (trans fats) is the partially hydrogenated fats present in margarines, salad and cooking oils. When ingested, trans fats are deposited in tissues but disappear when the nutritional stimulus is removed. They have no adverse effects on growth or reproduction in rats. Trans fats are hypercholesterolemic for rabbits and monkeys but no more atherogenic than their cis counterparts. In man, trans fats elevate cholesterol but the extent of elevation may depend on the level of dietary linoleic acid. In some, but not all, studies they elevate Lp(a); the difference may reflect the presence of specific trans isomers--an area that merits further studies. Tissue of subjects with coronary disease contain no more trans fatty acids than those of controls. Reviews of the literature by expert committees in the US and UK conclude that at current levels of intake dietary trans fats pose no health problems. However, more research is needed especially with regard to pregnancy, lactation, and neonatal health. Current concerns should not deflect our attention from the larger aspects of fat and health.

Animals↗
PubMed1997

Dietary fibre and cancer.

Early epidemiological studies suggested that dietary fibre could be protective against colon cancer. Many isolated fibres were tested for anticarcinogenic activity in carcinogen-treated rats. Wheat bran was consistently protective. Some human studies suggest that dietary wheat bran may protect against growth of colon adenomas. The precise mechanism by which fibre exerts its effects is still elusive. Fibre exerts many influences in the digestive tract. It can dilute the tract contents, and studies show that decreased concentration of faecal bile acids is correlated with reduced cancer risk. Fibre may enhance energy excretion and caloric intake has been correlated positively with cancer risk. Bacterial degradation of fibre produces, among other compounds, butyric acid which may affect colonic and faecal pH and also shows antiproliferative activity. More data are needed vis-à-vis effects of dietary fibre on human colon cancer. These should include studies of specific fibres as well as of high fibre diets. The mechanism(s) of fibre action, including effects on oncogenes, steroid metabolites and short chain fatty acids, requires elucidation.

Animals↗
PubMed1997

Dietary conjugated linoleic acid reduces plasma lipoproteins and early aortic atherosclerosis in hypercholesterolemic hamsters.

Conjugated linoleic acid is a collective term used to designate a mixture of positional and geometric isomers of linoleic acid in which the double bonds are conjugated. Unlike linoleic acid, there is a paucity of information regarding the effect of dietary conjugated linoleic acid on plasma lipoproteins and aortic atherosclerosis. Therefore, fifty hamsters were divided into five groups of ten and fed 0 (Control), 0.06 (LOW), 0.11 (MEDIUM), and 1.1 (HIGH) en% conjugated linoleic acid or 1.1 en% linoleic acid. Blood samples were taken at 4, 8 and 11 weeks for plasma lipid analyses and for plasma tocopherol assay at sacrifice. Animals fed the conjugated linoleic acid-containing diets collectively had significantly reduced levels of plasma total cholesterol, non-high density lipoprotein cholesterol, (combined very low and low density lipoprotein) and triglycerides with no effect on high density lipoprotein cholesterol, as compared to CONTROLs. Linoleic acid-fed animals relative to CONTROLs also had reduced plasma total cholesterol, non-high density lipoprotein cholesterol and triglycerides, but only the latter was statistically significant. Compared to the CONTROL group, plasma tocopherol/total cholesterol ratios determined from plasma pools for the LOW, MEDIUM and HIGH conjugated linoleic acid and linoleic acid groups were increased by 48%, 48%, 86% and 29%, respectively, suggesting a tocopherol-sparing effect, at least for the conjugated linoleic acid treatment. Morphometric analysis of aortas revealed less early atherosclerosis in the conjugated linoleic acid and linoleic acid-fed hamsters compared to the CONTROL group.

Animals↗
PubMed1996

A new dietary model to study colorectal carcinogenesis: experimental design, food preparation, and experimental findings.

Experimental dietary studies of human colorectal carcinogenesis are usually based on the AIN-76A diet, which is dissimilar to human food in source, preparation, and content. The aims of this study were to examine the feasibility of preparing and feeding rats the diet of a specific human population at risk for colorectal neoplasia and to determine whether changes in the colonic morphology and metabolic contents would differ from those resulting from a standard rat diet. The mean daily food intake composition of a previously evaluated adenoma patient case-control study was used for the "human adenoma" (HA) experimental diet. Foods were prepared as for usual human consumption and processed by dehydration to the physical characteristics of an animal diet. Sixty-four female Sprague-Dawley rats were randomized and fed ad libitum the HA or the AIN-76A diet. Every eight weeks, eight rats from each group were sacrificed, and the colons and contents were examined. Analysis of the prepared food showed no significant deleterious changes; food intake and weight gain were similar in both groups. Compared with the controls, the colonic contents of rats fed the HA diet contained significantly less calcium, concentrations of neutral sterols, total lipids, and cholic and deoxycholic acids were increased, and there were no colonic histological changes other than significant epithelial hyperproliferation. This initial study demonstrated that the HA diet can be successfully processed for feeding to experimental animals and is acceptable and adequate for growth but induces significant metabolic and hyperproliferative changes in the rat colon. This dietary model may be useful for studies of human food, narrowing the gap between animal experimentation and human nutritional research.

Adenoma↗
PubMed1996

Effect of sesame oil on serum and liver lipid profiles in the rat.

In our previous study (Satchithanandam, S., Reicks, M., Calvert, R.J., Cassidy, M.M. and Kritchevsky, D. (1993) J. Nutr. 123, 1852-1858), we found that the absorption of lymphatic cholesterol by rats fed diets containing 24% sesame oil was about 50% less than that by rats fed the control diet containing no sesame oil. The effect of sesame oil on serum cholesterol levels was not determined at that time. In the present study, three groups of male Wistar rats (75-100 g) were fed a control diet or a diet containing 12 or 24% sesame oil. To increase serum cholesterol levels, 1% cholesterol and 0.5% cholic acid were added to each diet. After rats were fed for 4 weeks, total cholesterol, LDL-cholesterol, HDL-cholesterol, and triglyceride levels were measured in the serum. Liver weight and cholesterol and triglyceride levels were determined. Liver cholesterol levels were significantly lower in rats fed the 24% sesame oil diet, and the liver lipid level was significantly higher in the 24% sesame oil-fed group, compared with levels in the group fed the control diet. Liver weights and esterified cholesterol and liver triglyceride levels were not significantly different among the groups. Levels of serum total cholesterol and LDL-cholesterol were significantly lower in rats fed the 24% sesame oil diet, compared with levels in the control group. Serum triglyceride and HDL-cholesterol levels did not differ significantly among the groups. The mechanism by which a diet containing 24% sesame oil reduces levels of serum and liver cholesterol, liver LDL cholesterol, and liver lipids is not known. However, the high degree of unsaturation (85%) of sesame oil and the presence of linoleic acid may be important factors.

Animals↗
PubMed1995

Dietary protein, cholesterol and atherosclerosis: a review of the early history.

The first purely nutritional investigation into experimental atherosclerosis was carried out by Ignatowski in 1908. Believing that a toxic metabolite of animal protein led to atherosclerosis, he fed meat to adult rabbits and milk and egg yolk to weanling rabbits and caused atherosclerosis. For the next two decades experimental efforts from many laboratories were directed at determining which, if any, animal protein was the most atherogenic. The discovery in 1912 that dietary cholesterol per se was atherogenic turned attention to fat and cholesterol, eclipsing work on dietary protein. In 1926 Clarkson and Newburgh showed that the amount of cholesterol present in the animal protein they fed was insufficient to be atherogenic, demonstrating that some factor other than lipid determined atherogenicity. In 1940 Meeker and Kesten showed that animal protein (casein) was more atherogenic that plant protein (soy). Carroll and his co-workers showed that most proteins of animal origin were more cholesterolemic for rabbits than were proteins of vegetable origin, although there was some overlap. Cholesterol turnover is slower and fecal excretion of cholesterol is reduced in rabbits fed casein as opposed to those fed soy protein. The mechanisms underlying this effect are moot.

Animals↗
PubMed1995

The effect of over- and undernutrition on cancer.

Overnutrition, as a factor in carcinogenesis, has been a matter of concern for over 80 years. Overnutrition relates to excess intake of calories, and fat is the major contributor to caloric burden. Thus, fat has been the focus of many epidemiological studies, but as long ago as 1975 some investigators were suggesting that excess energy intake might be the major factor relating to cancer incidence. Ecological studies support the idea that a high fat (high energy?) diet may represent a risk for cancer but case-control or follow-up studies generally do not. The effects of undernutrition have been studied experimentally. Mostly conducted in rats or mice, they show virtually uniformly that caloric (energy) restriction inhibits the growth of spontaneous, transplanted or induced tumours. The effect is observed even when the calorie-restricted animals ingest more fat than do the controls. Energy utilization via exercise reduces tumour growth in rats and a life history of physical labour reduces risk in man. The mechanism(s) by which caloric restriction exerts its effects are moot, but it has been shown to reduce insulin levels and to reduce oncogene expression. Energy restriction also increases activity of antioxidant enzymes and leads to enhanced DNA repair. Increased energy flux (by means of decreased intake or increased output) may provide a simple and inexpensive approach to reducing the risk of cancer in man.

Animals↗
PubMed1995

Influence of psyllium preparations on plasma and liver lipids of cholesterol-fed rats.

Rats were fed a semi purified diet containing 0.5% cholesterol and 10% fiber (cellulose, pectin, psyllium seed and defatted psyllium husk). One additional group of rats was fed cholesterol (0.5%) as part of a fiber-free diet and another was fed the fiber free diet without cholesterol. Cellulose had virtually no effect on serum or liver lipids. Pectin had a lipid lowering effect. Psyllium seed exerted an effect on total serum cholesterol equal to that of pectin but gave higher levels of HDL-cholesterol. The effects of psyllium seed on liver lipids were more pronounced than those of pectin. Defatted psyllium husk feeding virtually normalized liver size and serum triglyceride levels and produced lower serum total cholesterol levels and higher HDL-cholesterol than observed in normal controls. Defatted psyllium husk feeding also yielded liver lipid values which were in the normal range. Fecal wet and dry weights were significantly higher in rats fed either psyllium preparation.

Analysis of Variance↗