| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Removal of cholesterol from the rat spleen by phospholipid-apolipoprotein mixtures Mindham, M. A. and P. A. Mayes (1992), Biochem Soc Trans 20(2): 105S. |
| Removal of intrahepatic cholesterol stones by the combination of percutaneous pneumatic balloon dilatation and cholangioscopic lithotomy Satoh, H., Y. Hirohashi, et al. (1992), Fukuoka Igaku Zasshi 83(6): 275-80. Abstract: A 53-year-old man presented with a common hepatic duct stone and was also found to have an incarcerated stone, which was thought to consist of cholesterol, in the intrahepatic bile duct of the right lobe. After operative choledocholithotomy, removal of the intrahepatic cholesterol stone was accomplished with percutaneous cholangioscopic lithotomy (PCL) via a choledochal drainage route after pneumatic balloon dilation of a stricture, followed by internal stenting. Although case reports of primary cholesterol hepatolithiasis with some characteristic clinical features have increased recently in Japan, the natural history and clinical course after non-surgical intervention remain uncertain because of the rarity of this disease entity and lack of long-term follow-up studies. We concluded that intrahepatic cholesterol stones can be removed with percutaneous cholangioscopic lithotomy (PCL) without hepatectomy because ductal inflammatory changes and liver parenchymal atrophy, which are indications for surgical intervention, are seldom encountered in primary cholesterol hepatolithiasis. |
| Removal of intravenous Intralipid in patients with familial hypercholesterolemia during inhibition of cholesterol absorption and synthesis Ketomaki, A., H. Gylling, et al. (2004), Clin Chim Acta 344(1-2): 83-93. Abstract: BACKGROUND: While plant stanols are known to upregulate low density lipoprotein (LDL) receptors, we studied the effects of plant stanol (STA) and sterol (STE) ester spreads on triglyceride-rich lipoprotein (TRL) removal in statin-treated patients with familial hypercholesterolemia (FH) using intravenous Intralipid-squalene fat tolerance test. METHODS: Five patients consumed STA and STE in a randomized, crossover study for 4 weeks. TRL removal was studied at baseline and at the end of both periods. Serum, chylomicron (CM), and very low density lipoprotein lipids, squalene, and plant sterols were measured. RESULTS: LDL cholesterol was decreased by both spreads (15-16%, p<0.05). Plant sterol concentrations were doubled in serum and CM by STE vs. STA. After the injection of Intralipid, CM squalene and sitosterol, but not triglycerides (TG), reached higher peak levels (and area under the incremental curve (AUIC) of squalene) by both spreads than at baseline. Despite different plant sterol concentrations by STE vs. STA, the incremental curves for plant sterols were similar by the spreads. CONCLUSIONS: Despite the retarded removal of TRL lipids by STA and STE in the statin-treated subjects with FH, improvement of the fasting lipid profile was suggested important in consideration of combination of cholesterol absorption inhibitor with statins even in FH. |
| Renal cholesterol accumulation: a durable response after acute and subacute renal insults Zager, R. A., T. Andoh, et al. (2001), Am J Pathol 159(2): 743-52. Abstract: Proximal tubular cholesterol levels rise within 18 hours of diverse forms of acute renal tubular injury (eg, myoglobinuria, ischemia/reperfusion, urinary tract obstruction). These increments serve to protect against further bouts of tubular attack (so-called "acquired cytoresistance"). Whether these cholesterol increments are merely transitory, or persist into the maintenance phase of acute renal failure (ARF), has not been previously defined. Furthermore, whether subacute/insidious tubular injury eg, cyclosporine A (CSA), tacrolimus toxicity, nontubular injury (eg, acute glomerulonephritis), or physiological stress (eg, mild dehydration) impact renal cholesterol homeostasis have not been addressed. This study sought to resolve these issues. Male CD-1 mice were subjected to glycerol-induced ARF. Renal cortical-free cholesterol (FC) and cholesterol ester (CE) levels were determined 3, 5, 7, or 14 days later, and the values contrasted to prevailing blood-urea nitrogen concentrations. The impact of 40 minutes of unilateral renal ischemia plus reflow (3 to 6 days) on mouse cortical FC/CE content was also assessed. Additionally, FC/CE levels were measured in rat renal cortex either 10 days after CSA or tacrolimus therapy, or 48 hours after induction of nephrotoxic serum nephritis. Finally, the impact of overnight dehydration on mouse renal cortical/medullary FC/CE profiles was determined. Compared to sham-treated animals, glycerol, CSA, tacrolimus, ischemia-reperfusion, and nephrotoxic serum each induced dramatic CE +/- FC elevations, rising as much as 10x control values. In the glycerol model, striking correlations (r |
| Renal cholesterol embolism. Apropos of 13 cases Fleury, D., B. Mougenot, et al. (1990), Presse Med 19(22): 1040-4. Abstract: Between January 1981 and April 1988, histologically proven renal cholesterol embolism was diagnosed in 13 men over 60 years of age with a previous history of hypertension and atherosclerosis. Six patients developed acute renal failure, usually induced by a triggering factor such as angiographic procedure or anticoagulation, and associated with peripheral and visceral cholesterol embolism, eosinophilia and a high sedimentation rate. In this group of patients, whose protean clinical manifestations and laboratory data mimicked necrotizing angiitis despite the absence of antineutrophil cytoplasmic antibodies, skin lesion biopsy established the diagnosis and made renal biopsy unnecessary. Six patients had chronic renal failure and elevated sedimentation rate, and the last patient had isolated microhematuria. In these 7 patients, percutaneous renal biopsy was an adequate procedure for the diagnosis of cholesterol embolism. As medical management of cholesterol embolism is essentially preventive, these unusual presentations must be emphasized. |
| Renal cortical cholesterol accumulation is an integral component of the systemic stress response Zager, R. A. and A. Johnson (2001), Kidney Int 60(6): 2299-310. Abstract: BACKGROUND: Direct tubular injury (such as ischemia or myohemoglobinuria) increases renal cortical cholesterol content. This study explored whether systemic forms of stress (such as heat shock or sepsis) can trigger renal cholesterol accumulation, and if so, whether increased 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (HMGCR) expression might be involved. METHODS: Male CD-1 mice were subjected to glycerol-induced myohemoglobinuria (MH), systemic heat shock (HS), or E. coli sepsis. Free cholesterol (FC), cholesteryl esters (CE), and HMGCR (Western blot) levels were assessed 18 hours later. Statin effects on renal cholesterol levels and on the severity of MH-acute renal failure (ARF) were also determined. RESULTS: Sepsis and HS each induced dramatic FC and CE increments, comparable to those observed with myohemoglobinuria, and without inducing acute tubular necrosis (ATN). Part of the cholesterol increments was localized within plasma membrane (detergent resistant) microdomains (for example, rafts/caveolae). HS and MH each increased renal HMGCR, as well as HS protein (HSP-72) expression. Oxidant stress (Fe) imposed on cultured proximal tubule (HK-2) cells also enhanced HMGCR content. Conversely, sepsis did not raise renal HMGCR or HSP-72 levels. Statin therapy decreased the severity of MH-ARF and renal cholesterol content. However, this appeared to arise from a statin-mediated decrease in glycerol-induced extrarenal tissue damage (myolysis/LDH release). CONCLUSIONS: Cholesterol appears to be a renal 'acute phase reactant' with tissue levels increasing with either systemic stress (such as, heat shock, sepsis), or direct tissue damage (such as ATN). Increased HMGCR expression can contribute to this result. Mechanisms other than HMGCR induction also can mediate stress-induced cholesterol increments (for example, in the case of sepsis), and statins can mitigate MH-ARF. However, systemic anti-inflammatory effects, rather than a primary renal action, appear more likely to be involved. |
| Renal dysfunction does not alter the pharmacokinetics or LDL-cholesterol reduction of atorvastatin Stern, R. H., B. B. Yang, et al. (1997), J Clin Pharmacol 37(9): 816-9. Abstract: The objective of this study was to determine the effects of renal dysfunction on the steady-state pharmacokinetics and pharmacodynamics of atorvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Nineteen subjects with calculated creatinine clearances ranging from 13 mL/min to 143 mL/min were administered 10 mg atorvastatin daily for 2 weeks. Pharmacokinetic parameters and lipid responses were analyzed by regression on calculated creatinine clearance. Correlations between steady-state atorvastatin pharmacokinetic or pharmacodynamic parameters and creatinine clearance were weak and, in general, did not achieve statistical significance. Although the elimination rate constant, lambda z (0.579), was significantly correlated with creatinine clearance, neither maximum plasma concentration (Cmax, -0.361) nor oral clearance (Cl/F, 0.306) were; thus, steady-state exposure is not altered. Renal impairment has no significant effect on pharmacodynamics and pharmacokinetics of atorvastatin. |
| Renal embolism caused by cholesterol crystals: late onset of renal insufficiency de la Casa Monje, R., J. Martinez Ara, et al. (1992), Med Clin (Barc) 98(15): 597-8. |
| Renal failure and cholesterol crystal embolization: a report of 4 surviving cases and a review of the literature Mannesse, C. K., P. J. Blankestijn, et al. (1991), Clin Nephrol 36(5): 240-5. Abstract: Four patients with end-stage renal failure (suspected to be) caused by cholesterol crystal emboli are described. Although cholesterol crystal embolization is generally considered to be fatal specifically when it is associated with renal failure, all four patients survived and in three renal function improved after periods of 3 weeks to 14 months of hemo- or peritoneal dialysis. The literature on cholesterol crystal embolization is reviewed and possible mechanisms of (partial) recovery of renal function are discussed. |
| Renal failure due to cholesterol emboli Fraser, I., B. Ihle, et al. (1991), Aust N Z J Med 21(4): 418-21. Abstract: Renal failure due to cholesterol embolisation is an uncommonly recognised condition. It is usually associated with severe aortic atherosclerosis and in most cases follows a vascular event, such as angiography, vascular surgery, or aneurysm rupture. We report nine patients, all males, who presented to our unit. Six patients survived the initial event, although two died six and eight weeks later. This report emphasises that, although this condition has a high mortality, long term survival is not a rare event. |
| Renal failure due to cholesterol embolization following percutaneous transluminal renal angioplasty Koga, T., S. Okuda, et al. (1991), Jpn J Med 30(1): 35-8. Abstract: Percutaneous transluminal renal angioplasty was performed in a 63-year-old diabetic woman who had renovascular hypertension with solitary functioning kidney and diffuse atherosclerosis. Angioplasty was technically successful, while thereafter, fever and myalgia of legs occurred with gradual increases in blood urea nitrogen and creatinine. The patient became uremic over a month after angioplasty and was placed on dialysis. She died six months after angioplasty. Autopsy revealed cholesterol embolization in bilateral kidney, pancreas and spleen, causing subacute renal failure. It is suggested that careful assessment of the patient should be made when determining the need for renal angioplasty for renovascular hypertension with a solitary functioning kidney. |
| Renal impairment and intraglomerular mononuclear phagocytes in cholesterol-fed rabbits Yoshimura, N., S. Arima, et al. (1994), Nephron 68(4): 473-80. Abstract: Morphological and immunohistochemical studies using the anti-macrophage monoclonal antibody RbM2 were performed in cholesterol-fed rabbits. From the beginning of the experiment, the levels of lipoproteins showed the pattern of familial type III hyperlipoproteinemia patients, and glomerular endothelial and mesangial cells had lipid deposits. By the 3rd week, RbM2-positive cells appeared in the capillary lumina. These cells became larger and increased in number after the 8th week. Although they had become very large and had increased noticeably by the 20th week, few sclerotic glomeruli were observed. We could hardly detect any proliferation of or foamy changes in the mesangial cells, and monocyte/macrophages showed no proliferative capacity within the glomeruli. These findings suggest that hyperlipidemia alone did not cause proliferation or foam transformation of the mesangial cells. The glomerular macrophages, probably derived from circulating monocytes, did not induce a glomerular injury under the short-term hyperlipidemic conditions of these experiments. |
| Renal vasoconstriction caused by short-term cholesterol feeding is corrected by thromboxane antagonist or probucol Kaplan, R., H. S. Aynedjian, et al. (1990), J Clin Invest 86(5): 1707-14. Abstract: Recent studies indicate that short-term cholesterol feeding causes vascular hyperreactivity and/or increased tone in certain vascular beds. The present study in rats examined the effect of 3 wk of cholesterol-supplemented diet (CSD) on renal hemodynamics. We tested the hypothesis that LDL oxidized in vivo is causally related to increased renal vascular tone by adding the antioxidant drug probucol to the CSD (CSD + P). Micropuncture of surface nephrons in the CSD rats demonstrated that single nephron glomerular filtration rate (SNGFR) and single nephron afferent plasma flow (QA) were markedly lower than in normal rats, whereas glomerular capillary pressure (PGC), afferent arteriolar resistance (RA), and single nephron filtration fraction (SNFF) were higher. In the CSD + P animals, almost all of these hemodynamic abnormalities were absent. TXB2 and PGE2 were increased in proximal tubule fluid and urine in the CSD rats, but normal in the CSD + P group. Infusion of a TXA2 receptor antagonist into the suprarenal aorta of CSD rats caused a rapid return to normal of RBF (renal blood flow), GFR (glomerular filtration rate), SNGFR, QA, RA, PGC, and Kf (ultrafiltration coefficient). Our observations demonstrate that cholesterol feeding leads to renal vasoconstriction, which appears to be mediated largely by increased TXA2 production. The fact that probucol prevented the hemodynamic abnormalities as well as the increased TX production is consistent with the hypothesis that LDL oxidized in vivo initiates events leading to TX mediated vasoconstriction. |
| Repeated bile acid therapy for the long-term management of cholesterol gallstones Petroni, M. L., R. P. Jazrawi, et al. (1996), J Hepatol 25(5): 719-24. Abstract: BACKGROUND/AIMS: Following non-surgical treatment, cholesterol gallstones recur in a high proportion of patients, and recurrence cannot be predicted nor effectively prevented. Our aim was to test prospectively the viability and the efficacy of repeated bile acid therapy, in which recurrent stones are diagnosed at an early stage by regular ultrasound monitoring and promptly retreated, as a strategy for the management of these patients in clinical practice. METHODS: One hundred and seventy-two consecutive patients were recruited upon achieving complete gallstone dissolution using non-surgical therapy (bile acids or lithotripsy plus bile acids), and followed up at 6-monthly intervals by ultrasound scan. Gallstone recurrence was promptly treated by a combination of ursodeoxycholic acid plus chenodeoxycholic acid (5 mg/kg per day each) for a period of 2 years, or less if complete redissolution was achieved. Median follow-up period was 34 months (range 6-70). RESULTS: Forty-five patients had gallstone recurrence; of these, 39 underwent one or more repeated courses of bile acid therapy (follow-up data available in 27). Gallstone recurrence rate was 15% at 1 year and 47% at 5 years. Average annual redissolution rate of recurrent gallstones (intention to treat) was 41%. The proportion of gallstone-free patients in the whole population was 88%, 84%, 77%, 78%, 75% at 1-5 years, respectively, and rose to > 90% at 3 years onwards in patients with single primary stones. CONCLUSIONS: We conclude that repeated bile acid therapy maintains the majority of patients gallstone free, and is therefore an effective long-term management strategy, especially in patients with primary single gallstones. |
| Repeated measurements of serum cholesterol and blood pressure in relation to long-term incidence of myocardial infarction. The Zutphen Study de Vries, C. L., E. J. Feskens, et al. (1993), Cardiology 82(2-3): 89-99. Abstract: Repeated risk factor measurements reduce the amount of random error due to intraindividual variation. Annual measurements of serum cholesterol and systolic blood pressure were done in a cohort of 878 men, aged 40-59 years, between 1960 and 1970. This study examined for both risk factors the association with the incidence of myocardial infarction (MI) during follow-up till 1985. Mean values from repeated measurements yielded stronger statistical associations with MI incidence than single observations. However, when measurements were extended over too many years in this middle-aged cohort, a bias occurred due to selective loss of high-risk individuals as early cases. This was especially the case of serum cholesterol. Taking account of trends in regression analysis did not show any advantage over the use of mean values. |
| Replacement of butter on bread by rapeseed oil and rapeseed oil-containing margarine: effects on plasma fatty acid composition and serum cholesterol Seppanen-Laakso, T., H. Vanhanen, et al. (1992), Br J Nutr 68(3): 639-54. Abstract: The effects of zero-erucic acid rapeseed oil and rapeseed oil-containing margarine on plasma fatty acid composition and serum cholesterol were studied in butter users (n 43). Compliance to the substitution was followed by fatty acid analysis of total plasma and plasma phospholipids. The amount of substitute fats represented, on average, 21% of total fat and 8% of total energy intake. Changes in the relative fatty acid composition of plasma phospholipids indicated further fatty acid metabolism, and were closely related to the serum cholesterol level. The reduction in saturated fatty acids led to a significant increase in the proportion of n-3 and n-6 polyunsaturated fatty acids (PUFA) with the rapeseed oil diet, whereas the margarine caused a significant rise in n-6 PUFA only. The increase in the proportions of the two PUFA families occurred in accordance with their competitive order, most completely with the rapeseed oil diet. When butter was replaced by rapeseed oil, low-density-lipoprotein-cholesterol decreased by an average of 9.1% without a reduction in high-density-lipoprotein-cholesterol. During margarine substitution the reduction was 5.2%, on average. Of the plasma phospholipids, alpha-linolenic acid and the linoleic:stearic acid ratio, but not oleic acid, were the components most significantly correlated with serum cholesterol levels or the decrease in these levels. The results show that rapeseed oil can act primarily as a source of essential fatty acids, rather than that of monoenes, in the diet of butter users. |
| Replacement of carbohydrate by protein in a conventional-fat diet reduces cholesterol and triglyceride concentrations in healthy normolipidemic subjects Wolfe, B. M. and L. A. Piche (1999), Clin Invest Med 22(4): 140-8. Abstract: OBJECTIVE: To determine the effect on plasma lipid profiles of replacement of dietary carbohydrate by low-fat, high-protein foods. DESIGN: Cross-over randomized controlled trial. PARTICIPANTS: Ten healthy, normolipidemic subjects (8 women and 2 men). INTERVENTIONS: Subjects were randomly allocated to either a low-protein (12%) or high-protein (22%) weight-maintaining diet for 4 weeks and then switched to the alternate diet for 4 more weeks. The first 2 weeks of each diet served as an adjustment/washout period. Fat was maintained at 35% of energy, mean cholesterol intake at 230 mg per day and mean fibre intake at 24 g per day. Compliance was promoted by the use of written dietary protocols based on the food preferences of the subjects and weekly dietary consultation as required. OUTCOME MEASURES: Mean plasma levels of total, very-low-density-lipoprotein (VLDL), low-density-lipoprotein (LDL), and high-density-lipoprotein (HDL) cholesterol, and of total and very-low-density-lipoprotein (VLDL) triglycerides. Satiety levels were self-rated on a 10-point scale. RESULTS: Consumption of the high- versus the low-protein diet resulted in significant reductions in mean plasma levels of total cholesterol (3.8 v. 4.1 mmol/L, p < 0.05), VLDL cholesterol (0.20 v. 0.26 mmol/L, p < 0.02), LDL cholesterol (2.4 v. 2.6 mmol/L, p < 0.05), total triglycerides (0.69 v. 0.95 mmol/L, p < 0.005) and VLDL triglycerides (0.35 v. 0.57 mmol/L, p < 0.001), as well as in the ratio of total cholesterol to HDL cholesterol (3.1 v. 3.5, p < 0.01). A trend towards an increase in HDL cholesterol (1.26 v. 1.21 mmol/L, p = 0.30) was observed but was not statistically significant. Satiety levels tended to be higher among those eating the high-protein diet (6.1 v. 5.4, p = 0.073). CONCLUSIONS: Moderate replacement of dietary carbohydrate with low-fat, high-protein foods in a diet containing a conventional level of fat significantly improved plasma lipoprotein cardiovascular risk profiles in healthy normolipidemic subjects. |
| Replacement of cholesterol gallstones by murideoxycholyl taurine gallstones in prairie dogs fed murideoxycholic acid Cohen, B. I., N. Ayyad, et al. (1991), Hepatology 14(1): 158-68. Abstract: The effect of two hydrophilic bile acids, murideoxycholic acid (3 alpha,6 beta-dihydroxy-5 beta-cholanoic acid) and ursodeoxycholic acid, on cholesterol and bile acid metabolism and hepatic pathology and gallstone composition was studied in the prairie dog. Cholesterol gallstones were induced by feeding a diet containing 1.2% cholesterol for 75 days. The animals were divided into six groups, and gallstone regression was studied as follows: groups 2 and 5, chow plus 0.2% cholesterol; groups 3 and 6, chow plus 0.2% cholesterol plus 0.15% ursodeoxycholic acid; groups 4 and 7, chow plus 0.2% cholesterol plus 0.15% murideoxycholic acid. Animals in groups 2 to 4 were killed after an additional 6 wk; animals in groups 5 to 7 were killed after an additional 12 wk. Gallstone dissolution did not occur in any group. The gallstones in groups 2, 3, 5 and 6 were typical cholesterol aggregates, as determined by polarized light microscopy and Fourier transform infrared spectrometry. The gallstones of the murideoxycholic acid group were large, solitary, dark stones that appeared radiopaque under 22 kVp x-ray examination. Scanning electron microscopy showed that in these stones the cholesterol crystals had been replaced by an amorphous material, both within the stone and on the stone surface. Chemical analysis indicated that at the end of 12 wk the calcium/sodium salt of the taurine conjugate of murideoxycholic acid (murideoxycholyl taurine) comprised 70% of the stones; protein, cholesterol and small amounts of other bile salts were also present. In vitro studies confirmed the insolubility of the sodium and calcium salts of murideoxycholyl taurine. These studies indicate that the hydrophilic bile acids, murideoxycholic acid and ursodeoxycholic acid, did not achieve gallstone dissolution under the conditions used. In the animals fed murideoxycholic acid, an insoluble calcium salt of murideoxycholyl taurine replaced cholesterol as the major constituent of gallbladder stones. This is the first example of an insoluble dihydroxy taurine-conjugated bile acid; administration of the unconjugated bile acid induced precipitation of a kind of gallstone not previously reported. The final result was transformation of cholesterol stones to bile salt stones. |
| Replacement of dietary saturated fat with monounsaturated fat: effect on atherogenesis in cholesterol-fed rabbits clamped at the same plasma cholesterol level Nielsen, L. B., P. Leth-Espensen, et al. (1995), Br J Nutr 74(4): 509-21. Abstract: The aim was to compare the effect on atherogenesis of dietary monounsaturated and saturated fatty acids in cholesterol-clamped rabbits. To obtain an average plasma cholesterol concentration of 20 mmol/l in each rabbit during the 13-week cholesterol-feeding period, dietary cholesterol was adjusted weekly. The amount of fat fed daily was 10 g per rabbit in Expts A (n 23), C (n 36), and D (n 58) and 5 g per rabbit in Expt B (n 24). The source of monounsaturated fatty acids was olive oil in all four experiments. The source of saturated fatty acids was butter in Expt A, lard in Expt B, coconut oil in Expt C, and butter or lard in Expt D. Generally, olive oil-fed groups received more cholesterol and tended to have more cholesterol in VLDL and less in LDL compared with groups receiving saturated fat. Analysis of variance of the combined results of all four experiments showed that, in comparison with saturated fat, olive oil lowered aortic cholesterol by 13 (-9-30, 95% confidence interval) % in the aortic arch, and by 10 (-10-26) % in the thoracic aorta, which was not significant. In the comparison with olive oil, no differences in effects on aortic cholesterol content were detected between butter, lard and coconut oil. These findings do not support the view that replacement of dietary saturated fat with olive oil has a major impact on the development of atherosclerosis in addition to that accounted for by changes in plasma cholesterol levels. |
| Replacement of dietary saturated fatty acids by trans fatty acids lowers serum HDL cholesterol and impairs endothelial function in healthy men and women de Roos, N. M., M. L. Bots, et al. (2001), Arterioscler Thromb Vasc Biol 21(7): 1233-7. Abstract: We tested whether trans fatty acids and saturated fatty acids had different effects on flow-mediated vasodilation (FMD), a risk marker of coronary heart disease (CHD). Consumption of trans fatty acids is related to increased risk of CHD, probably through effects on lipoproteins. Trans fatty acids differ from most saturated fatty acids because they decrease serum high-density lipoprotein (HDL) cholesterol, and this may increase the risk of CHD. We fed 29 volunteers 2 controlled diets in a 2x4-week randomized crossover design. The "Trans-diet" contained 9.2 energy percent of trans fatty acids; these were replaced by saturated fatty acids in the "Sat-diet." Mean serum HDL cholesterol after the Trans-diet was 0.39 mmol/L (14.8 mg/dL), or 21% lower than after the Sat-diet (95% CI 0.28 to 0.50 mmol/L). Serum low density lipoprotein and triglyceride concentrations were stable. FMD+SD was 4.4+/-2.3% after the Trans-diet and 6.2+/-3.0% after the Sat-diet (difference -1.8%, 95% CI -3.2 to -0.4). Replacement of dietary saturated fatty acids by trans fatty acids impaired FMD of the brachial artery, which suggests increased risk of CHD. Further studies are needed to test whether the decrease in serum HDL cholesterol caused the impairment of FMD. |