| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Effect of plasma cholesterol on red blood cell oxygen transport Buchwald, H., T. J. O'Dea, et al. (2000), Clin Exp Pharmacol Physiol 27(12): 951-5. Abstract: 1. Oxygen (O2) transfer from the blood to tissues is a function of the red blood cell (RBC) O2 saturation (SO2), the plasma O2 content being negligible. Under conditions of increased tissue O2 demand, the SO2 of arterial blood does not change appreciably (97%); however, the SO2 of mixed venous blood, equal to that of the perfused tissues, can go as low as 20%. 2. Tissue O2 availability is limited by the exposure time to a RBC, which decreases under conditions of maximum stress (< 1 s). If the O2 unloading time was to increase significantly, because of a decrease in the RBC diffusion constant or an increase in the RBC membrane thickness, the RBC O2 unloading time would exceed tissue (e.g. cardiac) transit time and O2 transfer would be impaired. 3. Cholesterol constitutes the non-polar, hydrophobic lipid of the enveloping layer of the RBC membrane. As the cholesterol content of the RBC increases, the fluidity of the membrane decreases and the lipid shell stiffens. 4. Early studies demonstrated that high blood cholesterol concentrations were associated with reduced blood O2 transport; in essence, the haemoglobin dissociation curve was shifted to the left. 5. Current investigations have shown that the cholesterol RBC membrane barrier to O2 diffusion delayed O2 entry into the RBC during saturation and delayed O2 release from the RBC during desaturation. In an analysis of 93 patients divided by their cholesterol concentration into five groups, the percentage change in blood O2 diffusion was inversely proportional to the cholesterol concentration. 6. The RBC membrane cholesterol is in equilibrium with the plasma cholesterol concentration. It stands to reason that as the plasma cholesterol increases, the RBC membrane becomes impaired and O2 transport is reduced. 7. The implications of this new perspective on O2 transport include the ability to increase tissue oxygenation by lowering plasma cholesterol. |
| Effect of plasma cholesterol reduction by pravastatin on the functional properties of forearm arteries in hypercholesterolemic patients Baldassarre, D., G. Busnach, et al. (1999), Nutr Metab Cardiovasc Dis 9(3): 108-17. Abstract: BACKGROUND AND AIM: Since functional properties in the vasculature of hypercholesterolemic subjects are impaired, a six-month pravastatin treatment (20 mg/die) was tested in an open design, on the impaired unstimulated forearm arterial compliance (Un-FAC(AUC)) of 14 asymptomatic type IIa familial hypercholesterolemic patients. In order to evaluate whether FAC(AUC) changes might be related to the extent of cholesterol reduction achieved, this evaluation was carried out in five severely hypercholesterolemic patients, undergoing LDL-apheresis. METHODS AND RESULTS: Arterial functional properties, i.e. FAC(AUC) responses to glyceryl trinitrate (GTN-FAC(AUC)) and acetylcholine (ACh-FAC(AUC), four patients) and the effects on rest and peak forearm blood flow and vascular resistance were evaluated on the non-dominant arm using plethysmographic methods, that also allow the direct assessment of the non-linear "compliance-blood pressure" curve. Selective LDL-apheresis was performed by using a dextran-sulphate column. Pravastatin effectively lowered plasma total (-16%, p = 0.002) and LDL cholesterol levels (-22%, p = 0.006 vs baseline). Rest and peak flow, basal and post ischemic vascular resistance were not affected as well as Un-FAC(AUC) and GTN-FAC(AUC). However, in the four hypercholesterolemic patients undergoing ACh infusion, there was an improvement in the ACh-FAC(AUC) of borderline statistical significativity (p = 0.056). LDL-apheresis reduced plasma total and LDL cholesterol levels by 55% and 59%, without affecting blood pressure. In this series of five patients Un-FAC(AUC) increased, the Un-FAC(AUC) rise being inversely related to the absolute reduction of plasma total (r = 0.92, p < 0.05) and LDL cholesterol (r = 0.89, p < 0.05) levels. CONCLUSIONS: In hypercholesterolemic patients a short-term hypocholesterolemic treatment with pravastatin, although able to improve the lipid profile, cannot alter significantly blood flow, vascular resistance, Un-FAC(AUC) and GTN-FAC(AUC). A possible selective improvement in the ACh-receptor-activated signal transduction pathway has been observed and the importance of a drastic reduction of cholesterol concentrations in order to affect the Un-FAC(AUC) is suggested. |
| Effect of Pluronic L81, a hydrophobic surfactant, on intestinal mucosal cholesterol homeostasis Pool, C., D. F. Nutting, et al. (1991), Am J Physiol 261(2 Pt 1): G256-62. Abstract: Addition of triglyceride and phospholipid to sodium taurocholate when chylomicron output was blocked by L81 did not increase lymphatic total cholesterol output or mucosal unesterified (UC) content more than with sodium taurocholate alone, but mucosal esterified cholesterol (CE) was increased slightly. In these animals with defective chylomicron formation, excess cholesterol accumulated in the intestinal mucosa mainly as CE. The mucosal cholesterol content of animals with normal chylomicron transport expanded during cholesterol and triglyceride absorption, and the expansion led to increased lymphatic secretion of CE. These animals accumulated significantly less CE in their mucosa than did rats treated with L81, but had about the same amount of mucosal UC. However, the overall uptake of cholesterol from the lumen, as determined by either radioactivity or mass of cholesterol in mucosa and lymph, was significantly less in the L81 rats. Also, more radioactive cholesterol remained in the lumen of the L81-treated rats. Finally, the data on specific activities of free and esterified cholesterol showed that the mucosal cholesterol derived from the lumen does not mix evenly with the free cholesterol pool in the enterocytes and is preferentially esterified for export in lymph as triglyceride-rich lipoprotein. |
| Effect of policosanol on the hepatic cholesterol biosynthesis of normocholesterolemic rats Menendez, R., A. M. Amor, et al. (1996), Biol Res 29(2): 253-7. Abstract: We have suggested previously, measuring 14C-acetate incorporation into free cholesterol, that oral administration of policosanol inhibits hepatic cholesterol biosynthesis in rats. Nevertheless, since acetate has limitations to study cholesterol synthesis in vivo, we now investigate rates of incorporation of labeled water into hepatic sterol after policosanol treatment. Absolute rates of incorporation of 3H-water in sterols were depressed by policosanol by about 20%, giving a more accurate degree of cholesterol biosynthesis inhibition in this species. Since policosanol did not inhibit labeled mevalonate incorporation into cholesterol in rat liver, we also studied the effect of policosanol on hydroxy-methylglutaryl-coenzyme A (HMG-CoA) reductase. Reductase activity assayed in microsomes treated with policosanol remained unchanged, suggesting that cholesterol synthesis is not inhibited by a direct action of policosanol on this enzyme. |
| Effect of polydextrose on absorption of triglyceride and cholesterol in mesenteric lymph-fistula rats Ogata, S., K. Fujimoto, et al. (1997), Proc Soc Exp Biol Med 215(1): 53-8. Abstract: In most experimental designs, the inhibitory effect of water-soluble dietary fibers on lipid absorption is evaluated by the decrease in plasma lipid concentration or the increase in fecal lipid output. The aim of this study was to evaluate the acute effect of a water-soluble polysaccharide, polydextrose, on lipid transport to the mesenteric lymph using lymph-fistula rats. The mesenteric lymph duct of rats was cannulated, and an infusion tube was introduced into the duodenum. After recovery, a lipid emulsion containing radioactive triolein and cholesteryl oleate was infused into the duodenum for 8 hr. The tested group was infused with the lipid emulsion containing 5% or 10% polydextrose as dietary fiber. Samples from the lymph-fistula were collected, and the luminal contents and mucosa were collected at the end of infusion. Lymph flow in the mesenteric lymph decreased in the polydextrose group after the infusion. The amounts of both triglyceride and cholesterol remaining in the lumen were greater in the polydextrose group, due to decreased transport of lipid into the lymph. These effects were dose dependent in the 5% and 10% polydextrose groups. The results of this study indicate that polydextrose retarded the transport of triolein and cholesterol into the mesenteric lymph. |
| Effect of pore sizes and cholesterol-lipid solution on the fracture toughness of pure titanium sintered compacts Teoh, S. H., R. Thampuran, et al. (1993), Biomaterials 14(6): 407-12. Abstract: Commercial pure titanium has been widely used as an implant material because of its excellent biocompatibility and good ductility. To determine the effect of pore size on the fracture resistance of porous titanium compacts, a series of fracture toughness (KQ) tests were performed on commercial pure titanium powder compacted to 0.17 and 0.62 GPa. Pore sizes ranged from 25 to 103 microns, with porosity between 8.5 and 35%. Two sets of fracture toughness tests using disc-shaped compacts (ASTM E 399-90) were performed, the first in air at 37 degrees C and the second with compacts treated in cholesterol-lipid solution at 37 degrees C. The KQ value of compacts with a smaller mean pore size (ca. 50 microns) was approximately twice that of the compacts with a larger mean pore size (100 microns). The effect of cholesterol-lipid solution treatment was detrimental, perhaps due to preferential lipid absorption by the titanium oxide and/or the presence of chlorides. For the smaller pore size compacts, the KQ values decreased by up to 20%. For the larger pore size compacts, the effect of cholesterol-lipid solution was less significant. Morphologically, compacts with smaller pore size had a predominantly ductile fracture with significantly higher dimple density than the larger pore size compacts. |
| Effect of potentially probiotic lactobacilli on faecal enzyme activity in minipigs on a high-fat, high-cholesterol diet-a preliminary in vivo trial Haberer, P., M. du Toit, et al. (2003), Int J Food Microbiol 87(3): 287-91. Abstract: Minipigs were fed a "Western-style", high-cholesterol diet for a baseline period, followed by the diet containing a mixture of three Lactobacillus strains with potential probiotic features, after which a normal pig diet was followed. The faecal enzyme activity for beta-glucuronidase and azoreductase, which are commonly considered as markers for procarcinogenic activity, was significantly reduced during the 5 weeks of "probiotic" supplementation. During the period of Lactobacillus administration, the cell counts for total anaerobes increased, whereas the total number of aerobes showed no change. |
| Effect of pravastatin (10 mg/day) on progression of coronary atherosclerosis in patients with serum total cholesterol levels from 160 to 220 mg/dl and angiographically documented coronary artery disease. Coronary Artery Regression Study (CARS) Group Tamura, A., Y. Mikuriya, et al. (1997), Am J Cardiol 79(7): 893-6. Abstract: To evaluate the effect of pravastatin on progression of coronary atherosclerosis in normocholesterolemic patients with coronary artery disease (CAD), 90 patients with CAD and serum cholesterol levels of 160 to 220 mg/dl were randomized into a pravastatin (10 mg/day) group (n = 45) and control group (n = 45) in a 2-year study. The proportions of patients with progression (an increase of > or = 15% in percent stenosis) and regression (a decrease of > or = 15% in percent stenosis) of coronary atherosclerosis were compared between the 2 groups. Of 90 patients, 80 (89%) had a final angiogram: the pravastatin (n = 39) and control group (n = 41). Percent changes in total cholesterol, low-density lipoprotein cholesterol, and apoprotein B levels were significantly greater in the pravastatin group than in the control group (total cholesterol -11 +/- 12% vs 3 +/- 15%, p < 0.01; low-density lipoprotein cholesterol -18 +/- 16% vs 4 +/- 21%, p < 0.01; apoprotein B -5 +/- 20% vs 6 +/- 20%, p < 0.05). The proportion of patients with progression of coronary atherosclerosis was significantly smaller in the pravastatin group than in the control group (21% vs 49%, p < 0.05). The proportion of patients with disease regression did not differ in the 2 groups (3% vs 2%, p = NS). In conclusion, this study indicates that cholesterol-lowering therapy with pravastatin can prevent the progression of coronary atherosclerosis even in normocholesterolemic patients with established CAD. |
| Effect of pravastatin on cardiovascular events in older patients with myocardial infarction and cholesterol levels in the average range. Results of the Cholesterol and Recurrent Events (CARE) trial Lewis, S. J., L. A. Moye, et al. (1998), Ann Intern Med 129(9): 681-9. Abstract: BACKGROUND: A majority of all myocardial infarctions occur in patients who are 65 years of age or older and have average cholesterol levels, but little information is available on whether cholesterol lowering in such patients reduces the rate of recurrent cardiovascular disease. OBJECTIVE: To determine whether pravastatin reduces the rate of recurrent cardiovascular events in older patients. DESIGN: Subset analysis of a randomized, controlled trial. SETTING: 80 hospitals and affiliates in the United States and Canada. PATIENTS: 1283 patients aged 65 to 75 years who had had myocardial infarction and had a plasma total cholesterol level less than 6.2 mmol/L (240 mg/dL) and a low-density lipoprotein cholesterol level of 3.0 to 4.5 mmol/L (115 to 174 mg/dL). INTERVENTION: Pravastatin, 40 mg/d, or placebo. MEASUREMENTS: Five-year event rates of major coronary events (coronary death, nonfatal myocardial infarction, angioplasty, or bypass surgery) and stroke. RESULTS: Major coronary events occurred in 28.1% of placebo recipients and 19.7% of pravastatin recipients (difference, 9.0 percentage points 95% CI, 4 to 13 percentage points; relative risk reduction, 32%; P < 0.001). Coronary death occurred in 10.3% of the placebo group and in 5.8% of the pravastatin group (difference, 4.6 percentage points CI, 1.9 to 6.5 percentage points; relative risk reduction, 45%; P = 0.004). Stroke incidence was 7.3% in the placebo group and 4.5% in the pravastatin group (absolute reduction, 2.9 percentage points CI, 0.3 to 4.5 percentage points; relative reduction, 40%; P = 0.03). The numbers of older patients needed to treat for 5 years were 11 (CI, 8 to 24) to prevent a major coronary event and 22 (CI, 15 to 53) to prevent a coronary death. For every 1000 older patients treated, 225 cardiovascular hospitalizations would be prevented compared with 121 hospitalizations in 1000 younger patients. CONCLUSIONS: In older patients with myocardial infarction and cholesterol levels in the average range, pravastatin is associated with a clinically important reduction in risk for major coronary events and stroke. Given the high cardiovascular event rate in older patients, the potential for absolute benefit in this age group is substantial. |
| Effect of pravastatin on cardiovascular events in women after myocardial infarction: the cholesterol and recurrent events (CARE) trial Lewis, S. J., F. M. Sacks, et al. (1998), J Am Coll Cardiol 32(1): 140-6. Abstract: OBJECTIVES: We sought to determine the effect of pravastatin on recurrent cardiovascular events in women with average cholesterol levels after myocardial infarction (MI). BACKGROUND: Little information is available on the effectiveness of lipid lowering in secondary prevention of coronary heart disease (CHD) in women; in particular, those with CHD and average cholesterol levels. METHODS: In the Cholesterol and Recurrent Events (CARE) trial, 576 postmenopausal women, between 3 and 20 months after MI, with a total cholesterol level <240 mg/dl and a low density lipoprotein cholesterol level 115 to 174 mg/dl, were randomized to receive pravastatin 40 mg/day or matching placebo for a median follow-up period of 5 years. The main outcome measures were combined coronary events (coronary death, nonfatal MI, percutaneous transluminal coronary angioplasty PTCA or coronary artery bypass graft surgery CABG), the primary trial end point (coronary death or nonfatal MI) and stroke. RESULTS: Women treated with pravastatin had a risk reduction of 43% for the primary end point (p = 0.035), 46% for combined coronary events (p = 0.001), 48% for PTCA (p = 0.025), 40% for CABG (p = 0.14) and 56% for stroke (p = 0.07). The 3,583 men in the CARE trial also showed a reduction in risk, but the magnitude tended to be less. Pravastatin improved plasma lipids similarly in men and women. There were no differences in risk of coronary events in the placebo group between men and women. Minor differences between men and women were present in baseline characteristics and treatment for MI, in general, conferring a higher risk status and a lower incidence of CABG in the women. CONCLUSIONS: Pravastatin led to significant early reduction of a wide range of cardiovascular events in post-MI women with average cholesterol levels. |
| Effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels Willerson, J. T. (1996), Circulation 94(12): 3054. |
| Effect of pravastatin on endothelial function in patients with coronary artery disease (cholesterol-independent effect of pravastatin) Masumoto, A., Y. Hirooka, et al. (2001), Am J Cardiol 88(11): 1291-4. |
| Effect of pravastatin on hepatic cholesterol metabolism Reihner, E., M. Rudling, et al. (1991), Fortschr Med 109(8): 189-94. Abstract: BACKGROUND: Inhibitors of the rate-limiting enzyme of cholesterol biosynthesis, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, are now used frequently to treat hypercholesterolemia. We studied the effects of specific inhibition of cholesterol synthesis by one of these agents (pravastatin) on the hepatic metabolism of cholesterol in patients with gallstone disease who were scheduled to undergo cholecystectomy. METHODS: Ten patients were treated with pravastatin (20 mg twice a day) for three weeks before cholecystectomy; 20 patients not treated served as controls. A liver specimen was obtained from each patient at operation, and the activities of rate-determining enzymes in cholesterol metabolism as well as low-density-lipoprotein (LDL)-receptor binding activity were determined. RESULTS: Pravastatin therapy reduced plasma total cholesterol by 26 percent and LDL cholesterol by 39 percent (p less than 0.005). Serum levels of free lathosterol, a precursor of cholesterol whose concentration reflects the rate of cholesterol synthesis in vivo, decreased by 63 percent (p less than 0.005), indicating reduced de novo biosynthesis of cholesterol. Microsomal HMG-CoA reductase activity, when analyzed in vitro in the absence of the inhibitor, was increased 11.8-fold (1344 +/- 311 vs. 105 +/- 14 pmol per minute per milligram of protein in the controls; p less than 0.001). The expression of LDL receptors was increased by 180 percent (p less than 0.005), whereas the activities of cholesterol 7 alpha-hydroxylase (which governs bile acid synthesis) and of acyl-coenzyme A: cholesterol O-acyltransferase (which regulates cholesterol esterification) were unaffected by treatment. CONCLUSIONS: Inhibition of hepatic HMG-CoA reductase by pravastatin results in an increased expression of hepatic LDL receptors, which explains the lowered plasma levels of LDL cholesterol. |
| Effect of pravastatin, a HMG CoA reductase inhibitor, on blood lipids and aortic lipidosis in cholesterol-fed White Carneau pigeons Hadjiisky, P., D. Hermier, et al. (1993), Biochim Biophys Acta 1181(3): 279-86. Abstract: The effect of pravastatin, an inhibitor of HMG CoA reductase, on blood lipids and aortic lipidosis was studied in young cholesterol-fed White Carneau pigeons. The birds were fed with normal ('N group', n = 20) or atherogenic diet (grains + 0.4% cholesterol + 4% lard) alone ('C group', n = 20) and in association with pravastatin ('P group', n = 20). Plasma lipids and aortic intima lipidosis were studied after 3-5 and 8-12 months of the diet. Compared to the N group, pigeons from C group exhibited hypercholesterolemia (TC = 1000 mg/dl) and hyperlipoproteinemia of which level was independent of the duration of the diet. Total VLDL (VLDL+LDL)-cholesterol and apolipoprotein-B levels rose significantly 15, 8 and 4 times, respectively, whereas HDL were increased two times (P < 0.01) in females only. Macroscopically visible intima lipidosis areas covered 40% and 80% of aortic surface after 3-5 and 8-12 months of the diet. In P group, the increase in plasma lipid values was significantly lower than in WC from C group: -40% for total cholesterol (600 mg/dl) (P < 0.01), -71% for VLDL (P < 0.001), -53% for (VLDL+LDL)-cholesterol (P < 0.01) and -54% for apo-B (P < 0.05). HDL remained as high as in C group. Consequently TC/HDL-C ratio was improved and atherogenic risk of cholesterol was reduced by 41% (P < 0.05). Intima lipidosis areas were lowered by 35% (P < 0.01). We conclude that pravastatin treatment involves (1) a decrease in hypercholesterolemia and hyperlipoproteinemia and (2) a lowering in extensiveness and severity of macroscopically visible aortic lipidosis in cholesterol-fed White Carneau pigeon. |
| Effect of pravastatin-induced LDL-cholesterol reduction on coronary heart disease and cerebrovascular disease in Japanese: Hokuriku lipid coronary heart disease study-pravastatin atherosclerosis trial (Holicos-PAT) Koizumi, J., M. Shimizu, et al. (2002), J Atheroscler Thromb 9(5): 251-9. Abstract: The purpose of Holicos-PAT was to investigate the efficacy of serum lipid lowering by pravastatin against coronary heart disease (CHD) and cerebrovascular disease (CVD) in the Japanese population.Hypercholesterolemic men and women (n = 2,232), aged 40-70 years, were followed up for 5 years, while they were receiving pravastatin (group P, n = 1,422) or only diet therapy (group C, n = 810).The primary endpoint was CHD (a composite of onset or worsening of angina pectoris, performing CABG or PTCA, non-fatal myocardial infarction, death from CHD including heart death or sudden death).The secondary endpoints were comprised of CVD, total mortality, variation of serum lipid and apoprotein levels, and a relationship between the LDL-C level and occurrence of CHD.For several reasons (proving to meet the exclusion criteria after registration, etc.), 1,290 cases of group P and 749 cases of group C were used as subjects for the primary analysis.The mean follow-up period was 4.5 years in group P and 4.2 years in group C for events of CHD.The mean LDL-C level (SD) in group P was 176 (29) mg/dl and decreased to 134 (29) mg/dl one year later.This effect continued during the follow-up period.CHD events occurred in 9.2/1000 patient-years for men and 2.4/1000 patient-years for women without a history of CHD.CHD events occurred in 55.3/1000 patient-years for men and 23.6/1000 patient-years for women with a history of CHD, which was 6 times higher in men and 10 times higher in women than in those without a history of CHD, respectively.The adjusted relative risk ratio of group P to group C for CHD events was 0.74 (95%CI: 0.47-1.19).In the patients with a history of CHD, the ratio was 0.55 (95%CI: 0.30-1.00).The effect was apparent in the patients with a history of CHD.The incidence of myocardial infarction in Japanese patients with hypercholesterolemia living in the Hokuriku district was apparently lower, than the worldwide incidence, indicative that pravastatin may have a tendency to inhibit the occurrence of events of arteriosclerotic disease. |
| Effect of pravastatin-to-simvastatin conversion on low-density-lipoprotein cholesterol Ito, M. K., J. C. Lin, et al. (2001), Am J Health Syst Pharm 58(18): 1734-9. Abstract: The effects of a pravastatin-to-simvastatin conversion program on low-density-lipoprotein (LDL) cholesterol levels were studied. Patients receiving pravastatin at a Veterans Affairs medical center were switched to simvastatin beginning in 1997. The dosage of simvastatin was based on the additional percent reduction in LDL cholesterol needed to achieve the goal specified by the National Cholesterol Education Program. The primary endpoint was the change in the percentage of patients meeting their LDL cholesterol goal at baseline and follow-up. Changes in lipid indices, the relative risk (RR) of coronary heart disease (CHD), and program costs were also evaluated. A total of 1032 patients completed the program. The mean +/- S.D. daily doses of pravastatin and simvastatin were 25.2 +/- 11.3 and 22.7 +/- 13.3 mg, respectively. Median baseline and follow-up LDL cholesterol concentrations were 116 and 99 mg/dL, respectively (p < 0.001). Overall, 44% of the patients met their LDL cholesterol goal while taking pravastatin, compared with 69% after conversion to simvastatin (p < 0.001). The predicted mean RR of a future CHD event (based on changes in serum lipids) was 0.87 (95% confidence interval, 0.83-0.91) four years after conversion. The total cost of the program was $40,644 in the first year, and there was a net saving thereafter. Therapeutic interchange between pravastatin and simvastatin increased the number of patients meeting their LDL cholesterol goal. |
| Effect of precipitation and centrifugation conditions on high-density lipoprotein cholesterol measured with phosphotungstate-magnesium reagent Masson, D., F. Mainard, et al. (1992), Clin Chem 38(1): 148. |
| Effect of pregnancy and lactation on lipoprotein and cholesterol metabolism in the rat Smith, J. L., S. R. Lear, et al. (1998), J Lipid Res 39(11): 2237-49. Abstract: Origins of hyperlipidemia and cholestasis that occur during pregnancy were investigated by examining expression of key elements related to plasma and hepatic cholesterol metabolism during pregnancy, lactation, and post-lactation in the rat model. Among major findings were: during pregnancy, the activities of hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase, acyl coenzyme A:cholesterol acyltransferase, acyl coenzyme A:diacylglycerol acyltransferase, cholesterol 7alpha-hydroxylase, cholesterol ester hydrolases, low density lipoprotein receptors, LRP, and mdr2 were significantly lower or similar to non-pregnant controls while SR-B1 was elevated. Once lactation began, reductase, cholesterol acyltransferase, 7alpha-hydroxylase activities, low density lipoprotein receptors, and mdr2 increased while SR-B1 decreased. In later stages of lactation most hepatic elements returned to near control levels. Plasma cholesterol levels were higher than control at birth and during lactation with increase in LDL-size particles. By 24 h post-lactation, plasma triglycerides were 3.7-fold higher while cholesterol remained unchanged. Very large lipoproteins were present while LDL-size particles were now absent. Hepatic cholesterol acyltransferase had decreased to 27% of control while diacylglycerol acyltransferase increased 3-fold and low density lipoprotein receptors doubled. Most elements were normalized 3 weeks after weaning except for LRP and low density lipoprotein receptors which were elevated.These studies provide an integrated picture of expression of key elements of hepatic and plasma cholesterol metabolism during pregnancy and lactation and advance understanding of hyperlipidemia and cholestasis during these states. |
| Effect of probiotic supplementation on growth, nitrogen utilisation and serum cholesterol in broilers Mohan, B., R. Kadirvel, et al. (1996), Br Poult Sci 37(2): 395-401. Abstract: 1. The effect of dietary probiotic supplementation on the growth, nitrogen utilisation and serum cholesterol content of broiler chickens was studied in 2 trials. 2. In experiment 1, the birds receiving the 0, 75, 100, 125 mg probiotic/kg diets had weight gains of 1204.0, 1272.0, 1268.3 and 1210.5, respectively at the end of 8 weeks of feeding. The group of birds fed on the 75 mg probiotic supplemented diet retained significantly (P < 0.01) more nitrogen than the control birds. Serum cholesterol content was lower in the probiotic-supplemented birds (93.3 mg/100 ml) compared to the control birds (132.2 mg/100 ml). 3. In the second experiment the probiotic plus antibiotic-supplemented group of birds had the maximum weight gain (1148.5 g) followed by antibiotic (1141.3 g), probiotic-supplemented (1128.4 g) and control birds (1045.6 g) after 6 weeks. Nitrogen retention was greatest in the antibiotic--(48.5%) followed by the probiotic--(46.5%), probiotic plus antibiotic-supplemented groups (46.3%) compared to 40.2% in control birds. 4. The apparent metabolisable energy was greatest in birds receiving the probiotic plus antibiotic-supplemented diet (12.37 MJ/kg) followed by antibiotic--(12.00 MJ/kg), probiotic-supplemented birds (11.92 MJ/kg) than in control birds (11.62 MJ/kg). Serum cholesterol was significantly (P < 0.01) lower in probiotic-supplemented birds (86.1 mg/dl) compared to 118.4 mg/dl in control birds. |
| Effect of probiotic supplementation on laying hen diets on yield performance and serum and egg yolk cholesterol Kurtoglu, V., F. Kurtoglu, et al. (2004), Food Addit Contam 21(9): 817-23. Abstract: The effects of dietary supplementation of a commercial probiotic (BioPlus 2B) on daily feed consumption, egg yield, egg weight, specific gravity, body weight, feed conversion ratio, serum and egg yolk cholesterol, and serum trigylceride in layer hens were investigated. In 12 replicates, 480 27-week-old Brown-Nick layers were fed with diets containing 0, 250, 500 or 750 mg kg(-1) probiotic for 90 days. When compared with the controls, supplementation of 250, 500 and 750 mg kg(-1) probiotic increased egg production, but decreased the damaged egg ratio (p < 0.05), egg yolk cholesterol and serum cholesterol (p < 0.001) levels. In addition, serum triglyceride levels were reduced by using 500 and 750 mg kg(-1) probiotic supplementation (p < 0.001). Feed conversion ratios were positively affected by supplementation of 250 and 500 mg kg(-1) probiotic compared with controls (p < 0.05). There was no statistically significant difference between the control and all treatment groups on feed consumption, egg weight, specific gravity, body weight, and egg yolk weight. |