| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Dietary intervention and plasma cholesterol level in electricity workers Ciorlia, L. A. (1997), Arq Bras Cardiol 68(1): 21-5. Abstract: PURPOSE: To evaluate the efficacy of the diet on plasma cholesterol level above 200 mg/dL and to relate these values to age and occupation at the CPFL (Electricity Supply Company). METHODS: The participants were divided into 3 different groups (A, B and C), according to total cholesterol (TC): < 200 mg/dL (A), > or = 200 mg/dL and < 239 mg/dL (B) and > or = 240 mg/dL (C). Between 1983 and 1991, 688 workers of the company between 21 and 60 years, underwent dosages of TC with diet orientation: those having TC > 200 mg/dL, were identified in groups B and C. In addition to that, the participants were grouped according to their functions at the company. The TC level was dosed by Huang's modified colorimetric method. RESULTS: The mean TC level was 206 mg/dL. The nondiet group presented mean TC of 168 +/- 22.9 mg/dL in 1983 and 192 +/- 27.4 mg/dL in 1991 significantly higher compared to the initial value. Groups B and C, under standard diet, presented mean TC levels of 218 +/- 11.2 mg/dL and 266 +/- 22.5 mg/dL in 1983, respectively, 211 +/- 25.2 mg/dL and 229 +/- 34.4 mg/dL in 1991, with a significant decrease over time (p < 0.0001). In the working status, the managers presented mean TC values significantly higher than other occupations. CONCLUSION: The mean TC level of 206 mg/dL is considered high for Brazilians, and the distribution curve is similar to the American. The response to the standard diet was efficient, decreasing the TC in workers with values > 200 g/dL. Managers presented higher TC levels in relation to other functions, in addition to older age and different job conditions. |
| Dietary intervention for cholesterol reduction in public clinic patients Hyman, D. J., K. S. Ho, et al. (1998), Am J Prev Med 15(2): 139-45. Abstract: OBJECTIVES: To test the feasibility and effectiveness of a diet intervention (consisting of interactive mailings, computer-generated phone calls, and classes) in hypercholesterolemic low-income public clinic patients. METHODS: Clinic patients with serum cholesterol > 200 mg/dl, referred by their primary care physician were randomized to a 6-month special intervention (SI) or usual care (UC). The intervention included mailings, computer phone calls, and four 1-hour classes. Serum total cholesterol (TC) was measured before and after intervention, and participation was monitored. RESULTS: One hundred sixty-five of the 212 patients referred (77.8%) agreed to participate. A medical records review revealed 123 (74.5%) met eligibility criteria. Eligible subjects had a mean age of 56.7 years, 80.0% were African American, 74.8% were female, 33.6% were married, and 89.4% had a high school or lower education. Subjects were randomized with 80.5% (99) completing follow-up cholesterol measures. SI subjects were encouraged to use all three components, with 84.6% (55 of 65) actively participating in at least one component. Seventy-two percent (47 of 65) returned at least one mailing, 49.1% (28 of 57) of those with touch-tone phones accessed the computer system, and 43.1% (28 of 65) attended classes. The TC in SI decreased from 273.2 mg/dl to 265.0 mg/dl (P = 0.05) and in UC 272.4 mg/dl to 267.6 mg/dl (P = 0.32). The net reduction in SI compared with UC was 3.4 mg/dl (P = 0.58). CONCLUSIONS: (1) Low-income public clinic patients will participate in diet interventions, (2) computer-generated interactive phone calls are feasible in this population, and (3) clinically meaningful decreases in serum cholesterol are difficult to achieve with interventions of practical intensity. |
| Dietary inulin lowers plasma cholesterol and triacylglycerol and alters biliary bile acid profile in hamsters Trautwein, E. A., D. Rieckhoff, et al. (1998), J Nutr 128(11): 1937-43. Abstract: The mechanisms by which inulin may elicit its lipid-lowering effect are not well elucidated. To examine the lipid-lowering potential of inulin and especially its effect on bile acid metabolism, male golden Syrian hamsters were fed semipurified diets containing 20 g/100 g fat, 0.12 g/100 g cholesterol and 0 (control), 8, 12 or 16% inulin for 5 wk. Plasma total cholesterol concentrations were significantly lowered by 18, 15 and 29% in hamsters fed 8, 12 and 16% inulin, respectively. Dietary inulin specifically decreased VLDL cholesterol, which was significantly lower in hamsters fed 16% inulin compared with controls (1.1 +/- 0.3 vs. 2.9 +/- 0.6 mmol/L). LDL and HDL cholesterol were not significantly affected by dietary inulin. Plasma triacylglycerol was significantly reduced by 40 and 63% in hamsters fed 12 and 16% inulin, respectively. Hepatic total cholesterol and particularly esterified cholesterol accumulation were significantly lower in hamsters fed 8% inulin compared with controls. All three levels of dietary inulin caused distinct alterations in the bile acid profile of gallbladder bile. Taurochenodeoxycholic acid was significantly lower, whereas glycocholic and glycodeoxycholic acid were greater in hamsters fed inulin. Daily fecal bile acid excretion (micromol/d) tended to be greater (P = 0.056) in inulin-fed hamsters compared with controls, whereas daily neutral sterol excretion was not affected. These data demonstrate that the lipid-lowering action of inulin is possibly due to several mechanisms, including altered hepatic triacylglycerol synthesis and VLDL secretion and impaired reabsorption of circulating bile acids. |
| Dietary iron elevates LDL-cholesterol and decreases plasma antioxidant levels: influence of antioxidants Pool, G. F. and H. van Jaarsveld (1998), Res Commun Mol Pathol Pharmacol 100(2): 139-50. Abstract: High body iron and LDL-cholesterol concentrations, and antioxidant deficiency, are regarded as risk factors for ischemic heart disease. Iron is well known for causing oxidative damage and antioxidants for their beneficial effects on radical scavenging. It is, however, unknown whether or not dietary iron causes depletion of plasma antioxidants; causes lipid peroxidation; alters HDL- and LDL-cholesterol, and triglyceride concentrations. Rats received diets differing only in iron concentration--15 mg/Kg, 35 mg/Kg, 150 mg/Kg or 300 mg/Kg diet. The second group of rats received antioxidants (alpha-tocopherol and beta-carotene) in their drinking water. Increasing dietary iron increased plasma lipid hydroperoxide and LDL-cholesterol concentrations, but did not affect HDL-cholesterol or triglyceride concentrations. It decreased antioxidants, alpha-tocopherol and retinol. Antioxidant supplementation inhibited the above changes. |
| Dietary isoflavones reduce plasma cholesterol and atherosclerosis in C57BL/6 mice but not LDL receptor-deficient mice Kirk, E. A., P. Sutherland, et al. (1998), J Nutr 128(6): 954-9. Abstract: Susceptibility to atherosclerosis is determined by a combination of genetic and environmental factors, including diet. Consumption of diets rich in soy protein has been claimed to protect against the development of atherosclerosis. Potential mechanisms include cholesterol lowering, inhibition of lipoprotein oxidation and inhibition of cell proliferation by soy proteins or isoflavones, such as genistein, that are present in soy. This study was designed to determine whether soy isoflavones confer protection against atherosclerosis in mice and whether they reduce serum cholesterol levels and lipoprotein oxidation. C57BL/6 and LDL receptor-deficient (LDLr-null) mice were fed soy protein-based, high fat diets with isoflavones present (IF+, 20.85 g/100 g protein, 0.027 g/100 g genistein, 0.009 g/100 g daidzein) or diets from which isoflavones, and possibly other components, had been extracted (IF-, 20.0 g/100 g protein, 0.002 g/100 g genistein, 0.001 g/100 g daidzein). Because LDLr-null mice develop extensive atherosclerosis and hypercholesterolemia after minimal time on a high fat diet, they were fed the diets for 6 wk, whereas C57BL/6 mice were fed the diets for 10 wk. Plasma cholesterol levels did not differ between LDLr-null mice fed IF- and those fed IF+, but were 30% lower in C57BL/6 mice fed the IF+ diet than in those fed the IF- diet. Susceptibility of LDL to oxidative modification, measured as the lag phase of conjugated diene formation in LDLr-null mice, was not altered by isoflavone consumption. All LDLr-null mice developed atherosclerosis, and the presence or deficiency of dietary isoflavones did not influence atherosclerotic lesion area. In contrast, atherosclerotic lesion area was significantly reduced in C57BL/6 mice fed IF+ compared with those fed IF-. Thus, this study demonstrates that although the isoflavone-containing diet resulted in a reduction in cholesterol levels in C57BL/6 mice, it had no effect on cholesterol levels or on susceptibility of LDL to oxidative modification in LDLr-null mice. Further, dietary isoflavones did not protect against the development of atherosclerosis in LDLr-null mice but did decrease atherosclerosis in C57BL/6 mice. These findings suggest that soy isoflavones might lower cholesterol levels by increasing LDL receptor activity, and the reduction in cholesterol may offer some protection against atherosclerosis. |
| Dietary isohumulones, the bitter components of beer, raise plasma HDL-cholesterol levels and reduce liver cholesterol and triacylglycerol contents similar to PPARalpha activations in C57BL/6 mice Miura, Y., M. Hosono, et al. (2005), Br J Nutr 93(4): 559-67. Abstract: The effects of dietary isohumulones, the main components accounting for the bitter taste of beer, on lipid metabolism were examined. Young female C57BL/6N mice were fed diets containing isomerized hop extract (IHE), which consists mainly of isohumulones. Administration of IHE with an atherogenic (high-fat and high-cholesterol) diet for 2 weeks resulted in a significant increase in plasma HDL-cholesterol (P<0.01), along with a concomitant reduction in the atherosclerosis index, an increase in liver weight and a decrease in body weight gain in a dose-dependent manner. When animals received IHE with either a cholesterol or a basal diet for 1 week, significant decreases in the liver content of cholesterol (P<0.01) and triacylglycerol (cholesterol diet, P<0.01) were observed. Quantitative analyses of hepatic mRNA levels revealed that IHE administration resulted in up-regulation of mRNA for acyl-CoA oxidase, acyl-CoA synthetase, hydroxymethylglutaryl-CoA synthetase, lipoprotein lipase and fatty acid transport protein, and down-regulation of mRNA for Apo CIII and Apo AI. Administration of purified isohumulones effectively resulted in the same changes as IHE. Administration of fenofibrate, an agonist for PPARalpha, with a cholesterol diet caused marked hepatomegaly, an increase in plasma HDL-cholesterol, a decrease in hepatic cholesterol content, and alterations in hepatic mRNA levels similar to those observed in mice given IHE. Taken together, these results suggest that the modulation of lipid metabolism observed in mice fed diets containing isohumulones is, at least in part, mediated by activation of PPARalpha. |
| Dietary L-arginine decreases myointimal cell proliferation and vascular monocyte accumulation in cholesterol-fed rabbits Boger, R. H., S. M. Bode-Boger, et al. (1998), Atherosclerosis 136(1): 67-77. Abstract: L-arginine, the precursor of endogenous nitric oxide (NO), has been shown to enhance endothelial function and to reduce the progression of atherosclerosis in cholesterol-fed rabbits. In the present study, we investigated whether myointimal cell proliferation is enhanced in hypercholesterolaemic rabbit aorta and whether chronic treatment of the rabbits with L-arginine or with the NO synthase inhibitor L-NAME influences this proliferative response and vascular monocyte accumulation. Rabbits were fed 1% cholesterol or normal rabbit chow for 12 weeks. Subgroups of cholesterol-fed rabbits were treated with oral L-arginine (2.25%) or L-NAME (3 mg/dl) in drinking water. Myointimal cell proliferation was quantified in aortic segments by immunohistochemical detection of bromodeoxyuridine (BrdU) incorporation into nuclear DNA; vascular monocyte accumulation was assessed by immunohistochemistry using a monoclonal anti-macrophage/monocyte antibody (RAM-11). Plasma levels of L-arginine and the endogenous NO synthase inhibitor, ADMA, were quantified by high-performance liquid chromatography (HPLC). Cholesterol feeding increased the aortic intima/media (I/M) ratio, which was not measurable in the control group, to 1.9 +/- 0.3. This was paralleled by enhanced cell proliferation (cholesterol, 2.4 +/- 0.2%; P < 0.05; control, 0.02 +/- 0.001% BrdU-positive cells per 72 h) and vascular monocyte accumulation. Double immunostaining for BrdU and alpha-actin showed that about two thirds of the proliferating cells were smooth muscle cells. ADMA levels increased from 0.8 +/- 0.1 micromol/l to 2.2 +/- 0.2 micromol/l in cholesterol-fed rabbits, but were unchanged by L-arginine or L-NAME treatment. Myointimal proliferation and intima/media ratios were correlated with ADMA plasma levels. Dietary L-arginine reduced monocyte accumulation by 85 +/- 2% (P < 0.05 vs cholesterol), myointimal cell proliferation (1.8 +/- 0.3% per 72 h; P < 0.05) and intimal thickening (I/M ratio: 0.7 +/- 0.2), whereas the inhibitor of NO synthase, L-NAME, further increased cell proliferation to 3.1 +/- 0.4% per 72 h (P < 0.05). No significant difference was observed in vascular monocyte infiltration between the cholesterol and L-NAME groups. We conclude that cell proliferation and vascular monocyte accumulation are enhanced in hypercholesterolaemic rabbit aorta. These atherogenic effects can be attenuated by dietary L-arginine. Decreased NO formation might underlie the enhanced monocyte accumulation and cell proliferation in hypercholesterolaemic rabbit aorta. The observed inhibition of cell proliferation adds to our understanding of the antiatherosclerotic effects of L-arginine in vivo. |
| Dietary L-arginine normalizes endothelin-induced vascular contractions in cholesterol-fed rabbits Phivthong-ngam, L., S. M. Bode-Boger, et al. (1998), J Cardiovasc Pharmacol 32(2): 300-7. Abstract: The endothelium regulates vascular function by releasing the vasodilator autacoid nitric oxide (NO) and the vasoconstrictor peptide endothelin-1 (ET-1). Impaired activity of NO as well as excessive activity of ET-1 have been demonstrated in hypercholesterolemia and atherosclerosis. Because dietary L-arginine can restore NO function and improve abnormal endothelium-dependent relaxation in hypercholesterolemic rabbits, we examined the effects of dietary supplementation with L-arginine in cholesterol-fed rabbits on endothelium-dependent vascular relaxation and ET-1-induced vascular contraction, as well as the systemic synthesis of ET-1. Rabbits were initially fed a diet enriched with 1% cholesterol for 4 weeks, followed by 0.5% cholesterol alone or supplemented with 2% L-arginine in drinking water during the next 12 weeks. Cholesterol feeding impaired endothelium-dependent relaxation of rabbit aortic rings ex vivo and increased urinary immunoreactive ET-1 excretion, along with decreased urinary nitrate excretion, an index of NO production. L-Arginine partially restored endothelium-dependent relaxation in parallel to increased urinary nitrate excretion and decreased urinary immunoreactive ET-1 excretion. Selective inhibition of ET-A receptors with BQ123 partially restored endothelium-dependent relaxation in hypercholesterolemic rabbits but had no effect on arterial rings from rabbits supplemented with L-arginine or from control animals. The contractile vascular response of aortic rings to exogenous ET-1 was increased in rabbits fed a high-cholesterol diet; this enhanced contractility to ET-1 was completely reversed by L-arginine. These data suggest that L-arginine restores endothelial function and normalizes the synthesis and vasoconstrictor response to ET-1 in hypercholesterolemia. |
| Dietary L-arginine reduces the progression of atherosclerosis in cholesterol-fed rabbits: comparison with lovastatin Boger, R. H., S. M. Bode-Boger, et al. (1997), Circulation 96(4): 1282-90. Abstract: BACKGROUND: We investigated whether L-arginine induces regression of preexisting atheromatous lesions and reversal of endothelial dysfunction in hypercholesterolemic rabbits, whether similar effects can be obtained by cholesterol-lowering therapy with lovastatin, and which mechanism leads to these effects. METHODS AND RESULTS: Rabbits were fed 1% cholesterol for 4 weeks and 0.5% cholesterol for an additional 12 weeks. Two groups of cholesterol-fed rabbits were treated with L-arginine (2.0% in drinking water) or lovastatin (10 mg/d) during weeks 5 through 16. Systemic nitric oxide (NO) formation was assessed as the urinary excretion rates of nitrate and cGMP in weekly intervals. Cholesterol feeding progressively reduced urinary nitrate excretion to approximately 40% of baseline (P<.05) and increased plasma concentrations of asymmetrical dimethylarginine (ADMA), an endogenous NO synthesis inhibitor. Dietary L-arginine reversed the reduction in plasma L-arginine/ADMA ratio and partly restored urinary excretion of nitrate and cGMP (each P<.05 vs cholesterol) but did not change plasma cholesterol levels. L-Arginine completely blocked the progression of carotid intimal plaques, reduced aortic intimal thickening, and preserved endothelium-dependent vasodilator function. Lovastatin treatment reduced plasma cholesterol by 32% but did not improve urinary nitrate or cGMP excretion or endothelium-dependent vasodilation. Lovastatin had a weaker inhibitory effect on carotid plaque formation and aortic intimal thickening than L-arginine. L-Arginine inhibited but lovastatin potentiated superoxide radical generation in the atherosclerotic vascular wall. CONCLUSIONS: Dietary L-arginine improves NO-dependent vasodilator function in cholesterol-fed rabbits and completely blocks the progression of plaques via restoration of NO synthase substrate availability and reduction of vascular oxidative stress. Lovastatin treatment has a weaker inhibitory effect on the progression of atherosclerosis and no effect on vascular NO elaboration, which may be due to its stimulatory effect on vascular superoxide radical generation. |
| Dietary L-aspartate and L-glutamate inhibit fatty streak initiation in cholesterol-fed rabbit Yanni, A. E., H. A. Yatzidis, et al. (2003), Nutr Metab Cardiovasc Dis 13(2): 80-6. Abstract: BACKGROUND AND AIM: Low-density lipoprotein (LDL) oxidation is a potential atherogenic agent, and protecting LDL from oxidation prevents atherogenesis. It has been shown that L-aspartate and L-glutamate decrease lipid peroxidation after reoxygenation by means of the initiation of the cardiopulmonary bypass circuit (CPB), when supplemented to the CPB prime, and so they may protect against atherogenesis. The aim of this study was to evaluate the effect of the dietary administration of L-aspartate and L-glutamate on fatty streak onset in cholesterol-fed rabbit. METHODS AND RESULTS: Male New Zealand white rabbits were fed for four weeks with either a high-cholesterol plus corn oil diet (control group) or the same diet supplemented with 12.5 mM L-aspartate and 12.5 mM L-glutamate in drinking water (Asp + Glu group). The mononuclear cells adhering to the endothelium and the intimal foam cells of the thoracic aorta were used to quantify the extent of atherosclerosis. Total serum cholesterol and lipid peroxidation activity, measured as thiobarbituric acid reactive substances (TBARS), were determined 0, 1 and 4 weeks after a 2-week adaptation period. There were no between-group differences in body weight or food intake during the intervention. Serum TBARS were significantly increased in both groups during the experimental period but without any statistical difference between groups. At the end of the dietary intervention, there was a ten-fold increase in total serum cholesterol concentration in both groups vs baseline. The numbers of adherent mononuclear cells and intimal foam cells were both significantly lower in the Asp + Glu group. CONCLUSIONS: Our results suggest that dietary supplementation with L-aspartate and L-glutamate seems to protect the arterial wall from atherogenesis in an experimental animal. |
| Dietary levels of chia: influence on yolk cholesterol, lipid content and fatty acid composition for two strains of hens Ayerza, R. and W. Coates (2000), Poult Sci 79(5): 724-39. Abstract: Four hundred fifty H&N laying hens, half white and half brown, were fed for 90 d to compare a control diet to diets containing 7, 14, 21, and 28% chia (Salvia hispanica L.) seed. Cholesterol content, total fat content, and fatty acid composition of the yolks were determined 30, 43, 58, 72, and 90 d from the start of the trial. Significantly less cholesterol was found in the egg yolks produced by the hens fed the diets with 14, 21, and 28% chia compared with the control, except at Day 90. Palmitic fatty acid content and total saturated fatty acid content decreased as chia percentage increased and as the trial progressed. Total omega-3 fatty acid content was significantly greater (P < 0.05) for both strains for all chia diets compared with the control diet. Total polyunsaturated fatty acid (PUFA) content of the yolks from the chia diets was significantly greater (P < 0.05) than from the control diet. Generally, total PUFA content tended to be highest in the yolks of the white hens. |
| Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies Clarke, R., C. Frost, et al. (1997), Bmj 314(7074): 112-7. Abstract: OBJECTIVE: To determine the quantitative importance of dietary fatty acids and dietary cholesterol to blood concentrations of total, low density lipoprotein, and high density lipoprotein cholesterol. DESIGN: Meta-analysis of metabolic ward studies of solid food diets in healthy volunteers. SUBJECTS: 395 dietary experiments (median duration 1 month) among 129 groups of individuals. RESULTS: Isocaloric replacement of saturated fats by complex carbohydrates for 10% of dietary calories resulted in blood total cholesterol falling by 0.52 (SE 0.03) mmol/l and low density lipoprotein cholesterol falling by 0.36 (0.05) mmol/l. Isocaloric replacement of complex carbohydrates by polyunsaturated fats for 5% of dietary calories resulted in total cholesterol falling by a further 0.13 (0.02) mmol/l and low density lipoprotein cholesterol falling by 0.11 (0.02) mmol/l. Similar replacement of carbohydrates by monounsaturated fats produced no significant effect on total or low density lipoprotein cholesterol. Avoiding 200 mg/day dietary cholesterol further decreased blood total cholesterol by 0.13 (0.02) mmol/l and low density lipoprotein cholesterol by 0.10 (0.02) mmol/l. CONCLUSIONS: In typical British diets replacing 60% of saturated fats by other fats and avoiding 60% of dietary cholesterol would reduce blood total cholesterol by about 0.8 mmol/l (that is, by 10-15%), with four fifths of this reduction being in low density lipoprotein cholesterol. |
| Dietary lipids and the low blood cholesterol-cancer association Kritchevsky, S. B. (1992), Am J Epidemiol 135(5): 509-20. Abstract: The role of dietary fat and cholesterol in the low blood cholesterol-cancer association was examined in the National Health and Nutrition Survey Epidemiologic Follow-up Study (NHEFS) conducted during 1971-1984. Of the 9,593 male and female participants, aged 25-74 years, 638 developed cancer during the median of 10.2 years of follow-up. Diet was assessed using a 24-hour dietary recall. Despite an inverse association between serum cholesterol and cancer, male cases consumed, on average, more dietary cholesterol, a larger proportion of calories as saturated fat, but a similar proportion of calories as linoleic acid. Among females, cases consumed less fat and cholesterol than noncases. Among males with central adiposity (subscapular-to-triceps skinfold ratio greater than or equal to 1), cases ate more dietary cholesterol both absolutely and as a proportion of calories. Among males with peripheral adiposity, cases tended to eat less dietary cholesterol than noncases. Among females, serum cholesterol was inversely associated with cancer risk among those with central adiposity but directly associated among those with peripheral adiposity. Dietary comparisons were adjusted for age, race, body mass index, smoking status, alcohol consumption, education, and economic status. The results indicate that diet cannot explain the low blood cholesterol-cancer association in men. Furthermore, inconsistencies in the literature in this area may be due, in part, to differing proportions of central adiposity in study populations. |
| Dietary maltitol causes increased serum and liver cholesterol concentrations in rats Zhang, X. Z., G. W. Meijer, et al. (1990), Int J Vitam Nutr Res 60(3): 296-7. |
| Dietary meat, dairy products, fat, and cholesterol and pancreatic cancer risk in a prospective study Michaud, D. S., E. Giovannucci, et al. (2003), Am J Epidemiol 157(12): 1115-25. Abstract: Case-control studies suggest that meat and cholesterol intakes may be related to elevated risks of pancreatic cancer. Few prospective studies have examined associations between diet and pancreatic cancer, although in one recent study saturated fat consumption was related to higher risk. In a cohort of US women, the authors confirmed 178 pancreatic cancer cases over 18 years of follow-up. A mailed 61-item food frequency questionnaire was self-administered at baseline, and health and lifestyle variables were updated biennially. Analyses were performed using Cox proportional hazards models to adjust for potential confounders. Intakes of total fat, different types of fats, and cholesterol were not associated with pancreatic cancer risk. Similarly, total meat, red meat, and dairy products were not related to risk. Individual food items contributing to intakes of total meat and dairy products, as well as fish and eggs, did not reveal any specific association. Updating dietary exposures by using questionnaires from 1980, 1984, 1986, and 1990 produced similar findings. The authors' data do not support previous findings that meat or saturated fat intakes are related to pancreatic cancer risk. Future prospective studies should examine the influence of cooking practices as well as other dietary habits on the risk of pancreatic cancer. |
| Dietary modification of high density lipoprotein phospholipid and influence on cellular cholesterol efflux Gillotte, K. L., S. Lund-Katz, et al. (1998), J Lipid Res 39(10): 2065-75. Abstract: African green monkeys fed fat-specific diets served as a model to investigate the effect of phospholipid acyl chain modification on high density lipoprotein (HDL)-mediated cellular cholesterol efflux. Diets enriched in saturated, monounsaturated, n-6 polyunsaturated, or n-3 polyunsaturated fats were provided during both low cholesterol and cholesterol-enriched stages; sera and HDL3 samples were obtained at specific points during the treatment period. Analysis of the HDL phospholipid composition revealed significant acyl chain modification, consistent with the respective fat-specific diet. Cholesterol efflux from mouse L-cell fibroblasts to HDL3 isolated from the specific diet groups was measured and revealed no differences in the abilities of the particles to accept cellular cholesterol; determination of the bidirectional flux of cholesterol between the cells and HDL3 species further demonstrated no effect of phospholipid acyl chain modification on this process. The effects of dietary modification of phospholipid acyl chains on cellular cholesterol efflux were directly examined by isolating the HDL phospholipid and combining it with human apolipoprotein A-I to form well-defined reconstituted HDL particles. These complexes did not display any differences with respect to their ability to stimulate cellular cholesterol efflux. Incubations with 5% sera further confirmed that the fat-specific diets do not influence cholesterol efflux. These results suggest that the established influences of specific dietary fats on the progression of atherosclerosis are due to effects on cholesterol metabolism other than the efflux of cellular cholesterol in the first step of reverse cholesterol transport. |
| Dietary monounsaturated fatty acids enhance cholesterol efflux from human fibroblasts. Relation to fluidity, phospholipid fatty acid composition, overall composition, and size of HDL3 Sola, R., C. Motta, et al. (1993), Arterioscler Thromb 13(7): 958-66. Abstract: This study was designed to determine whether modifications induced by dietary fats on the high-density lipoprotein3 (HDL3) physicochemical characteristics could affect cholesterol efflux and intracellular cholesterol content, leading to upregulation of low-density lipoprotein (LDL) receptor activity from cultured fibroblasts. Serum HDL3S were obtained from 12 healthy women aged 26 to 49 years who adhered to four 7-week isocaloric diets containing 30% of the caloric intake as fat. Of the total calories, 15.6% of each diet was provided by (1) milk fats, rich in saturated fatty acids; (2) sunflower oil, rich in n-6 polyunsaturated fatty acids; (3) olive oil, rich in monounsaturated fatty acids; and (4) rapeseed oil, rich in n-3 polyunsaturated fatty acids. HDL3 isolated after the monounsaturated fatty acid diet induced the greatest cellular 3Hfree cholesterol efflux, reduced the content of intracellular cholesterol, and enhanced 125I-LDL degradation. Univariate regression analyses suggested that the increased capacity of HDL3 to promote cellular 3Hfree cholesterol efflux was in part due to its greater fluidity, higher cholesteryl ester content, elevated linoleic to linolenic acid ratio in phospholipids, and its smaller size. In conclusion dietary fats induced physicochemical changes in HDL3, which strongly modulated cellular cholesterol homeostasis in vitro. These data also suggest a novel mechanism by which dietary fats exert their effect on atherosclerosis. |
| Dietary myristic acid modifies the HDL-cholesterol concentration and liver scavenger receptor BI expression in the hamster Loison, C., F. Mendy, et al. (2002), Br J Nutr 87(3): 199-210. Abstract: The influence of myristic acid in a narrow physiological range (0.5 to 2.4% of total dietary energy) on the plasma and hepatic cholesterol metabolism was investigated in the hamster. The hamsters were fed on a diet containing 12.5 g fat/100 g and 0.05 g cholesterol/100 g with 0.5% myristic acid (LA diet) for 3 weeks (pre-period). During the following 3 weeks (test period), they were divided into four dietary groups with 0.5% (LA), 1.2% (LM), 1.8% (ML) or 2.4% (M) myristic acid. Finally, half the hamsters in each group were again fed the LA diet for another 3 weeks (post-period). At the end of the test period, the hepatic expression of the scavenger receptor BI (SR-BI) was lower in the LM, ML and M groups than in the LA group whereas the hepatic cholesteryl ester concentration was higher. Cholesterol 7alpha hydroxylase activity was lower in the ML and M groups than in the LA and LM groups while the sterol 27 hydroxylase and 3-hydroxy-3-methyl glutaryl coenzyme A reductase activities were not modulated by dietary myristic acid. This is the first time a negative correlation has been observed between the HDL-cholesterol concentration and the hepatic mass of SR-BI (r -0.69; P<0.0001) under physiological conditions. An inverse linear regression was also shown between SR-BI and the percentage of myristic acid in the diet (r -0.75; P<0.0001). The hepatic mass of SR-BI in the M group had increased at the end of the post-period compared with the test-period values. The present investigation shows that myristic acid modulates HDL-cholesterol via a regulation of the SR-BI expression. |
| Dietary N-3 polyunsaturated fatty acids decrease biliary cholesterol saturation in gallstone disease Berr, F., J. Holl, et al. (1992), Hepatology 16(4): 960-7. Abstract: Because fatty acid composition of biliary phospholipids influences cholesterol secretion into bile, we investigated whether replacement of n-1 monounsaturated or n-6 polyunsaturated fatty acids with n-3 polyunsaturated fatty acids in biliary phosphatidylcholines reduces supersaturation with cholesterol and prevents precipitation of cholesterol crystals in bile of gallstone patients. Seven patients with radiolucent gallstones in functioning gallbladders were studied before (control) and after 5 wk of dietary supplementation with marine fish oil (11.3 gm/day = 3.75 gm n-3 polyunsaturated fatty acids/day). Duodenal bile was collected for analysis during intravenous infusion of cholecystokinin. Gallbladder emptying in response to cholecystokinin was comparable before and during intake of n-3 polyunsaturated fatty acids. Intake of n-3 polyunsaturated fatty acids increased (p less than 0.001) the fractions of eicosapentaenoic and docosahexaenoic acids and decreased the fractions of linoleic (p less than 0.001) and arachidonic acids (p less than 0.02) in biliary phospholipids. Concomitantly, the molar ratio of cholesterol to phospholipids decreased (-19%; p less than 0.05). As a consequence, the cholesterol saturation index was reduced by -25% (p = 0.01), from 1.60 +/- 0.44 to 1.24 +/- 0.38. However, in vitro nucleation time of duodenal bile was not prolonged. The decrease in cholesterol saturation was not sufficient to prevent nucleation of cholesterol crystals in bile of gallstone patients. In conclusion, our data suggest that cholesterol saturation can be influenced by the fatty acid composition of the phosphatidylcholines secreted in bile. |
| Dietary non-starch polysaccharides interact with cholesterol and fish oil in their effects on plasma lipids and hepatic lipoprotein receptor activity in rats Abbey, M., C. Triantafilidis, et al. (1993), J Nutr 123(5): 900-8. Abstract: Male rats were fed the non-starch polysaccharides pectin, methylcellulose or guar gum with corn oil or with 60% of the corn oil replaced by fish oil. They were also fed these diets with or without cholesterol (+ cholic acid). Plasma total cholesterol concentration was higher overall in rats fed cholesterol and lower in those fed fish oil or fish oil + cholesterol. Plasma triacylglycerols were lower in rats fed fish oil with or without cholesterol. Hepatic LDL receptor activity was higher overall in rats fed fish oil or fish oil + cholesterol than in those fed cholesterol. Liver HDL receptor was lower overall in rats fed fish oil or cholesterol. Type of non-starch polysaccharide influenced these dietary effects so that in cholesterol-fed rats plasma cholesterol was highest in those fed methylcellulose, intermediate in those fed guar gum and in those fed pectin was unchanged from concentrations in rats fed pectin without cholesterol. Fish oil feeding lowered plasma cholesterol concentration in rats fed pectin or methylcellulose but not in those fed guar gum. Plasma triacylglycerols were lower in rats fed fish oil and all three non-starch polysaccharides, but concentrations were similar in rats fed pectin + fish oil + cholesterol and in those fed pectin. In rats fed methylcellulose + cholesterol and any non-starch polysaccharide + fish oils, HDL receptor activity was uniformly lower than in rats fed pectin, methylcellulose or guar gum. Low density lipoprotein receptor activity was higher in rats fed pectin + fish oil or pectin + fish oil + cholesterol than in rats fed pectin. |