scholarly journals Effect of Consumption Heated Oils with or without Dietary Cholesterol on the Development of Atherosclerosis

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1527 ◽  
Author(s):  
Che Idris ◽  
Kalyana Sundram ◽  
Ahmad Razis

Heating oils and fats for a considerable length of time results in chemical reactions, leading to the aggravation of a free radical processes, which ultimately contributes to atherosclerosis. Our study focused on elucidating the effect of feeding heated oils with or without dietary cholesterol on the development of atherosclerosis in rabbits. We heated palm olein and corn oil at 180 °C for 18 h and 9 h per day, respectively, for two consecutive days. Next, 20 male rabbits were divided into four groups and fed the following diet for 12 weeks: (i) heated palm olein (HPO); (ii) HPO with cholesterol (HPOC); (iii) heated corn oil (HCO); and (iv) HCO with cholesterol (HCOC). Plasma total cholesterol (TC) was significantly lower in the HCO group compared to the HCOC group. Atherosclerotic lesion scores for both fatty plaques and fatty streaks were significantly higher in the HCO and HCOC groups as compared to the HPO and HPOC groups. Additionally, fibrous plaque scores were also higher in the HCO and HCOC groups as compared to the HPO and HPOC groups. These results suggest that heated palm oil confers protection against the onset of atherosclerosis compared to heated polyunsaturated oils in a rabbit model.

1965 ◽  
Vol 209 (4) ◽  
pp. 773-780 ◽  
Author(s):  
Helen M. Tepperman ◽  
Jay Tepperman

The aggregate hexosemonophosphate dehydrogenase (HMPD) activity was found to be higher in livers of rats fed a diet containing saturated fat (hydrogenated coconut oil = H) for 7 days and fasted for 48 hr than it was in similarly prepared animals fed a corn oil (CO) diet. Later, a liver HMPD-increasing effect of feeding H was found in nonfasted animals. Lipogenesis (i.e., the incorporation of acetate-1-C14 into fatty acids by liver slices) was shown to be as low or lower in the H group as in the CO. Liver slices prepared from H and CO diet adapted rats were incubated with either acetate-1-C14 or palmitate-1-C14 and the extent of incorporation of C14 into individual fatty acids was measured. With both substrates more radioactivity was found in 16:1, 18:0, and 18:1 in the case of H-fed animals. It is proposed that a component of the signal for eliciting increased NADP-linked enzyme activity in the H rats was an increased rate of oxidation of NADPH attendant on monoene formation and chain lengthening.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
William S Kerwin ◽  
Jerry Ricks ◽  
Michael Rosenfeld

Recent studies have used dynamic contrast-enhanced (DCE) MRI to quantify the rate of uptake of gadolinium contrast agents in atherosclerotic plaque. The transfer constant K trans , that quantifies the blood supply and permeability of the plaque, shows strong association with plaque inflammation. The purpose of this study was to explore the link between K trans and plaque inflammation in a model of early atherosclerotic lesion development. Twelve NZW rabbits were placed on a 0.2% cholesterol diet and underwent balloon injury of the descending aorta. After 12 weeks, all rabbits underwent a DCE-MRI exam, after which 6 were euthanized and perfusion fixed to harvest the atherosclerotic aortas. The remaining 6 were imaged again at 24 weeks and their aortas were harvested. The DCE-MRI procedure utilized a unique, high-speed, small field-of-view imaging technique with quadruple inversion recovery blood suppression (turbo spin echo, TR=800 ms, TE=9ms, 3mm slice thickness, 0.5mm in-plane resolution). This allowed us to observe enhancement of the vessel wall without contamination from enhancement of the adjacent lumen. The DCE-MRI results were analyzed to determine the average, relative K trans in the vessel wall and compared to histological assessments of the aortas. K trans was significantly higher at 6 months compared to 3 months within the same animals (p<0.005) and compared to those euthanized at 3 months (p<0.001). No difference was observed between the two groups at 3 months (p=0.4). Histologically, aorta cross sections at 6 months had lesions that were no thicker than those at 3 months (0.49 vs. 0.45mm, p=0.6), but complex lesion features including necrotic cores, intraplaque hemorrhage, neovessels, and deep clusters of macrophages were significantly more common at 6 months (82% vs. 18%, p<0.001). The transformation of the lesions from simple to complex morphologies from 12 weeks to 24 coincided with a significant rise in K trans . We attribute this rise to the development of neovessels in response to pro-inflammatory stimuli. We conclude that K trans can be used to probe lesion characteristics and complexity in early atherosclerosis, with applications in early diagnosis and treatment monitoring. This research has received full or partial funding support from the American Heart Association, AHA Pacific/Mountain Affiliate (Alaska, Arizona, Colorado, Hawaii, Idaho, Montana, Oregon, Washington & Wyoming).


2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Govindasamy Ilangovan ◽  
Krishnamurthy Karthikeyan

Objective: Coronary heart disease and diabetes are highly prevalent among obese populations due to aberrant dietary cholesterol metabolism. Here we investigated the effect of heat shock factor-1 (HSF-1) on atherosclerosis and dietary cholesterol metabolism. Methods and Results: Atherogenic western diet-induced weight gain was reduced in HSF-1 and LDLr double knock out mice (HSF-1 -/- /LDLr -/- ), compared to LDLr -/- mice. Atherosclerotic lesion growth in aortic arch and carotid regions was retarded. Also, repression of PPAR-γ2 and AMPKα expression in adipose tissue, low hepatic steatosis, and lessened plasma adiponectins and lipoproteins were observed. Furthermore, reduced heat shock proteins and their mRNA levels in atherosclerotic lesions correlated with reduction in lesion burden. In HSF-1 -/- /LDLr -/- liver, higher cholesterol 7α hydroxylase (CYP7A1, the rate limiting enzyme in the synthesis of bile acid from cholesterol) and MDR1/p-glycoprotein (bile salt transporter across the hepatocyte canalicular membrane) gene expressions were observed, consistent with higher bile acid sequestration and larger hepatic bile ducts. HSF-1 deletion, however, upregulated both CYP7A1 enzyme and MDR1/p-glycoportein expression and activities, due to removal of its repressive binding in the CYP7A1 and MDR1 gene promoters. This increased the conversion of cholesterol into 7-α-hydroxycholesterol and bile acid, and dietary cholesterol metabolism. Conclusions: HSF-1 ablation not only eliminates heat shock response to retard atherosclerosis, but it also transcriptionally upregulates CYP7A1 and MDR1/P-gp axis to increase cholesterol metabolism. Therefore, HSF-1 is a metabolic regulator of dietary cholesterol and a major contributor to heart disease among obese population.


1961 ◽  
Vol 201 (1) ◽  
pp. 179-184 ◽  
Author(s):  
C. S. N. Setty ◽  
A. C. Ivy

Rats were fed a sterol, fat free synthetic diet plus 9% corn oil, the sterol content being known. One group received streptomycin and Sulfasuxidine in the diet at a level of 0.2% and 1%, respectively; another, 200 mg and 500 mg daily of Terramycin and Sulfathalidine (TS), respectively. Cholesterol-4-C14 was added to the diet, and the fecal C14 in the unsaponifiable (UM) and the digitonin-precipitable material (DM) and the "bile acid fraction" was determined. The antimicrobial agents had no significant effect on the output of C14 in the UM. In the TS, the output of C14 in the UM and DM was the same, showing that a marked reduction in intestinal flora prevents the change of digitonin-precipitable into nondigitonin-precipitable material. The C14 output in the UM or DM was used as a basis for calculation, and 68 and 76%, respectively, of the dietary cholesterol was absorbed. In the TS group, using either the UM or the DM, the absorption was 70%. The differences represented by the three percentages are not statistically significant.


1957 ◽  
Vol 190 (2) ◽  
pp. 214-220 ◽  
Author(s):  
T. M. Lin ◽  
Esko Karvinen ◽  
A. C. Ivy

The exclusion of pancreatic juice had no significant effect on elimination of endogenous cholesterol in the rat but increased it slightly in three dogs. Forty per cent of the dietary cholesterol was absorbed without and with pancreatic exclusion in the presence of a fat-free diet. Hence, pancreatic juice is not specifically necessary for the absorption of cholesterol. Pancreatic exclusion had no effect on the absorption of either dietary cholesterol or fatty acid, or both, when oleic and palmitic acid were fed. This indicates that any effect pancreatic exclusion may exert on cholesterol absorption when a fat containing diet is fed depends on the change in the utilization of the fat resulting from the exclusion. In the case of corn oil, triolein, trielaidin and tallow but not with tripalmitin, pancreatic exclusion was followed by an increased fecal elimination of both fatty acid and cholesterol. The increment of fatty acid elimination was large enough to dissolve the excess cholesterol excreted in the rats with pancreatic exclusion, except in the case of trielaidin. The only statistically significant decrease in the absorption of dietary cholesterol which resulted from pancreatic exclusion occurred when one of the unsaturated fatty acid esters, namely, corn oil, triolein, or trielaidin was the fat fed. These observations fail to show that pancreatic cholesterol esterase plays a specifically essential role in the absorption of free dietary cholesterol.


Nutrients ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1839
Author(s):  
Che Che Idris ◽  
Kalyana Sundram ◽  
Ahmad Abdull Razis

The authors wish to make the following change to their paper (Che Idris et al. [...]


2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Bradley K Wacker ◽  
Jingwan Zhang ◽  
Nagadhara Dronadula ◽  
David A Dichek

Background: Gene therapy, delivered directly to the vascular wall, could potentially protect against atherosclerotic lesion growth or regress existing lesions. Previously, we demonstrated that use of a helper-dependent adenoviral vector (HDAd) to express apolipoprotein (apo) A-I in carotid endothelium of fat-fed rabbits reduced carotid atherosclerosis measured 4 wk after vector infusion. Here we tested whether the same HDAd could promote atherosclerosis regression when delivered to existing lesions. Methods: To generate atherosclerotic lesions, rabbits were fed a high-fat diet for 4 wk, then underwent bilateral carotid artery surgery with brief intraluminal infusion of DMEM. This protocol yields large lipid- and macrophage-rich lesions within 6 mo. Postoperatively, diets were adjusted to maintain plasma cholesterol of 200 - 800 mg/dl. 6 mo later, rabbits underwent bilateral carotid gene transfer (HDAdApoAI on one side; HDAdNull on the other, with sides randomized) and were changed to chow diet. Carotids were harvested after 3 d (for RNA analysis) and after 7 wk (for analyses of RNA, DNA, and histology). Histologic sections were stained with H&E, oil red O, or antibodies that detect macrophages, smooth muscle actin, ICAM1, and VCAM1. Results: ApoA-I mRNA was detected only in arteries transduced with HDAdApoAI and was present in all HDAdApoAI-infused arteries both at 3 d and 7 wk after infusion. When compared to HDAdNull-infused arteries (n = 26), HDAdApoAI-infused arteries (n = 26) had 30 - 40% less median intimal lesion volume, lipid content, and macrophage content but these differences were not statistically significant (P = 0.3 - 0.9). Post-hoc subgroup analysis of small-to-moderate-sized lesions (n = 20 per group; excluding lesions with volume >1 SD above the mean of all lesions) showed that HDAdApoAI-infused lesions had 50 - 70% less median intimal volume (P = 0.04), lipid content (P = 0.02), and macrophage content (P = 0.03). Conclusions: 7 wk of vascular gene therapy with HDAdApoAI did not consistently cause lesion regression. However, subgroup analysis showed that HDAdApoAI significantly accelerated regression of small-to-moderate-sized atherosclerotic lesions. Prospective testing is required to evaluate the reproducibility of this finding.


2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Bernard G. Schreurs

A rabbit model of Alzheimer’s disease based on feeding a cholesterol diet for eight weeks shows sixteen hallmarks of the disease including beta amyloid accumulation and learning and memory changes. Although we have shown that feeding 2% cholesterol and adding copper to the drinking water can retard learning, other studies have shown that feeding dietary cholesterol before learning can improve acquisition and feeding cholesterol after learning can degrade long-term memory. We explore the development of this model, the issues surrounding the role of copper, and the particular contributions of the late D. Larry Sparks.


Sign in / Sign up

Export Citation Format

Share Document