| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Influence of FK506 on experimental atherosclerosis in cholesterol-fed rabbits Matsumoto, T., E. Saito, et al. (1998), Atherosclerosis 139(1): 95-106. Abstract: To investigate the role of activated T lymphocytes in the formation of atherosclerotic lesions, we studied the influence of FK506, an immunosuppressant, on the development of atherosclerosis in cholesterol-fed rabbits. New Zealand White rabbits fed on a 1.5% cholesterol diet were administered FK506 at 0.05 mg/kg (n = 12), 0.1 mg/kg (n = 12) or isotonic saline (as the control, n = 12) intramuscularly three times a week for 12 weeks. Although FK506 treatment did not affect plasma lipid levels, it caused an increase in the development of atherosclerotic lesions in a dose-dependent manner. Immunohistochemical analysis of the aorta after 8 weeks on the diet revealed that the ratio of T lymphocytes to the total number of cells in the plaques decreased significantly in the FK506 treated rabbits compared to the control rabbits. In culture, FK506 did not affect smooth muscle cell proliferation and cholesteryl ester formation in the macrophages. In contrast, culture medium from lymphocytes stimulated by concanavalin A decreased the accumulation of cholesteryl ester in the macrophages. This effect was inhibited by the culture medium in the presence of FK506. These findings suggest that activated T lymphocytes may inhibit intracellular cholesterol accumulation in atherosclerotic plaque. |
| Influence of formula versus breast milk on cholesterol synthesis rates in four-month-old infants Bayley, T. M., M. Alasmi, et al. (1998), Pediatr Res 44(1): 60-7. Abstract: We investigated whether supplementation of regular formula (RF) with cholesterol (Ch) (RF+Ch) influenced circulating Ch levels and de novo synthesis compared with their breast-fed (BF) counterparts in 4-mo-old infants. The incorporation rate of deuterium in body water into erythrocyte membrane-free Ch over 48 h was used as an index of cholesterogenesis. Plasma total-Ch and LDL-Ch concentrations were highest (p < 0.02) in BF infants, compared with infants in the RF-fed groups. Infants in the RF+Ch groups showed an intermediate response; their plasma total-Ch and LDL-Ch concentrations were not significantly different from the BF or the RF-fed groups. Plasma total/HDL-Ch and LDL/HDL-Ch ratios were higher (p < 0.05) in BF, and higher in RF+Ch-fed infants, compared with those fed RF, whereas not different between BF and RF+Ch-fed infants. At 4 mo of age, Ch FSR was 4-fold lower (p < 0.0001) in BF versus other groups, but not significantly different between RF- and RF+Ch-fed infants. Thus, despite addition of Ch to the concentration found in breast milk, FSR remained elevated compared with that of the group fed breast milk, with an intermediate response in circulating Ch levels. It is speculated that factors other than Ch intake account for the differential Ch metabolism between formula-fed and BF infants. |
| Influence of gender, body mass index, and age on response of plasma lipids to dietary fat plus cholesterol Clifton, P. M. and P. J. Nestel (1992), Arterioscler Thromb 12(8): 955-62. Abstract: We have conducted a crossover, randomized, double-blind dietary trial that tested the hypothesis that gender influences the response of plasma lipids, in particular high density lipoprotein (HDL) cholesterol, to dietary fat plus cholesterol. Twenty-six men and 25 women were matched for age, low density lipoprotein (LDL) cholesterol, triglyceride, and body mass index (BMI). After a 2-week baseline low-fat (27% of calories), low-cholesterol period, subjects were given two isocaloric liquid supplements for 3 weeks each, one containing 31 g fat (56% saturated) and 650 mg cholesterol, and the other fat free. The baseline HDL2 cholesterol level was significantly higher in women: 0.41 versus 0.26 mmol/l (p less than 0.01). Importantly, women also showed a greater rise in HDL2 cholesterol concentration with the fat/cholesterol supplement: 0.09 versus 0.03 mmol/l (p less than 0.01). The greater increment in women was related to their higher baseline HDL2 cholesterol levels. With the fat and cholesterol supplement, LDL cholesterol values rose from 3.76 to 4.04 mmol/l in women and from 3.77 to 4.13 mmol/l in men. The baseline LDL cholesterol value was found to account for about 35% of the variance in the rise in LDL cholesterol level with fat and cholesterol supplementation in both men and women less than 50 years. In men only, there was a significant effect of age: the change in LDL cholesterol with the fat/cholesterol supplement was 0.16 mmol/l in those less than 50 and 0.54 mmol/l in those greater than 50 years old (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS) |
| Influence of genetic polymorphisms on responsiveness to dietary fat and cholesterol Ye, S. Q. and P. O. Kwiterovich, Jr. (2000), Am J Clin Nutr 72(5 Suppl): 1275S-1284S. Abstract: Genes influence quantitative variations in plasma lipoprotein concentrations. For example, intake of dietary saturated fat and cholesterol raises the average serum cholesterol concentration, leading to a higher risk of coronary artery disease in populations. However, not all individuals within the population are susceptible: genetic factors appear to render individuals either "dietary responsive" or "dietary nonresponsive." In this review, we focus on current knowledge about the influence of genetic polymorphisms in certain genes on the lipoprotein response to dietary fat and cholesterol. Our preliminary studies in the Dietary Intervention Study in Children suggest a significant dose-response relation between the decrease in LDL cholesterol from baseline to 36 mo of follow-up in both the intervention group (who consumed a low-fat, low-cholesterol diet) and the usual care group (who consumed a regular diet) and the presence of the APOA1*A allele at the M1 site and the + site at the M2 site of the gene encoding apolipoprotein (apo) A-I. The DNA polymorphisms on the genes encoding apo A-IV, apo B, apo C-III, apo E, lipoprotein lipase, cholesteryl ester transfer protein, lecithin:cholesterol acyltransferase (phosphatidylcholine-sterol O:-acyltransferase), and LDL receptor were found by others to be associated with the plasma lipoprotein response to dietary intervention. Possible mechanisms involved in these effects are discussed and certain discrepancies in the literature about some genetic effects on responsiveness are analyzed. An improved understanding of the influence of specific genes on lipoprotein responsiveness to dietary fat and cholesterol may allow us to identify and counsel certain individuals to avoid high-fat diets so that they may reduce their risk of developing hyperlipidemia and coronary artery disease. |
| Influence of glucocorticoids and disease activity on total and high density lipoprotein cholesterol in patients with rheumatoid arthritis Boers, M., M. T. Nurmohamed, et al. (2003), Ann Rheum Dis 62(9): 842-5. Abstract: BACKGROUND: Glucocorticoids induce hypercholesterolaemia, a cardiovascular risk factor, in patients with diseases other than rheumatoid arthritis (RA), but the data in RA are contradictory. OBJECTIVE: To determine the effects of antirheumatic treatment, including prednisolone (combination) therapy on total and high density lipoprotein (HDL) cholesterol levels in RA, taking disease activity into account. METHODS: HDL cholesterol and total cholesterol levels were determined in:(a) established RA (b) two cohorts with early active RA, (c) a previously conducted 56 week trial among patients with early RA comparing the value of intensive combination therapy (that included glucocorticoids) with sulfasalazine alone (COBRA trial). RESULTS: In established RA total cholesterol levels were only slightly raised, irrespective of disease activity. However, HDL cholesterol was significantly higher in patients in remission than in patients with active disease. In contrast, in active early RA at baseline total cholesterol was low normal: between 4.6 and 5.1 mmol/l in the different populations. The level of HDL cholesterol was highly dependent on the duration of storage. In both COBRA groups total cholesterol increased by a mean of 0.6 mmol/l. HDL cholesterol increased by more than 50% after treatment, leading to an improvement of the total cholesterol/HDL ratio (atherogenic index). This increase (and index improvement) was much more rapid in the group receiving combination treatment. A similar pattern was seen in the 2001 cohort with early RA. In all the groups with active disease HDL and total cholesterol levels correlated inversely with disease activity. CONCLUSION: In established, but especially in early RA, disease activity is accompanied by atherogenic lipid levels. This dyslipidaemia can be rapidly reversed by aggressive antirheumatic treatment including glucocorticoids. |
| Influence of glutathione depletion on plasma membrane cholesterol esterification and on Tc-99m-sestamibi and Tc-99m-tetrofosmin uptakes: a comparative study in sensitive U-87-MG and multidrug-resistant MRP1 human glioma cells Le Jeune, N., N. Perek, et al. (2004), Cancer Biother Radiopharm 19(4): 411-21. Abstract: In our previous studies, we demonstrated a possible effect of cellular glutathione (GSH) depletion on plasma-membrane permeability and fluidity in glioma-cell lines. We therefore investigated the effect of GSH modulation on accumulation of two radiotracers, Tc-99m-sestamibi (MIBI) and Tc-99m-tetrofosmin (TFOS), and on plasma-membrane cholesterol content in sensitive U-87-MG and resistant U-87-MG-CIS and U-87-MG-MEL (MRP1 positive) human glioma-cell lines. GSH depletion was mediated by BSO pretreatment and addition of N-acetylcysteine reversed the effect. MIBI and TFOS uptakes, total cholesterol, and cholesteryl-ester contents were evaluated under each condition. In contrast with TFOS, MIBI accumulation was inversely proportional to the cell multidrug resistance phenotype. Similar cholesterol contents were observed in all cell lines, demonstrating that MRP1 did not modify lipid membrane composition. A decrease of intracellular GSH allows an increase of plasma-membrane cholesterol and a decrease of cholesteryl-ester content, which in turn results in spectacular TFOS uptake. The GSH status of the cells plays an important role in the plasma membrane cholesterol composition and TFOS uptake, which appears to be particularly sensitive to this modification. In contrast with MIBI, TFOS is not an MRP1 probe in glioma cells, and therefore appears to be a suitable tracer in this indication. |
| Influence of glycemic load on HDL cholesterol in youth Slyper, A., J. Jurva, et al. (2005), Am J Clin Nutr 81(2): 376-9. Abstract: BACKGROUND: The influence of dietary carbohydrate glycemic index on blood lipids has not been well studied. Assessment of glycemic load is not usually included in a standard dietary analysis. OBJECTIVE: The purpose of the present study was to examine relations between diet and blood lipids in youth with a broad range of cholesterol values and carbohydrate, fat, and protein intakes. DESIGN: Relations between blood lipids and dietary constituents were examined in 32 healthy males and females aged 11-25 y. Subjects exhibited a range of LDL-cholesterol values (1.71-6.67 mmol/L) and body mass index z scores (-1.18 to 2.64). Dietary constituents were assessed from 3-d food diaries. RESULTS: The only significant correlations evident were negative correlations between HDL cholesterol and glycemic load (in relation to white bread), percentage carbohydrate, total dietary sugar, total carbohydrate, and fructose. On stepwise multiple regression analysis, glycemic load accounted for 21.1% of the variation in HDL cholesterol. CONCLUSIONS: Glycemic load appears to be an important independent predictor of HDL cholesterol in youth. This relation is of concern and suggests that dietary restrictions without attention to a possible resulting increase in glycemic load may result in an unfavorable influence on blood lipids. |
| Influence of habits on masons' blood cholesterol Mallika, R., N. R. Prasad, et al. (2003), Indian J Physiol Pharmacol 47(4): 429-34. Abstract: Plasma total cholesterol, HDL cholesterol, glucose and total protein were estimated in (male) masons without any habits (normal masons) and masons with habits (cigarette smoking, alcohol consumption and betel-quid cum tobacco chewing) and compared with normal subjects. Masons had less total cholesterol and more HDL cholesterol when compared with normal subjects, which may be due to their occupational physical activities. Among masons, cigarette-smoking masons alone had more total cholesterol and less HDL cholesterol. Blood glucose also decreased in masons and more so in betel-quid cum tobacco chewing masons when compared with normal subjects while total protein content showed no variation. |
| Influence of heat exposure on serum lipid and lipoprotein cholesterol in young male subjects Yamamoto, H., K. C. Zheng, et al. (2003), Ind Health 41(1): 1-7. Abstract: The aims of the present study were to determine the effects of passive heat exposure on serum lipid concentrations in healthy young Japanese males and to analyze the relationship between subjects' physical characteristics and the extent of change in serum lipid concentrations. Thirteen subjects with mean ages of 22.6 +/- 1.0 (mean +/- SE) years were each exposed to control temperature (Tc: 25.2 +/- 0.0 degrees C), moderate (Tm: 35.5 +/- 0.2 degrees C) and high temperature(Th: 39.8 +/- 0.1 degrees C), at a relative humidity of 60.3 +/- 1.2% for one hour. Each exposure was carried out on a different day in random sequence. Blood samples were collected just before, during and after the exposure, and serum lipid concentrations were analyzed. In the Tc condition, the concentrations of total cholesterol (TC), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), triglyceride (TG), and free fatty acid (FFA) did not change significantly. In the Tm condition, HDL-C increased significantly after the exposure and FFA increased during and after exposure. While in the Th condition, TC and TG decreased significantly during and after exposure, and LDL-C decreased during exposure. The correlation between changes in serum lipid concentrations and physical characteristics was analyzed if lipid concentrations changed significantly during or after exposure, but no significant correlation was found. The results indicate passive heat exposure has an effect on serum lipid concentrations which is independent of physical characteristics. |
| Influence of high cholesterol diet and pravastatin sodium on the initiation of liver regeneration in rats after partial hepatectomy Zivna, H., P. Zivny, et al. (2002), Nutrition 18(1): 51-5. Abstract: OBJECTIVES: Liver regeneration is influenced by cholesterol and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA-reductase). HMG-CoA-reductase is a key enzyme for cholesterol synthesis. Recent studies have shown that inhibitors of HMG-CoA-reductase improve liver functions after 67% partial hepatectomy (PH). METHODS: Male Wistar rats (W) and Prague hereditary hypercholesterolemic rats (PHHC) were used. Aqua pro injectione (AI) or pravastatin (prava; 1 mg/kg) was administered orally once daily. Group 1: W, standard diet (SD) + AI; group 2: W, SD + prava; group 3: W, cholesterol-enriched diet (chol) + AI; group 4: PHHC, chol + AI; group 5: PHHC, chol + prava. After 27 d, PH was performed in all groups. RESULTS: Groups fed chol before PH had significantly higher liver triacylglycerol content (group 3: 25.8 +/- 2.6 mg/g of liver weight; group 4: 16.0 +/- 1.0 of liver weight; group 5: 22.0 +/- 1.0 of liver weight) than did the groups fed SD (group 1: 6.1 +/- 0.5; group 2: 5.9 +/- 0.7). Liver DNA synthesis after PH was significantly lower in chol-fed groups (group 3: 561 +/- 78; group 4: 472 +/- 92) than in SD-fed groups (group 1: 1645 +/- 574; group 2: 2935 +/- 1298), except the chol-fed PHHC given prava (group 5: 3230 +/- 527). CONCLUSIONS: In prava-treated rats, the induction of HMG-CoA activity overcame the inhibitory capability of pravastatin. The induction of HMG-CoA-reductase activity had a stimulatory effect on the initiation of liver regeneration. |
| Influence of high cholesterol feeding on the pattern and progression of experimental cerebral ischemia Chui, D. H., J. Marotta, et al. (1991), Biomed Pharmacother 45(9): 409-15. Abstract: The aim of our research was to study if cholesterol feeding might affect the ischemic changes in the vessels surrounding infarction foci in Sephadex G-75-induced cerebral ischemia model (SG-75). One hundred-twenty-four rabbits were divided as follows: group I was given standard food for 5 weeks; group II: as group I and then injected with SG-75; group III: standard food plus 1% cholesterol for 5 weeks; and group IV: as group III and then injected with SG-75. Rabbits were sacrificed 3 h, 6 h and 2, 5 and 7 days after ischemia had occurred. Vessels surrounding infarction foci (SIF) were identified by using a 6% carbon perfusion. Samples were examined by light microscopy and transmission electron microscopy (TEM). The occurrence of hemorrhagic infarction (HI) showed a clear time/course increase in group II whereas a decrease after 2 days in group IV was observed. The rate of HI was 40% and 20% in group II and IV, respectively. SIF vessels showed red blood cells leakage in group II, whereas multiple platelet thrombi appeared in group IV. This phenomenon caused a more extensive ischemic damage, when compared to group II. By making use of a widely employed model of high cholesterol diet and of a more physiological model of cerebral ischemia devised by us, we have provided the evidence that the hypercholesterolemia-induced changes in the SIF vessels strongly affect the pattern and progression of cerebral ischemia. |
| Influence of high density lipoprotein on esterified cholesterol stores in macrophages and hepatoma cells Bernard, D. W., A. Rodriguez, et al. (1990), Arteriosclerosis 10(1): 135-44. Abstract: The ability of high density lipoproteins (HDL) to induce the clearance of cholesteryl esters from cultured cells has been explored. Studies using the J774 mouse macrophage cell line showed that these cells are not stimulated to clear esterified cholesterol upon exposure to HDL. This was observed over a wide range of HDL concentrations (10 to 1000 micrograms/ml HDL protein), and the lack of stimulation was not influenced by a number of factors relating to the preparation of the HDL, such as HDL subfraction, varying extents of lecithin:cholesterol acyltransferase modification, or heparin-Sepharose chromatography to remove particles containing apo E. Neither the method of loading the cells with esterified cholesterol nor the physical state of the lipid droplets affected the inability of HDL to elicit esterified cholesterol clearance. In the presence of the acyl CoA:cholesterol acyltransferase inhibitor, Sandoz 58-035, where a high level of intracellular free cholesterol was generated, efflux of only a small fraction of the excess free cholesterol to HDL was observed. J774 cells were able to clear esterified cholesterol efficiently in the presence of cholesterol-free apolipoprotein HDL/phospholipid particles, indicating that the cells have the capacity to clear esterified cholesterol. Fu5AH hepatoma cells and P388.D1 mouse macrophage cells also failed to clear esterified cholesterol in response to HDL. In contrast, mouse peritoneal macrophages cleared esterified cholesterol efficiently to HDL, indicating that there are fundamental differences between mouse peritoneal macrophages and the other cells types studied in regard to cholesterol metabolism as influenced by HDL. |
| Influence of high-density lipoprotein cholesterol and rheological factors on the sex difference in cardiovascular disease Price, J. F., A. J. Lee, et al. (2000), J Cardiovasc Risk 7(1): 49-56. Abstract: BACKGROUND: It is well established that the incidence of cardiovascular disease among men is higher than that among women. OBJECTIVE: To determine whether differences between men and women in terms of a range of conventional and rheological risk factors could explain this sex difference. DESIGN: This was a population-based cohort study (the Edinburgh Artery Study). METHODS: Men and women aged 55-74 years (n = 1592) were selected at random from the general population of Edinburgh and followed up for 5 years. Baseline cardiovascular risk factors were measured and related to incidence of disease among men and women. RESULTS: Men had higher levels of cigarette smoking, haematocrit and blood viscosity and lower levels of low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol and plasma fibrinogen than did women. The incidences of cardiovascular events among men and women were 48.3 and 26.1 per 1000 person-years, respectively. Adjustment for level of HDL cholesterol reduced the male:female ratio for sex-specific incidence rates of cardiovascular events from 1.80 95% confidence interval (CI) 1.43-2.27 to 1.34 (95% CI 1.04-1.73). This reduction was partially reversed after further adjustment for the other cardiovascular risk factors. The impact of blood viscosity, plasma viscosity and plasma level of fibrinogen on the risk of cardiovascular disease was higher for men than it was for women (multivariate relative risk for blood viscosity were 1.24, 95% CI 1.08-1.43, for men and 0.81, 95% CI 0.61-1.06, for women). CONCLUSIONS: Levels of HDL cholesterol levels in women being higher than those in men may explain some, but not all, of the sex difference in incidence of cardiovascular disease. Greater susceptibility of men to rheological factors might also be important. |
| Influence of insulin on cholesterol removal from macrophages and cholesterol ester uptake by HepG2 cells Wybranska, I., E. Baczynska, et al. (1996), Eur J Clin Invest 26(11): 1004-10. Abstract: The fact that an increased blood insulin level is observed in patients with coronary artery disease (CAD) confirms the hypothesis that insulin promotes the development of atherosclerosis. The low high-density lipoprotein (HDL) concentration observed in such patients may contribute to alteration in reverse cholesterol transport and promote the accumulation of sterols in vascular tissue. We examined the effect of insulin (20-1000 microU mL-1) on cholesterol efflux into HDL3 particles from human blood monocyte/macrophages and rat peritoneal macrophages preloaded with labelled cholesterol esters, and the influence of insulin on the accumulation of sterols by rat liver cells and HepG2 cell line in vitro models. Insulin at concentrations up to 250 microU mL-1 inhibited the efflux of cholesterol from rat macrophages and promoted high uptake of sterols by both types of hepatic cells. Pharmacological concentrations higher than 250 microU mL-1 exerted the opposite effect. In the case of human macrophages, an insulin concentration of 20 microU mL-1 increased cholesterol removal, whereas 100-200 microU mL-1 insulin inhibited cholesterol removal from cells, and very high concentrations (> 350 microU mL-1) again increased cholesterol removal. We have shown that insulin excess counteracts the beneficial effects of HDL in removing cellular cholesterol and, therefore, may promote development of atherogenesis. |
| Influence of insulin resistance, secretion, and clearance on serum cholesterol, triglycerides, lipoprotein cholesterol, and blood pressure in healthy men Godsland, I. F., D. Crook, et al. (1992), Arterioscler Thromb 12(9): 1030-5. Abstract: Relations between serum lipids, lipoproteins, blood pressure, and insulin metabolism were investigated in 158 healthy men aged 19-77 years and with body mass indexes (BMIs) of 19-41 kg.m-2. Mathematical modeling analysis of glucose, insulin, and C-peptide concentrations during an intravenous glucose tolerance test was used to measure parameters of insulin metabolism. In univariate analysis, both fasting and postglucose insulin concentrations showed significant positive associations with fasting serum triglyceride levels (r = 0.33 and 0.38, respectively) and systolic (r = 0.22 and 0.26) and diastolic (r = 0.21 and 0.24) blood pressure and negative associations with high density lipoprotein subfraction 2 cholesterol (HDL2; r = -0.21 and -0.25). In multivariate analysis, the associations between insulin and HDL2 cholesterol concentrations were found to depend on triglyceride levels. Insulin resistance and basal pancreatic insulin secretion showed significant positive associations with serum triglycerides, which were independent of the effects of age, BMI, and fat distribution. Hepatic insulin throughout was independently associated with HDL2 cholesterol. Associations of insulin-related variables with blood pressure were generally dependent on age and BMI. These results underline the importance of insulin sensitivity and insulin concentrations as determinants of triglyceride metabolism. They also indicate a close relation between hepatic insulin handling and HDL2 concentration that is independent of triglyceride metabolism. |
| Influence of insulin sensitivity and the TaqIB cholesteryl ester transfer protein gene polymorphism on plasma lecithin:cholesterol acyltransferase and lipid transfer protein activities and their response to hyperinsulinemia in non-diabetic men Riemens, S. C., A. Van Tol, et al. (1999), J Lipid Res 40(8): 1467-74. Abstract: Lecithin:cholesteryl acyl transferase (LCAT), cholesteryl ester transfer protein (CETP), phospholipid transfer protein (PLTP), and lipoprotein lipases are involved in high density lipoprotein (HDL) metabolism. We evaluated the influence of insulin sensitivity and of the TaqIB CETP gene polymorphism (B1B2) on plasma LCAT, CETP, and PLTP activities (measured with exogenous substrates) and their responses to hyperinsulinemia. Thirty-two non-diabetic men without hyperlipidemia were divided in quartiles of high (Q(1)) to low (Q(4)) insulin sensitivity. Plasma total cholesterol, very low + low density lipoprotein cholesterol, triglycerides, and apolipoprotein (apo) B were higher in Q(4) compared to Q(1) (P < 0.05 for all), whereas HDL cholesterol and apoA-I were lowest in Q(4) (P < 0.05 for both). Plasma LCAT activity was higher in Q(4) than in Q(1) (P < 0. 05) and PLTP activity was higher in Q(4) than in Q(2) (P < 0.05). Insulin sensitivity did not influence plasma CETP activity. Postheparin plasma lipoprotein lipase activity was highest and hepatic lipase activity was lowest in Q(1). Insulin infusion decreased PLTP activity (P < 0.05), irrespective of the degree of insulin sensitivity. The CETP genotype exerted no consistent effects on baseline plasma lipoproteins and LCAT, CETP, and PLTP activities. The decrease in plasma PLTP activity after insulin was larger in B1B1 than in B2B2 homozygotes (P < 0.05). These data suggest that insulin sensitivity influences plasma LCAT, PLTP, lipoprotein lipase, and hepatic lipase activities in men. As PLTP, LCAT, and hepatic lipase may enhance reverse cholesterol transport, it is tempting to speculate that high levels of these factors in association with insulin resistance could be involved in an antiatherogenic mechanism. A possible relationship between the CETP genotype and PLTP lowering by insulin warrants further study. |
| Influence of lipolysis on chylomicron clearance and HDL cholesterol levels Patsch, J. (1998), Eur Heart J 19 Suppl H: H2-6. Abstract: Atherogenic risk is accurately defined by the turnover of the lipoprotein classes that transport cholesterol and triglycerides, and by the apolipoproteins that determine the fate of these particles. Post-prandial triglyceride levels have also been shown to be an accurate predictor of atherogenic risk. The post-prandial triglyceride levels and conversion of very low density lipoprotein (VLDL) to intermediate density lipoprotein (IDL) are controlled by a dynamic metabolic process involving lipoprotein lipase (LPL) and hepatic lipase. The interaction between the two enzymes modulates triglyceride transport through the plasma and influences the structure and serum concentrations of the denser cholesterol-rich low density lipoproteins (LDL) and high density lipoproteins (HDL). Inadequate LPL function, a consequence either of impaired enzyme function or simply post-prandial overloading, can have profound pathophysiological consequences. High levels of large HDL2 reflect effective catabolism of triglyceride-rich lipoproteins by LPL whereas low levels of this lipoprotein reflect inadequate LPL activity or elevated hepatic lipase activity. Individuals with low levels of HDL2 are prone to coronary artery disease. Overloading of LPL can occur in insulin resistance due to the absence of normal insulin-mediated suppression of VLDL secretion and the consequence is hypertriglyceridaemia. In addition, a deficiency in LPL can arise from a genetic defect which, in the homozygous state, results in pronounced hypertriglyceridaemia and pancreatitis. The correct management for patients with inadequate LPL activity is to optimize triglyceride metabolism, particularly in the post-prandial state. |
| Influence of lipoprotein lipase serine 447 stop polymorphism on tracking of triglycerides and HDL cholesterol from childhood to adulthood and familial risk of coronary artery disease: the Bogalusa heart study Chen, W., S. R. Srinivasan, et al. (2001), Atherosclerosis 159(2): 367-73. Abstract: The effects of the lipoprotein lipase (LPL) Serine 447 Stop (S447X) polymorphism on high-density lipoprotein cholesterol (HDLC) and triglycerides (TG) have been demonstrated. However, little is known about its effect on the tracking of HDLC and TG over time and familial risk of coronary artery disease (CAD). This aspect was examined in black and white individuals (n=829) aged 5-18 year at baseline, followed on average 18.8 yr. The frequency of the X447 allele was lower in Blacks than Whites (0.043 vs. 0.087, P=0.002). Carriers vs. noncarriers of the X447 allele had lower TG (99.3 vs 122.1 mg/dl, P<0.01) and higher HDLC (51.1 vs. 49.7 mg/dl, P<0.05) in adulthood, but not in childhood. The trends in genotype-specific means of childhood and adulthood levels of HDLC and TG in sex or race subgroups were similar to those in the total sample. With respect to tracking over time, of those in the bottom quartile of HDLC in childhood, 46.1% of the noncarriers vs. 23.1% of the carriers remained in this lowest quartile into adulthood (P=0.03); corresponding values for the top quartile of HDLC were 37.5% for the noncarriers vs. 57.1% for the carriers (P=0.03). Although TG tended to track better among the carriers in the bottom quartile and among the noncarriers in the top quartile, this trend was not significant. Carriers showed lower prevalence of parental history of CAD than noncarriers (6.9% vs. 14.1%, P=0.02) independently of lipoprotein variables, adiposity, blood pressure, age, sex and race. Thus, the X447 allele of the LPL gene is associated with an increase in HDLC and a decrease in TG in adults, tracking of HDLC since childhood, and a lower family history of CAD. |
| Influence of low cholesterol eggs enriched with vitamin-E and omega-3 fatty acid on blood lipid profile of Wistar rats Taneja, S. K. and A. Rakha (2005), Indian J Exp Biol 43(7): 601-5. Abstract: In the recent past, low cholesterol eggs enriched with vitamin-E and omega-3 fatty acid have been developed and are marketed under different brands claiming them as heart friendly. The influence of these eggs (smart eggs) on lipid profile of rats was evaluated in comparison to that of the standard eggs. Data of 4 week dietary treatment revealed that total plasma cholesterol, low density lipoprotein (LDL) and very low density lipoprotein (VLDL) cholesterol increased only 22% in rats fed on diet containing 4 smart eggs per kg of semi-synthetic diet in contrast to the increase of more than 100 % when fed on diet containing standard eggs. The results suggest that it is not the low cholesterol content alone but also vitamin E and omega-3 fatty acids present in smart eggs that act synergically to prevent a substantial change in blood lipid profile and impose no serious risk to the health of the consumers. |
| Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S Ballantyne, C. M., A. G. Olsson, et al. (2001), Circulation 104(25): 3046-51. Abstract: BACKGROUND: Patients with low HDL cholesterol (HDL-C) and elevated triglyceride had an increased risk for coronary heart disease (CHD) events and received the greatest benefit with fibrate therapy in substudy analyses of the Helsinki Heart Study and the Bezafibrate Infarction Prevention Study. METHODS AND RESULTS: In this post hoc analysis of the Scandinavian Simvastatin Survival Study, which enrolled patients with elevated LDL cholesterol (LDL-C) and CHD, subgroups defined by HDL-C and triglyceride quartiles were compared to examine the influence of HDL-C and triglyceride on CHD events and response to therapy. Patients in the lowest HDL-C (<1.00 mmol/L 39 mg/dL) and highest triglyceride (>1.80 mmol/L 159 mg/dL) quartiles (lipid triad; n=458) had increased proportions of other features of the metabolic syndrome (increased body mass index, hypertension, diabetes), men, prior myocardial infarction, prior revascularization, and beta-blocker use than patients in the highest HDL-C (>1.34 mmol/L 52 mg/dL) and lowest triglyceride (<1.11 mmol/L 98 mg/dL) quartiles (isolated LDL-C elevation; n=545). The major coronary event rate was highest in lipid triad patients on placebo (35.9%), and this subgroup had the greatest event reduction (relative risk 0.48, 95% CI 0.33 to 0.69); a significant treatment-by-subgroup interaction (P=0.03) indicated a greater treatment effect in the lipid triad subgroup than the isolated LDL-C elevation subgroup. CONCLUSIONS: Patients with elevated LDL-C, low HDL-C, and elevated triglycerides were more likely than patients with isolated LDL-C elevation to have other characteristics of the metabolic syndrome, had increased risk for CHD events on placebo, and received greater benefit with simvastatin therapy. |