| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Dietary cholesterol-oxidation products accumulate in serum and liver in apolipoprotein E-deficient mice, but do not accelerate atherosclerosis Ando, M., H. Tomoyori, et al. (2002), Br J Nutr 88(4): 339-45. Abstract: There are conflicting reports regarding the effect of dietary cholesterol-oxidation products (oxysterols) on the development of atherosclerosis in experimental animals. To address this issue, apolipoprotein (Apo) E-deficient mice were fed a purified diet (AIN-93) or the same purified diet containing 0.2 g cholesterol or 0.2 g oxysterols/kg. The dietary oxysterols had no significant effect on the serum lipid levels. Although all of the diet-derived oxysterols (cholest-5-en-3beta,7alpha-diol, cholest-5-en-3beta,7beta-diol, cholestan-5alpha,6alpha-epoxy-3beta-ol, cholestan-5beta,6beta-epoxy-3beta-ol, cholestan-3beta, 5alpha, 6beta-triol, cholest-5-en-3beta-ol-7-one and cholest-5-en-3beta, 25-diol) accumulated in the serum and liver, only cholest-5-en-3beta-ol-7-one and cholestan-3beta, 5alpha, 6beta-triol accumulated significantly (P<0.05) in the aorta. The oxysterol diet did not result in elevation of the aortic cholesterol level or the lesion volume in the aortic valve. These present results indicate that exogenous oxysterols do not promote the development of atherosclerosis in ApoE-deficient mice. |
| Dietary cholesterol--the role of eggs in the prudent diet Vorster, H. H., A. C. Beynen, et al. (1995), S Afr Med J 85(4): 253-6. Abstract: The recommendation that not more than 300 mg cholesterol be consumed daily to prevent high serum cholesterol levels and coronary heart disease is often used to justify a restriction of egg intake to three or four per week. One egg contains about 200 mg of cholesterol, but eggs are also excellent and relatively inexpensive sources of essential amino acids and certain vitamins. In this paper, the place of eggs in a prudent, cholesterol-lowering diet as a substitute for other animal products, is scrutinised. The extra cholesterol, where considered as the only variable, will increase serum cholesterol levels, but the effect is relatively small. The exclusion of eggs from the diet should be weighed against deprivation of essential nutrients especially in vulnerable groups. While restriction of egg intake in westernised populations seems justifiable, the upper limit of three or four per week may not always be applicable, depending on the overall diet and lipid profile of the individual. |
| Dietary conjugated linoleic acid lowers plasma cholesterol during cholesterol supplementation, but accentuates the atherogenic lipid profile during the acute phase response in hamsters Sher, J., A. Pronczuk, et al. (2003), J Nutr 133(2): 456-60. Abstract: Conjugated linoleic acid (CLA) reportedly exerts anticarcinogenic and antiatherosclerotic effects in animals. To test the hypothesis that the putative antiatherosclerotic effect of CLA might derive from an anti-inflammatory or antioxidant action on lipoprotein metabolism, an acute phase response (APR) was elicited in hamsters while varying dietary cholesterol and vitamin E intakes in two experiments. The effect of CLA intake (to 1%) was examined with 0% (Experiment 1, 7 wk) and 0 or 0.3% (Experiment 2, 12 wk) cholesterol, at which point APR was induced. In hamsters not fed dietary cholesterol (Experiment 1), CLA exaggerated the rise in plasma and LDL cholesterol observed during the APR. When CLA was fed concurrently with cholesterol (Experiment 2), plasma and liver cholesterol were reduced up to 40% independent of the APR. In addition, CLA decreased body weight gain and adipose reserves in Experiment 1, but not in Experiment 2. Because CLA failed to attenuate APR and was not influenced by vitamin E status, an antioxidant/anti-inflammatory role was not apparent. However, the reduced burden on liver and lipoprotein cholesterol induced by CLA during cholesterol feeding, suggests that CLA curtailed cholesterol absorption, whereas the rise during APR suggests that CLA exaggerated the impaired clearance of plasma cholesterol associated with acute inflammation. |
| Dietary conjugated linoleic acid mixture affects the activity of intestinal acyl coenzyme A: cholesterol acyltransferase in hamsters Thomas Yeung, C. H., L. Yang, et al. (2000), Br J Nutr 84(6): 935-41. Abstract: The present study was designed to study the mechanisms by which dietary conjugated linoleic acids (CLA) decrease serum cholesterol. Hamsters were fed a semi-synthetic diet containing 1 g cholesterol/kg diet with or without supplementation with 20 g linoleic acid (LA) and 20 g CLA/kg diet. After 8 weeks, serum fasting total cholesterol (TC) and triacylglycerol (TG) were significantly lower in the LA-supplemented and CLA-supplemented groups compared with those of the control (CTL) hamsters. In contrast to LA, CLA significantly lowered hepatic cholesterol but it increased the level of adipose tissue cholesterol, suggesting that the hypocholesterolaemic mechanism of CLA is different from that of LA. CLA decreased the activity of intestinal acyl CoA:cholesterol acyltransferase (ACAT) whereas LA had no effect on this enzyme. Consequently, CLA supplementation increased the faecal excretion of total neutral sterols, but it had no or little effect on the faecal acidic sterols. If the ACAT is associated with cholesterol absorption, the part of mechanisms by which CLA decreases serum cholesterol may involve down-regulation of intestinal ACAT activity. |
| Dietary copper in excess of nutritional requirement reduces plasma and breast muscle cholesterol of chickens Bakalli, R. I., G. M. Pesti, et al. (1995), Poult Sci 74(2): 360-5. Abstract: Male commercial broiler strain chickens were fed from hatching to 42 d of age either a control diet (based on corn and soybean meal) or the control diet supplemented with 250 mg copper/kg diet from cupric sulfate pentahydrate (for 35 or 42 d). Hypocholesterolemia (11.8% reduction) and decreased breast muscle cholesterol (20.4% reduction) were observed in copper-supplemented birds. There was a slight increase (P >.05) in breast muscle copper (14.5%), and all levels were very low (<.5 mg/kg). Feeding copper for 42 vs 35 d resulted in lower levels of cholesterol in the plasma (12.9 vs 10.8% reduction) and breast muscle (24.6 vs 16.2% reduction). Very similar results were found in two additional experiments in which hypocholesterolemia and reduced breast muscle cholesterol were associated with reduced plasma triglycerides and blood reduced glutathione. It is well known that hypercholesterolemia is a symptom of dietary copper deficiency. The data presented here indicate that blood and breast muscle cholesterol are inversely related to dietary copper in excess of the dietary requirement for maximal growth. The cholesterol content of the edible muscle tissue of broiler chickens can be reduced by approximately 25% after feeding a supranormal level of copper for 42 d without altering the growth of the chickens or substantially increasing the copper content of the edible meat. |
| Dietary copper supplementation reduces atherosclerosis in the cholesterol-fed rabbit Lamb, D. J., G. L. Reeves, et al. (1999), Atherosclerosis 146(1): 33-43. Abstract: There has been considerable debate about how copper status may affect the biochemical and cellular processes associated with atherogenesis. In the present study we have attempted to address this issue directly by investigating the effects of dietary copper supplementation on processes likely to contribute to atherogenesis, using the cholesterol-fed New Zealand White rabbit model. Age matched rabbits (n = 16) were fed a 0.25-1% cholesterol diet to maintain plasma cholesterol concentrations at approximately 30 mmol/l. Eight of these animals also received 0.2% copper acetate. Control animals (n = 8) received rabbit chow without supplements. After 13 weeks on the experimental diets the animals were killed. Integrated cholesterol levels were similar for the cholesterol-fed animals (31.1+/-2.5 vs. 29.9+/-1.9 mmol/l weeks; P>0.05). Although integrated plasma copper levels were higher in the animals receiving the copper supplements, these did not differ significantly (19.0+/-4.8 vs. 15.1+/-2.9 micromol/l weeks; P>0.05). Tissue concentrations of copper were higher in the copper fed animals compared to those on cholesterol alone in aortic 14.0+/-0.75 vs. 1.8+/-0.2 microg/g wet tissue; P<0.05), carotid artery (11.4+/-3.5 vs. 4.9+/-0.9 microg/g wet tissue; P<0.05), and hepatic (332.5+/-28.6 vs. 3.3+/-1.1 microg/g wet tissue; P<0.0001) samples. The concentration of copper within the carotid artery was also significantly higher than that within the aorta (7.5+/-1.8 vs. 2.4+/-0.4 microg/g wet tissue; P<0.05). In animals fed a normal rabbit chow aortic, carotid and hepatic copper concentrations were 3.7+/-0.8, 9.4+/-3.4, and 5.0+/-1.6 microg/g, respectively. These values did not differ significantly from the cholesterol-fed animals (P>0.05). Plasma concentrations of caeruloplasmin, the major copper carrying protein, were estimated as plasma ferroxidase activity and were similar for the groups (P>0.05), as were aortic superoxide dismutase activity levels (P>0.05). Copper supplementation was associated with increased mononuclear cell adhesion to the endothelium of the carotid endothelium, with 2.6+/-0.3 adherent monocytes/1000 endothelial cells in the cholesterol plus copper-fed animals compared to 1.3+/-0.3 in the cholesterol-fed group (P = 0.0006), and 0.1+/-0.1 in the control animals (P<0.002). This may reflect the higher concentrations of copper found within the carotid artery. Histology of the thoracic aorta at the level of the third and sixth intercostal arteries, showed that copper supplementation was associated with significantly smaller intimal lesions (P<0.05 and P<0.01, respectively). These data suggest that copper supplements possibly inhibit the progression of atherogenesis. |
| Dietary copper: cholesterol and lipoprotein metabolism Lei, K. Y. (1991), Annu Rev Nutr 11: 265-83. |
| Dietary corn oil versus olive oil enhances HDL protein turnover and lowers HDL cholesterol levels in hamsters van Tol, A., A. H. Terpstra, et al. (1999), Atherosclerosis 147(1): 87-94. Abstract: We studied the effect of dietary olive and corn oil on high-density lipoprotein (HDL) metabolism in golden Syrian hamsters. The animals were fed a semipurified diet containing 0.1% cholesterol and 40 energy % in the form of either olive or corn oil for a period of nine weeks. Hamsters fed corn oil had significantly lower very-low density and low-density lipoprotein (VLDL+LDL) cholesterol concentrations than those fed olive oil (0.98+/-0.24 vs. 1.40+/-0.34 mmol/l, means+/-S.D., n = 12), as well as significantly lower HDL cholesterol concentrations (3.31+/-0.50 vs. 3.91+/-0.12 mmol/l). The binding capacity of 125I-labelled HDL to liver membranes was 33% higher in the hamsters fed corn oil instead of olive oil (571+/-29 vs. 429+/-24 ng HDL protein/mg membrane protein, P<0.05, n = 4). HDL protein kinetics were studied with 125I-HDL using a constant infusion technique. Both HDL fractional catabolic rate (0.255+/-0. 058 vs. 0.121+/-0.023 /h, P<0.01, n = 5) and transport rate (2.386+/-0. 753 vs. 1.218+/-0.101 mg/h, P<0.01, n = 5) were about 2-fold higher in the hamsters fed corn oil. The rate of plasma cholesterol esterification by lecithin: cholesterol acyltransferase (LCAT) was essentially the same for the two diets. It is concluded that the low HDL level in the hamsters fed corn oil diets is linked with increased HDL binding and degradation in the liver and possibly other tissues. Due to increased HDL protein turnover, the capacity for reverse cholesterol transport is increased in hamsters fed corn oil despite the relative low HDL concentrations |
| Dietary effects on cardiovascular disease risk factors: beyond saturated fatty acids and cholesterol Nicolosi, R. J., T. A. Wilson, et al. (2001), J Am Coll Nutr 20(5 Suppl): 421S-427S; discussion 440S-442S. Abstract: Hypercholesterolemia represents a significant risk for cardiovascular disease (CVD). While diet intervention remains the initial choice for the prevention and treatment of CVD, the nature of the dietary modification remains controversial. For example, reducing calories from total fat, without decreasing saturated fat intake results in insignificant changes in low density lipoprotein cholesterol (LDL-C). Similarly, diet interventions that focus solely on lowering dietary cholesterol and saturated fat intake not only decrease LDL-C, but also high density lipoprotein cholesterol (HDL-C) and therefore may not improve the lipoprotein profile. This brief review summarizes dietary interventions that lower LDL-C without affecting HDL-C levels. These interventions include soy protein, soluble fiber, soy lecithin and plant sterols. This review also includes some of the reported dietary interventions, such as polyphenols, isoflavones, folic acid and vitamins B6 and B12, which reduce the risk of CVD without changes in lipoprotein cholesterol. |
| Dietary fat alters the distribution of cholesterol between vesicles and micelles in hamster bile Cohen, B. I., T. Mikami, et al. (1995), Lipids 30(4): 299-305. Abstract: The type of dietary fat strongly affects the incidence of gallstones in the hamster model of cholesterol cholelithiasis. The present study was designed to determine whether dietary fats could affect gallstone formation by altering the microstructure (vesicular/micellar ratio) of cholesterol in bile. Golden Syrian hamsters from Sasco (Omaha, NE) or Charles River (Wilmington, MA) were fed nutritionally adequate semipurified diets to which were added: (i) 4.0% butterfat without added cholesterol; (ii) 1.2% palmitic acid plus 0.3% cholesterol; or (iii) 4.0% safflower oil plus 0.3% cholesterol. Gallstone incidence and the percentage of cholesterol in vesicles and micelles were determined after two- or six-week feeding periods. Three out of ten Sasco hamsters fed the 1.2% palmitic acid diet for two weeks had cholesterol stones, while none of the eight Charles River animals had stones. In the Sasco hamsters, a significant proportion of the biliary cholesterol was found in void volume vesicles (28.8%) and small vesicles (17.1%); Charles River hamsters had negligible proportions (1.1%) of cholesterol in void volume vesicles and 15.4% in small vesicles. Cholesterol gallstones were most abundant in Sasco hamsters fed 1.2% palmitic acid for six weeks (nine out of ten animals); the mean cholesterol saturation index of the bile was 1.27. A significant proportion of the biliary cholesterol was eluted in the void volume vesicles (21.4%) and in small vesicles (15.0%). Five of the eight identically treated Charles River hamsters had cholesterol stones; the cholesterol saturation index averaged 1.36, and the biliary cholesterol was present in void volume vesicles (31.3%) and small vesicles (14.3%).(ABSTRACT TRUNCATED AT 250 WORDS) |
| Dietary fat and cholesterol and the risk of cardiovascular disease among women with type 2 diabetes Tanasescu, M., E. Cho, et al. (2004), Am J Clin Nutr 79(6): 999-1005. Abstract: BACKGROUND: Nutritional therapy is a cornerstone of diabetes management, but no epidemiologic studies have investigated the relation between specific dietary fatty acids and cholesterol and cardiovascular disease (CVD) risk among diabetic patients. OBJECTIVE: This study assessed the relation between specific dietary fatty acids and cholesterol and CVD risk among women with type 2 diabetes. DESIGN: Among 5672 women with type 2 diabetes from the Nurses' Health Study, diet was assessed prospectively and updated periodically. Relative risks of CVD were estimated from Cox proportional hazards analysis after adjustment for potential confounders. RESULTS: Between 1980 and 1998, we identified 619 new cases of CVD (nonfatal myocardial infarction, fatal coronary heart disease, and stroke). The relative risk (RR) of CVD for an increase of 200 mg cholesterol/1000 kcal was 1.37 (95% CI: 1.12, 1.68; P = 0.003). Each 5% of energy intake from saturated fat, as compared with equivalent energy from carbohydrates, was associated with a 29% greater risk of CVD (RR: 1.29; 95% CI: 1.02, 1.63; P = 0.04). The ratio of polyunsaturated to saturated fat (P:S) was inversely associated with the risk of fatal CVD. We estimated that replacement of 5% of energy from saturated fat with equivalent energy from carbohydrates or monounsaturated fat was associated with a 22% or 37% lower risk of CVD, respectively. CONCLUSIONS: A higher intake of cholesterol and saturated fat and a low P:S were related to increased CVD risk among women with type 2 diabetes. Among diabetic persons, replacement of saturated fat with monounsaturated fat may be more effective in lowering CVD risk than is replacement with carbohydrates. |
| Dietary fat and cholesterol induced modification of minipig lipoprotein fluidity and composition Berlin, E., M. A. Khan, et al. (1991), Comp Biochem Physiol A 98(1): 151-7. Abstract: 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. |
| Dietary fat and cholesterol intake in young children compared with recommended levels Stewart, K. J., C. M. Seemans, et al. (1999), J Cardiopulm Rehabil 19(2): 112-7. Abstract: PURPOSE: The National Cholesterol Education Program (1991) recommended that children 2 years of age or more derive less than 30% of their daily energy intake from total fat, less than 10% from saturated fat, up to 10% from polyunsaturated fat, and 10% to 15% from monounsaturated fat, and that they consume less than 300 mg/day of cholesterol. The purpose of this study was to assess whether preadolescent children were following these dietary guidelines in 1994 and to determine the relationship of diet to obesity. METHODS: This cross-sectional study was performed in elementary schools in southeast Baltimore, Maryland. The subjects were 468 children, grades 2 through 5 (mean age, 8.9 +/- 0.8 years). The main outcome measures were a 24-hour diet record, body mass index, and skinfold thickness. RESULTS: Mean percentage of total daily energy (TDE) from fat was 31.1%; saturated fat, 11.0%; monounsaturated fat, 10%; and polyunsaturated fat, 4.9%. Mean dietary cholesterol was 199.1 mg/day. Although the means for total and saturated fat are at recommended levels, the distribution of the dietary responses indicates that 50% of the children exceeded these targets. Twenty-five percent exceeded 35% of TDE derived from fat, and 25% exceeded 13% TDE derived from saturated fat. Fifty percent of children consumed below the desired level of monounsaturated fat, and almost no children consumed the desired 10% of polyunsaturated fat. Although mean dietary cholesterol was at a desired level, 16% of the children consumed more than 300 mg/day and 10% more than 377 mg/day. The negative correlation for sum of skinfold measurements with TDE (r = -0.14; P < 0.05), suggesting that fatter children consume fewer calories than thinner children, was the only correlate among dietary components and obesity. CONCLUSION: A substantial percentage of children in the United States are still not meeting recommended levels for dietary intake of fat and cholesterol. The trend for fatter children to consume fewer daily calories suggests that obesity is not entirely a result of overconsumption. |
| Dietary fat and cholesterol modulate the plasma lipoprotein distribution and production of pigment or cholesterol gallstones in hamsters Hayes, K. C., P. Khosla, et al. (1992), J Nutr 122(2): 374-84. Abstract: To evaluate the impact of key dietary factors on plasma lipoproteins and gallstone induction, male Syrian hamsters were fed either cholesterol and fat-supplemented purified diets containing glucose or lactose, or cholesterol and fat-free diets with or without fiber, for 13 wk. Fat-supplemented hamsters were hyperlipidemic in comparison to those fed fat-free diets. The former group revealed a greatly expanded VLDL fraction, whereas a normal HDL2 pool predominated in the latter group. Plasma fatty acids indicated that hamsters fed the fat-free diet were essential fatty acid deficient whilst the hamsters fed the fat-supplemented diet were subnormal in essential fatty acids. Ninety-three percent of the hamsters fed the fat-supplemented diet had gallstones (mostly cholesterol), whereas 62% of hamsters fed the fat-free diet had gallstones (almost all pigmented). Lactose increased cecal weight and prevented pigment stone formation in the fat-supplemented hamsters, whereas adding fiber to the fat-free diet contributed essential fatty acids, eliminated cholesterol stones and enhanced pigment stone formation. Thus, diets containing casein, rice flour, glucose and fiber with minimal essential fatty acids but no cholesterol promoted pigment stones (associated with a normal lipoprotein profile); a low fat diet limited in essential fatty acids but containing cholesterol and lactose, promoted cholesterol gallstones (associated with an expanded VLDL pool). |
| Dietary fat and fatty acids modulate cholesterol cholelithiasis in the hamster Cohen, B. I., E. H. Mosbach, et al. (1992), Lipids 27(7): 526-32. Abstract: We tested two hypotheses, i) whether the type and the amount of fat in the diet will affect the formation of cholesterol gallstones in the hamsters, and ii) whether palmitic acid, a major fatty acid component of butterfat, can act as a potentiator of cholesterol cholelithiasis in the hamster. Young, male golden Syrian hamsters (Sasco) were fed a semipurified diet containing casein, corn starch, cellulose and cholesterol (0.3%) to which various types and amounts of fat (butterfat, olive oil, menhaden oil, corn oil) were added. All diets contained 2% corn oil to supply essential fatty acids to the growing hamsters. No deaths or illness occurred during the experiment. Animals fed the semipurified diet plus 4% butterfat (group 1) had a gallstone incidence of 63%. Replacement of butterfat with either olive oil, corn oil or menhaden oil prevented the formation of cholesterol gallstones entirely (groups 2-4). When total butterfat was increased from 4% to 8% (group 8), the incidence of cholesterol gallstones increased to 80%. Substitution of 4% olive oil (group 5), corn oil (group 6), or menhaden oil (group 7) for the additional 4% butterfat significantly reduced gallstones to 35%, 45% and 30%, respectively. The replacement of 4% butterfat with 1.2% palmitic acid gave the highest incidence of cholesterol gallstones (95%). These results suggest that butterfat (and one of its components, palmitic acid) intensifies gallstone formation in this model whereas mono- and polyunsaturated fats act as inhibitors of cholesterol cholelithiasis. A fatty acid, possibly palmitic acid, appears to act as lithogen in our model. |
| Dietary fat and fiber alter large bowel and portal venous volatile fatty acids and plasma cholesterol but not biliary steroids in pigs Topping, D. L., R. J. Illman, et al. (1993), J Nutr 123(1): 133-43. Abstract: Male pigs were fed a low fiber beef diet (control) or that diet with additional fiber either as wheat bran, oat bran or baked beans. Total large bowel digesta and volatile fatty acid (VFA) pools were highest in pigs fed the diet with baked beans, intermediate in those fed the diets with oat bran and wheat bran and lowest in those fed the control diet. In all groups digesta mass and total VFA pools rose from the cecum and then fell to the distal colon, and incremental effects of diet were the same at all sampling sites. For acetate and propionate pools there was a significant interaction between diet and anatomical site, but data conversion to logarithms abolished this interaction, indicating that all dietary effects were proportionately the same across sections. Consumption of the diets with wheat bran, oat bran and baked beans increased the total large bowel butyrate pool compared with consumption of the control diet. Digesta H+ concentrations fell along the large bowel and correlated positively with VFA concentrations in the median colon. Portal venous VFA concentrations correlated with VFA in the proximal colon only. Plasma cholesterol and biliary steroids were unrelated to portal venous propionate concentrations. |
| Dietary fat increases high density lipoprotein (HDL) levels both by increasing the transport rates and decreasing the fractional catabolic rates of HDL cholesterol ester and apolipoprotein (Apo) A-I. Presentation of a new animal model and mechanistic studies in human Apo A-I transgenic and control mice Hayek, T., Y. Ito, et al. (1993), J Clin Invest 91(4): 1665-71. Abstract: In humans, diets high in saturated fat and cholesterol raise HDL-cholesterol (HDL-C) levels. To explore the mechanism, we have devised a mouse model that mimics the human situation. In this model, HuAITg and control mice were studied on low fat (9% cal)-low cholesterol (57 mg/1,000 kcal) (chow) and high fat (41% cal)-high cholesterol (437 mg/1,000 kcal) (milk-fat based) diets. The mice responded to increased dietary fat by increasing both HDL-C and apo A-I levels, with a greater increase in HDL-C levels. This was compatible with an increase in HDL size observed by nondenaturing gradient gel electrophoresis. Turnover studies with doubly labeled HDL showed that dietary fat both increase the transport rate (TR) and decreased the fractional catabolic rate of HDL cholesterol ester (CE) and apo A-I, with the largest effect on HDL CE TR. The latter suggested that dietary fat increases reverse cholesterol transport through the HDL pathway, perhaps as an adaptation to the metabolic load of a high fat diet. The increase in apo A-I TR by dietary fat was confirmed by experiments showing increased apo A-I secretion from primary hepatocytes isolated from animals on the high fat diet. The increased apo A-I production was not associated with any increase in hepatic or intestinal apo A-I mRNA, suggesting that the mechanism of the dietary fat effect was posttranscriptional, involving either increased translatability of the apo A-I mRNA or less intracellular apo A-I degradation. The dietary fat-induced decrease in HDL CE and apo A-I fractional catabolic rate may have been caused by the increase in HDL particle size, as was suggested by our previous studies in humans. In summary, a mouse model has been developed and experiments performed to better understand the paradoxical HDL-raising effect of a high fat diet. |
| Dietary fat intake in healthy adolescents: inverse relationships between the estimated intake of saturated fatty acids and serum cholesterol Samuelson, G., L. E. Bratteby, et al. (2001), Br J Nutr 85(3): 333-41. Abstract: The objective of the present study was to describe the intake of dietary fatty acids among healthy 15-year-old boys and girls and to relate the intake of specific fatty acids and the fatty acid composition of the serum cholesterol esters to serum lipid, apolipoprotein (Apo) and insulin concentrations respectively. Fifty-two girls and forty-two boys were randomly selected from the official population register. Unexpectedly, significant inverse associations were found between the dietary content of saturated fatty acids with a chain length of four to fifteen C atoms, mainly derived from milk fat, as well as the corresponding fatty acids in the serum cholesterol esters, on the one hand and the serum concentrations of cholesterol and ApoB on the other. The estimated dietary intake of 4:0-10:0, 12:0 and 14:0 respectively, were all significantly inversely related to the serum cholesterol (r -0.32, r -0.31, r -0.30, all and ApoB (r -0.42, r -0.42, and r -0.40, all concentrations in girls and 12:0 to the ApoB concentration (r -0.55, in boys. The proportions of 12:0 and 15:0 in the serum cholesterol esters were negatively correlated with the serum cholesterol concentrations in both girls (r -0.34, r -0.32, and boys (r -0.53, r -0.32, and with the ApoB concentrations among boys (r -0.61, r -0.43, It is conceivable that milk fat contains or is associated with some component in the diet, or some other characteristics of the food intake, which counterbalances the expected positive relationships between saturated fat intake and lipid levels. |
| Dietary fat quality and circulating cholesterol levels in humans: a review of actions and mechanisms Mazier, M. J. and P. J. Jones (1991), Prog Food Nutr Sci 15(1-2): 21-41. Abstract: Consumption of saturated fats contributes to elevated circulating cholesterol levels, whilst either polyunsaturated or monounsaturated fats are linked to depressed levels. Since elevated serum cholesterol is a risk factor for coronary heart disease, it is of interest to understand the factors responsible for the responses elicited by dietary fat quality. Changes in faecal sterol excretion, exogenous cholesterol absorption, lipoprotein composition, and lipoprotein catabolism can coincide with changes in fat intake but may not necessary cause them. Whether or not rates of whole-body cholesterol synthesis respond to dietary fat quality is not known. To date, animal studies suggest that shifts in LDL receptor-mediated cholesterol transport are to blame for responses of circulating cholesterol levels to dietary fat. |
| Dietary fat saturation and chain length modulate guinea pig hepatic cholesterol metabolism Fernandez, M. L. and D. J. McNamara (1994), J Nutr 124(3): 331-9. Abstract: The effects of dietary fat saturation and saturated fatty acid composition on plasma lipoprotein concentrations and hepatic cholesterol metabolism were investigated in guinea pigs. Animals were fed semipurified diets containing 15 g fat/100 g diet, as palm kernel, palm oil, beef tallow, lard, olive oil or corn oil. Plasma lipoprotein concentrations were significantly altered by the type of dietary fat. The LDL cholesterol concentration was highest in animals fed the diet with palm kernel and lowest in animals fed the diet with corn oil, whereas HDL cholesterol was lowest in beef tallow-fed guinea pigs (P < 0.01). Hepatic cholesteryl ester concentrations were 100% higher in animals fed diets containing polyunsaturated corn oil and monounsaturated olive oil compared with animals fed any of the saturated fat diets (P < 0.01). Hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity varied in the different dietary fat groups independent of hepatic cholesterol pools or plasma LDL concentrations. In contrast, hepatic acyl-CoA: cholesterol acyltransferase (ACAT) activity was significantly correlated with plasma LDL cholesterol across all dietary groups (r = 0.63, P < 0.001). These data demonstrate that regulation of hepatic HMG-CoA reductase activity is relatively independent of changes in plasma lipoprotein levels, whereas hepatic ACAT activity exhibits a positive correlation with plasma LDL cholesterol concentrations. |