PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “DIET, ATHEROGENIC”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2001

Maternal atherogenic diet in swine is protective against early atherosclerosis development in offspring consuming an atherogenic diet post-natally.

Atherosclerosis found early in life suggests that it may arise from fetal adaptations during development in utero. We evaluated the effect of a maternal atherogenic diet on atherosclerosis development in offspring. Aortic fat deposition was evaluated by Sudan IV staining and coronary atherosclerosis was assessed histologically. Sows were fed an atherogenic diet (ath) or standard diet (std) throughout gestation. Twelve neonates (six per maternal diet group) were evaluated with no significant differences noted (P>0.05) in serum lipids or aortic fat deposition and there was no evidence of coronary atherosclerosis. Twenty offspring (10 per maternal diet group) were followed for 5 months forming the pubertal age group. Half of these swine received an atherogenic (ATH) diet (std-ATH and ath-ATH) and half received a standard (STD) diet (std-STD and ath-STD). Pubertal age swine on the ATH diet had significantly greater (P<0.05) serum lipids and aortic fat deposition compared with those on the STD diet, with significantly greater fat deposition (P<0.05) occurring in the std-ATH versus ath-ATH group. Coronary atherosclerosis was exhibited only in the std-ATH diet group. Our findings suggest that gestational diet may alter the body's management of cholesterol later in life, possibly providing a protective effect from atherosclerosis.

Animals↗
PubMed1997

Effect of evening primrose oil on platelet aggregation in rabbits fed an atherogenic diet.

Evening primrose oil (Oenothera biennis) is a rich source of omega-6 series fatty acids. We report here the effects of dietary supplementation with evening primrose oil (EPO) on platelet aggregation as the main factor in arterial thrombus formation in an experimental model of atherogenesis in rabbits. A total of 40 male white New Zealand rabbits were divided into four groups (n = 10 animals/group): 1: normal diet, 2: atherogenic diet (ATD), 3: normal diet enriched with 15% EPO, 4: ATD + EPO. Each group was kept on the diet for 6 weeks. We determined serum lipid profile, platelet aggregation in whole blood, platelet thromboxane B2 production and platelet lipid peroxides. The atherogenic diet increased platelet aggregation (135% when ADP was used, and 185% when collagen was used as the inducer). Evening primrose oil reduced hyperaggregation to the values obtained in rabbits fed with the normal diet. Thromboxane synthesis was increased from 0.18 to 2.28 nmol/10(9) platelets); EPO reduced this value to 1.38 nmol/10(9) platelets. Lipid peroxides were increased by ATD from 0.27 to 0.81 nmol/10(8) platelets; EPO prevented this increase (0.35 nmol/10(8) platelets). In conclusion, EPO reduced platelet hyperaggregability in rabbits fed an atherogenic diet.

Animals↗
PubMedDate not supplied

Serum lipid picture of rabbits fed on silicate-supplemented atherogenic diet.

Silicon is recognised as a protective trace element in atherosclerosis by epidemiologic and biochemical studies. The goal of the present work was the evaluation of the antiatheromatous effect of the natrium silicate in an experimental trial on 30 rabbits given a standard diet (control), an atherogenic diet (L1 lot) and a natrium silicate-supplemented atherogenic diet (L2 lot), by comparing the variation of the lipid pictures between each of the experimental lots and control. Levels of total lipids, cholesterol, triglycerides (TG), free fatty acids (FFA) and phospholipids indicated that the natrium silicate supplemented to the atherogenic diet minimised the lipid metabolism unbalance by keeping constant the level of FFA and TG in rabbits.

Animals↗
PubMed1982

Endothelial morphology and plasma total and high density lipoprotein cholesterol changes in hypothalamically stimulated squirrel monkeys fed a modified atherogenic diet.

Experimental animals fed atherogenic diets show endothelial damage, impairment of endothelial regeneration and plasma lipid changes characterized by elevation of LDL and decrease of HDL cholesterol concentrations. Previous studies in this laboratory disclosed that chronic electrical stimulation of the lateral hypothalamus was associated with electron-microscopic evidence of endothelial injury in rats and squirrel monkeys maintained on basal (low fat/cholesterol-free) diets. In the present investigation squirrel monkeys fed similar diets supplemented with "modest" amounts of caloric fat and cholesterol were subjected to chronic lateral hypothalamic stimulation for periods as long as 20 months with the expectation that endothelial injury would be greater than in the absence of the supplements. The expectations were not substantiated. Endothelium was found to be surprisingly intact by electron microscopy and similar to that of implanted nonstimulated controls. A further observation of interest was the cholesterolemic response, notably in the HDL fraction, observed in both groups, but more striking in experimental animals. The data suggest that an interaction between a modified lipid/cholesterol diet and hypothalamic stimulation may lead to elevation of plasma HDL cholesterol concentration and preservation of endothelial integrity. Further investigation is required to determine whether these two events are causally related.

Animals↗
PubMed1983

Early morphological changes in the endothelium of a peripheral artery of rabbits fed an atherogenic diet.

The effect of an atherogenic diet on the endothelium of the central artery of the rabbit ear was studied by scanning and transmission electron microscopy. Examination of the inner surface of the artery after only 5 weeks on the diet revealed morphological changes including irregularly shaped cells, breaks at intercellular junctions, swelling of the membrane over the central part of the cells, and occasional holes in the cells. By 9 weeks more severe damage was seen including lifting off of cells and some holes. In addition, arrays of dark spots were seen by scanning electron microscopy in some cells in arteries of rabbits fed the diet for 5 to 9 weeks. The dark spots may correspond to abnormally large vacuoles seen inside endothelial cells by transmission electron microscopy. The central ear artery and aorta of some rabbits were tested for their ability to convert arachidonic acid into prostacyclin and thromboxane A2 by radioimmunoassay of the stable metabolites 6-keto-prostaglandin F1 alpha and thromboxane B2. The vessels from rabbits fed the atherogenic diet did not differ from vessels of rabbits on the control diet in their production of either metabolite.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Apo E levels and distribution in rhesus monkeys consuming an atherogenic diet.

The effect of an atherogenic diet on serum apo E levels and distribution among the lipoproteins of rhesus monkeys was studied. Animals able to maintain their serum cholesterol levels below 250 mg/dl (hyporesponders) showed no significant change in their serum apo E levels; however, in monkeys whose serum cholesterol concentrations ranged from 250 to 850 mg/dl, serum apo E levels appeared to have increased in direct proportion to plasma cholesterol concentration (r2 = 0.92) such that in monkeys whose serum cholesterol concentration exceeded 650 mg/dl (hyperresponders), the apo E levels had increased 5-6-fold. The majority of the apo E (60%) in hyporesponders consuming the atherogenic diet was associated with HDL, whereas only 10% of the serum apo E was associated with HDL in hypercholesterolemic hyperresponders. Nonetheless, the absolute amount of HDL-associated apo E was the same in both phenotypes. Thus, essentially all of the increase in serum apo E levels in hyperresponders was due to an increase in non-HDL-associated apo E. The mean density of the fraction showing the greatest increase in apo E, and accounting for the majority of the d less than 1.063 g/ml apo E in hyperresponders, was 1.010 g/ml. That fraction was distinct from the lipoproteins principally responsible for the increase in apo B and cholesterol levels in those animals. The latter were smaller in size and higher in density than the major apo E-rich fraction. Nonetheless, the d less than 1.063 g/ml apo E apparently circulates on apo B-containing particles, since it was retained on an anti-apo B immunoaffinity column. These data show that a diet-induced hypercholesterolemia is accompanied by a marked increase in serum apo E levels in rhesus monkeys, but that the lipoproteins principally responsible for the increase in apo E levels are distinct from those mainly responsible for the hypercholesterolemia. They also suggest that the levels of apo E-containing HDL in hypercholesterolemic hyperresponders are not significantly lowered by the diet, even though those animals' apo A-I levels were severely reduced. Thus, both the LDL and the HDL of the hypercholesterolemic primate contain apo E-rich subfractions which are metabolically distinct from the principal lipoprotein family in each fraction.

Animals↗
PubMedDate not supplied

Structural and hemodynamic response of peripheral arteries of macaque monkeys to atherogenic diet.

The arteries of monkeys given atherogenic diets develop marked intimal thickening and medial thinning, but luminal size apparently changes minimally. The hemodynamic significance of the atherosclerotic changes is therefore uncertain. To evaluate vascular function in atherosclerotic arteries, we studied the hind-limb vessels of adult male rhesus and cynomolgus monkeys to assess the structural and hemodynamic responses to an atherogenic diet given for about 1.5 years or for much longer periods (6.5 years for rhesus and 4.3 years for cynomolgus monkeys). The intimal cross-sectional area greatly increased after the atherogenic diet, but there was no significant luminal narrowing after either the 1.5-year diet or the longer diet periods. The media of atherosclerotic arteries showed focal atrophy and focal thinning after pressure fixation, but the total medial mass was not decreased even after the long diet periods. Hemodynamic studies indicated mild functional impairment in the atherosclerotic vessels; resting resistance increased and vasodilator responses decreased, but adrenergic responses were preserved. Thus, the marked changes that occur in the arterial wall in experimental primate atherosclerosis include adaptations to lesion formation that permit a long prestenotic phase of atherosclerosis in which vascular dysfunction is minimal.

Animals↗
PubMed2003

Effect of chronic treatment with the vasopeptidase inhibitor AVE 7688 and ramipril on endothelial function in atherogenic diet rabbits.

Cardiovascular disease is the major cause of death in Western nations, although improved possibilities regarding diagnosis and therapy now exist. Endothelial dysfunction is triggered by cardiovascular risk factors such as hypercholesterolaemia, hypertension, adiposity and smoking, contributing to the common endpoint of atherosclerosis. This study examined the pharmacological effects of angiotensin-converting enzyme (ACE) and combined ACE-neutral endopeptidase (NEP) (vasopeptidase) inhibitors on endothelial dysfunction in the model of hyperlipidaemic rabbits. The focus of the study was to assess endothelial function after treatment with the ACE-NEP inhibitor AVE 7688 (30 mg/kg/day) in comparison to the ACE inhibitor (ACE-I) ramipril (1 mg/kg/day). Different parameters, such as endothelial function, blood pressure (BP), expansion of plaques, endothelial nitric oxide (NO) and superoxide (O2-) release and plasma levels of various lipidaemic parameters were analysed. Control groups consisted of one group fed only with normal diet, one group fed only with atherogenic diet and the direct control group fed with varied diets (six weeks atherogenic diet followed by 12 weeks normal diet). Since for the treatment of atherosclerosis, a change in feeding is absolutely necessary, in the present study, at the start of the treatments with AVE 7688 and ramipril, the rabbits food was changed to a normal diet. At the end of the study, mean arterial blood pressure (MAP) was measured in the anaesthetised animals. The values in standard, atherogenic and varied diet-fed rabbits were around 73 2 mmHg. Angiotensin I (Ang I) given intravenous (i.v.) induced a strong increase in MAP of about 20%. In both the treated groups Ang I-induced BP increase was inhibited. In contrast, i.v. bradykinin led to a strong reduction in MAP in both the treated groups of around 50%. Six weeks feeding with an atherogenic diet in the rabbits induced an enduring endothelial dysfunction despite the food subsequently being changed to a normal chow. All measured parameters indicated a significant favourable effect on endothelial dysfunction as a result of the two treatment regimens. Endothelial function measured in the organ chamber showed somewhat greater improvement in the ACE-NEP treated group than in the ACE-I treated group. The treatment with ramipril, as well as with AVE 7688, restored endothelial function by increasing the ratio of NO to O2- concentration and bioavailability of NO. In this study, a similar protective effect on endothelial function was shown by ACE-NEP inhibition as already seen with ACE inhibitors in an animal model of atherosclerosis.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Clostridium difficile infection in hamsters fed an atherogenic diet.

Diarrhea and unexpected death were encountered in a group of young Syrian hamsters (Mesocricetus auratus) used for hyperlipoproteinemia and atherosclerosis research. The animals were fed an atherogenic diet containing 18% saturated fat and 0.366% cholesterol. Mortality began 45 days after hamsters were placed on this atherogenic diet. The atherogenic studies were aborted at 74 days because of high mortality. Toxigenic Clostridium difficile was isolated from animals found dead or euthanatized because of illness. Signs observed were unexpected death and acute liquid diarrhea. Characteristic pathologic changes were necrosis and hemorrhage of the intestinal mucosa with acute inflammation. Hepatic lipidosis was a consistent finding presumed to be associated with the consumption of the atherogenic diet. The study was repeated by placing 23 hamsters on the atherogenic diet and 10 hamsters on the control diet. In animals fed the atherogenic diet, the average time to mortality differed between studies, but clinical signs, gross and histologic lesions, culture findings, and toxin results in both atherogenic diet groups were similar. C. difficile was not isolated from the feeds. No antibiotics were found in the atherogenic diet. The results from these studies suggest that hamsters fed an atherogenic diet have increased susceptibility to disease caused by C. difficile as compared with hamsters fed a normal fat and cholesterol diet.

Animals↗
PubMed1991

Alterations in some lipid components and Ca2+ ATPase activity in brain of rats fed an atherogenic diet.

Male Wistar rats were fed an atherogenic diet for four months to investigate possible diet-induced lipid alterations and brain Ca2+ ATPase activity. Total cholesterol and triglyceride levels were found to be increased significantly in both serum and brain while the phospholipid level was decreased in both. The distribution of serum cholesterol between high-density and low-density lipoproteins was altered when compared to control rats with a decrement in HDL-cholesterol and a pronounced increment in LDL-cholesterol. The atherogenic diet resulted in about 50% depression in brain Ca2+ ATPase activity. It is concluded that alterations in ion transport and neurotransmitter release may be expected due to pronounced inhibition of brain Ca2+ ATPase activity in rats fed an atherogenic diet.

Animals↗
PubMed1992

Effect of fenofibrate on the tail artery contraction of rats fed with an atherogenic diet.

The feeding of rats by an atherogenic diet for 4 weeks modified the postsynaptic effect of noradrenaline in the perfused rat tail artery. When fenofibrate (100 mg/kg p.o.) was administered simultaneously, with an atherogenic diet, at the first onset of the experiment this effect was completely inhibited, while when it was administered from the 15th day of the experiment it had no effect on vasoconstrictor responses to noradrenaline. The atherogenic diet decreased the contraction of the rat tail artery at the lower concentrations (3 x 10(-8) - 3 x 10(-7) M) and increased vasoconstrictor response to a maximal concentration (10(-5) M) of noradrenaline. These results suggest that fenofibrate can prevent the changes in the contractile profile of an isolated atherogenic rat tail artery.

Animals↗
PubMed1982

Effect of plant proteins on cholesterol metabolism in growing rats fed atherogenic diets.

Weanling rats were fed atherogenic diets containing 2% cholesterol and 0.5% bile acids for 4 weeks. The experimental diets contained 10% protein derived from soy protein, wheat gluten, or wheat gluten supplemented with lysine and threonine. The control diet contained 10% protein derived from casein. Rats fed the plant proteins were found to have lower serum cholesterol and triglyceride levels, no detectable amounts of low density lipoprotein, a smaller amount of very low density lipoprotein and a higher concentration of high density lipoprotein (HDL) as compared to the control animals. There were no differences in the serum HDL-cholesterol level between the control and the experimental groups. It was shown that the hypocholesterolemic effect of wheat gluten is independent of the low lysine concentration or the ratio of lysine/arginine in it.

Animals↗
PubMedDate not supplied

Ascorbic acid and glycosaminoglycan and lipid metabolism in guinea pigs fed normal and atherogenic diets.

The effect of low and high doses of ascorbic acid on glycosaminoglycan and lipid metabolism was studied in guinea pigs fed both normal and atherogenic diets. The high dose of ascorbic acid (25 mg/100 g body weight/day) decreased the cholesterol level in the liver and aorta but not in the serum in animals fed the normal diet in comparison with those fed the low dose of ascorbic acid (0.1 mg/100 g body weight/day). In animals fed the atherogenic diet, cholesterol decreased in the serum and liver, but not in the aorta. Serum triglycerides were not affected by the dose of ascorbic acid in the group on the normal diet, but in the animals receiving the atherogenic diet, the high dose of ascorbic acid caused serum triglycerides to decrease when compared with the low dose. Hepatic and aortic triglycerides decreased in groups on normal and atherogenic diets receiving the high dose of ascorbic acid. Lipoprotein lipase activity was not affected in the aorta by the dose of ascorbic acid either in the normal or atherogenic diet group. It was increased in the liver and heart in both the groups receiving the low dose of ascorbic acid but decreased in the high dose group. The concentration of all the glycosaminoglycans significantly increased in the aorta of animals on normal diet receiving the high dose of ascorbic acid when compared with the low dose group. In the group on the atherogenic diet, hyaluronic acid was not affected, but all the sulphated glycosaminoglycans increased in the animals receiving the high dose when compared with those receiving the low dose. In the liver all the sulphated glycosaminoglycans increased while hyaluronic acid decreased in both the normal and atherogenic diet groups receiving the high rather than the low dose of ascorbic acid. L-Glutamine:D-fructose-6-phosphate aminotransferase and UDPG dehydrogenase, two key enzymes in the biosynthesis of precursors of glycosaminoglycans, were studied in relation to the dose of ascorbic acid. Hepatic aminotransferase activity was higher both in the normal and atherogenic diet groups when receiving the high rather than the low dose of ascorbic acid. UDPG dehydrogenase was not affected by the dose of ascorbic acid. The activities of the degrading enzymes -- hyaluronidase, beta-glucuronidase, beta-hexosaminidase and aryl sulphatase -- significantly increased both in the normal and atherogenic diet groups when receiving the low rather than the high dose of ascorbic acid. The concentration of PAPS, sulphate activity and sulphotransferase activity were all increased in both the normal and atherogenic diet groups receiving the high dose of ascorbic acid.

Animals↗