| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Systolic and pulse blood pressures (but not diastolic blood pressure and serum cholesterol) are associated with alterations in carotid intima-media thickness in the moderately hypercholesterolaemic hypertensive patients of the Plaque Hypertension Lipid Lowering Italian Study. PHYLLIS study group Zanchetti, A., G. Crepaldi, et al. (2001), J Hypertens 19(1): 79-88. Abstract: OBJECTIVE: The Plaque Hypertension Lipid Lowering Italian Study (PHYLLIS), is the first study in patients with hypertension (diastolic blood pressure (DBP) 95-115 mmHg; systolic blood pressure (SBP) 150-210 mmHg), moderate hypercholesterolaemia (LDL-cholesterol 4.14-5.17 mmol/l (160-200 mg/dl) and initial carotid artery alterations (maximum intima-media thickness (IMT) Tmax > or = 1.3 mm). The primary objective of PHYLLIS is investigating whether in these patients administration of an angiotensin converting enzyme inhibitor, fosinopril, and a statin, pravastatin, is more effective than administration of a diuretic and a lipid-lowering diet in retarding or regressing alterations in carotid IMT. While the study is in progress, baseline data are here reported to clarify the association of various risk factors with carotid IMT in these medium-high risk hypertensive patients. METHODS: Patients numbering 508 have been randomized to PHYLLIS by 13 peripheral units, in Italy. Age was (mean +/- SD) 58.4 +/- 6.7 years, males were 40.2%, current smokers 16.5%, means +/- SD of serum total, low-density lipoprotein (LDL), high-density lipoprotein (HDL) cholesterol and triglycerides concentrations were 6.79 +/- 0.67, 4.69 +/- 0.51, 1.37 +/- 0.38, 1.59 +/- 0.64 mmol/l (262.4 +/- 25.8, 181.3 +/- 19.8, 53.0 +/- 14.6, 141.0 +/- 56.7 mg/ dl). Means +/- SD of clinic sitting SBP/DBP were 159.8 +/- 9.0/98.3 +/- 4.2 mmHg. 483 of the 508 patients also had 24 h ambulatory BP monitoring, edited and read at a centralized unit (mean +/- SD 24 h SBP/DBP averages 136.3 +/- 14.1/84.0 +/- 10.0 mmHg). Quantitative B-mode ultrasound (Biosound 2000 II 5A, Biosound, Indianapolis, Indiana, USA) recordings of carotid arteries were taken by certified sonographers in the peripheral units and tracings were all read at a central unit. CBMmax (mean IMT of eight sites at common carotids and bifurcations) was 1.21 +/- 0.17; Mmax (mean of 12 sites also including internal carotids) 1.16 +/- 0.17, and Tmax (single maximum) 1.85 +/- 0.48 mm. RESULTS: Ambulatory SBP and pulse pressure (PP) (24 h, daytime, night-time averages) and their variability indices (24 h SD) were always significantly correlated with CBMmax and Mmax (P0.01 -0.001), and the correlations remained significant after adjustment for age, gender and smoking. No measurement of DBP was ever associated with any IMT measurement. Likewise, no lipid variable was found associated with any IMT measurement. CONCLUSIONS: Baseline data from PHYLLIS indicate that in this population of hypertensive patients with moderate hypercholesterolaemia, SBP and PP are with age among the most significant factors associated with carotid artery alterations. However, the narrow range of inclusion LDL-cholesterol and DBP values may have obscured an additional role of these variables. |
| T helper cell infiltration and foam cell proliferation are early events in the development of atherosclerosis in cholesterol-fed rabbits Drew, A. F. and P. G. Tipping (1995), Arterioscler Thromb Vasc Biol 15(10): 1563-8. Abstract: The involvement of T cells in the early cellular events in atherosclerosis was studied in rabbits fed a 1% cholesterol diet by use of specific monoclonal anti-rabbit CD5 and CD4 antibodies. T cells were not seen in the aortic intimas of rabbits not fed cholesterol but were seen in intimal lesions in cholesterol-fed rabbits. Accumulation of T cells in plaques occurred between 2 and 4 weeks after commencement of cholesterol feeding, and the greatest density of CD5-positive T cells were observed after 4 weeks (11.2 +/- 6.0 cells/mm2 mean +/- SEM; P <.02 compared with normal control rabbits, P <.03 compared with 2-week plaques). Staining for CD4 indicated that the majority of these T cells were T helper cells (9.9 +/- 4.9 cells/mm2). At this time, plaques showed a dense cellular infiltrate of macrophages (3623 +/- 467 cells/mm2) and macrophage proliferation was evident (2.1 +/- 1.1% of total plaque cells). As the cross-sectional area of intimal lesions increased progressively in subsequent weeks, their cellularity declined (8 weeks, 2239 +/- 271 cells/mm2; 12 weeks, 1535 +/- 55 cells/mm2; 16 weeks, 1747 +/- 242 cells/mm2, P <.05 for all groups compared with the 4-week group). The density of the T cell infiltrate (8 weeks, 6.7 +/- 3.0 cells/mm2; 12 weeks, 0.6 +/- 0.2 cells/mm2; 16 weeks, 1.0 +/- 0.4 cells/mm2) and the proliferative index of cells within plaques (8 weeks, 0.6 +/- 0.2%; 12 weeks, 0.8 +/- 0.3%; 16 weeks, 0.2 +/- 0.2%) also declined.(ABSTRACT TRUNCATED AT 250 WORDS) |
| T lymphocytes increase the synthesis of esterified cholesterol in human monocyte-derived macrophages by activation of the scavenger pathway Kotake, H., S. Oikawa, et al. (1992), Biochim Biophys Acta 1138(4): 327-33. Abstract: Immunohistochemical analyses have shown the presence of T lymphocytes (T-cells) in atherosclerotic places in addition to macrophages and smooth muscle cells. To elucidate the role of T-cells in the formation of atherosclerotic lesions, we studied whether T-cells can stimulate the scavenger pathway and promote esterified cholesterol (EC) synthesis by 14Coleate incorporation in macrophages. Macrophages and T-cells were co-cultured in two ways. In one culture, macrophages were in direct contact with T-cells (direct contact form). In the other, macrophages and T-cells were separated by Transwell membrane, but shared the same culture medium via the membrane (indirect contact form). Based on the incorporation of 14Coleate into EC, macrophages strikingly increased EC synthesis in both forms of co-culture. This increase was proportional to the number of T-cells present and was inhibited by cyclosporin A. When macrophages were co-cultured indirectly in contact with T-cells in the presence of AcLDL for 24 h, and the T-cells were subsequently removed, EC synthesis in macrophages increased. However, this increase was not observed in macrophages that were rinsed twice with PBS. When macrophages, previously incubated with AcLDL for 24 h, were co-cultured indirectly in contact with T-cells for 24 h, the medium were prepared as activated T-cell-conditioned medium (aTCM). EC synthesis in macrophages cultured with aTCM increased. The ability of aTCM to increase EC synthesis disappeared upon repeated freezing/thawing, boiling and trypsin treatment. T-cells (indirect contact form) and aTCM similarly increased AcLDL-binding and -degradation in macrophages. These results indicated that T-cells secreted an active substance(s), protein in nature, which could activate the scavenger pathway and increase EC synthesis in macrophages. These observations suggest that T-cells can promote the uptake of modified lipoproteins by macrophages to induce foam cell-formation. |
| Tamoxifen and estrogens as membrane antioxidants: comparison with cholesterol Wiseman, H. (1994), Methods Enzymol 234: 590-602. |
| Tamoxifen and norethisterone: effects on plasma cholesterol and total body calcium content in the estrogen-deficient rat Gold, E., S. Stapley, et al. (1994), Horm Metab Res 26(2): 100-3. Abstract: It is important that drugs which are used to protect bone from the osteoporotic effects of estrogen deficiency should not affect plasma lipids adversely. Effects of a) norethisterone acetate and b) tamoxifen citrate on plasma cholesterol and on bone conservation in rats with normal plasma 17B-estradiol and in rats made estrogen-deficient with the LHRH agonist, buserelin are reported. Tamoxifen halved total plasma cholesterol (p < 0.01), whereas norethisterone did not lower plasma cholesterol. Furthermore tamoxifen fully protected bone from estrogen-deficiency osteopenia whereas norethisterone conserved bone less well. Reductions in cholesterol elicited by tamoxifen were similar in estrogen-deficient rats and in rats with normal ovarian function. This is the first report in the rat that tamoxifen has lipid-lowering actions. It is suggested the rat may be useful for future investigations of the lipid-lowering mechanisms of tamoxifen. |
| Tamoxifen and toremifene lower serum cholesterol by inhibition of delta 8-cholesterol conversion to lathosterol in women with breast cancer Gylling, H., S. Pyrhonen, et al. (1995), J Clin Oncol 13(12): 2900-5. Abstract: PURPOSE: Long-term effects of tamoxifen and toremifene, a new antiestrogen that closely resembles tamoxifen, were investigated on serum lipids and cholesterol metabolism. PATIENTS AND METHODS: The study group consisted of 24 postmenopausal Finnish women with advanced breast cancer from an international multicenter study of 415 patients. Cholesterol metabolism was evaluated by measuring the cholesterol precursor (delta 8-cholestenol, desmosterol, and lathosterol, reflecting cholesterol synthesis) and plant sterol (markers of cholesterol absorption) and cholestanol levels by gas-liquid chromatography. RESULTS: Tamoxifen and toremifene lowered significantly serum low-density lipoprotein (LDL) cholesterol levels after 12 months of treatment by 16% and 15%, with no change in high-density lipoprotein (HDL) cholesterol or serum triglyceride levels. Serum delta 8-cholestenol was increased 40- and 55-fold during toremifene and tamoxifen treatment, respectively, while the increase of desmosterol less than doubled and was lacking for lathosterol by toremifene. Plant sterols and cholestanol were only inconsistently increased in serum. CONCLUSION: Tamoxifen and toremifene inhibit the conversion of delta 8-cholestenol to lathosterol so that serum total and LDL cholesterol levels are lowered by downregulation of cholesterol synthesis. Thus, inhibition of the delta 8-isomerase may be the major hypolipidemic effect of these agents. Reduced risk of coronary artery disease will probably occur also during long-term toremifene treatment, because the drug reduces cholesterol and its synthesis, similarly to tamoxifen. |
| Tamoxifen decreases cholesterol sevenfold and abolishes lipid lesion development in apolipoprotein E knockout mice Reckless, J., J. C. Metcalfe, et al. (1997), Circulation 95(6): 1542-8. Abstract: BACKGROUND: Apolipoprotein E (apo E) knockout mice develop severe vascular lipid lesions resembling human atherosclerotic plaques, irrespective of the fat content of their diet. METHODS AND RESULTS: Oral tamoxifen (TMX) at a dose of 1.9 mg.kg body wt-1.d-1 abolished lipid lesion development, assayed by oil red O staining, whether the mice were fed a normal diet or a diet with high fat content. The TMX-treated mice showed a sevenfold decrease in total cholesterol. However, the proportion of plasma cholesterol present in VLDL remained unchanged, whereas the proportion in LDL decreased by 37%, and that in HDL increased by 64%. Consistent with the shift from LDL to HDL cholesterol, there was a 62% decrease in total triglycerides. The concentrations of active and acid-activatable latent plus active TGF-beta in the aorta were substantially elevated by TMX (87% and 24% increase, respectively). CONCLUSIONS: Although the mechanism of cardiovascular protection by TMX in apo E knockout mice is unknown, the inhibition of lipid lesion formation may be attributable to the changes in lipoprotein profile and the elevated levels of TGF-beta, both of which are thought to be protective against atherosclerosis in humans and animal models. |
| Tamoxifen decreases serum cholesterol by inhibiting cholesterol synthesis Gylling, H., E. Mantyla, et al. (1992), Atherosclerosis 96(2-3): 245-7. |
| Tamoxifen is a potent inhibitor of cholesterol esterification and prevents the formation of foam cells de Medina, P., B. L. Payre, et al. (2004), J Pharmacol Exp Ther 308(3): 1165-73. Abstract: Tamoxifen is a selective estrogen receptor modulator (SERM) used for the treatment and prevention of breast cancer. Tamoxifen has been reported to protect against the progression of coronary artery diseases in human and different atherosclerosis animal models by blocking the appearance of the atheromatous plaque. However, the molecular mechanism of this effect remains unknown. Acyl-CoA:cholesterol acyl transferase (ACAT) catalyzes the biosynthesis of cholesteryl esters, which are the major lipids found in the atheromatous plaque. In this paper we have tested whether ACAT might be inhibited by tamoxifen. We show, using molecular modeling, that tamoxifen displays three-dimensional structural homology with Sah 58-035 (3-decyldimethylsilyl-N-2-(4-methylphenyl)-1-phenylethyl-propanamide), a prototypical inhibitor of ACAT. We report that tamoxifen inhibits ACAT in a concentration-dependent manner on rat liver microsomal extract. We show that the presence on estrogen receptor ligands of a backbone isosteric to the diphenyl ethane backbone of Sah 58-035 constitutes a pharmacophore for ACAT inhibition. More importantly, tamoxifen was able to inhibit ACAT on intact macrophages stimulated with acetylated low-density lipoproteins and blocked the formation of foam cells, a step that precedes the formation of the atheromatous plaque. This work constitutes the first evidence that tamoxifen is an inhibitor of ACAT and foam cell formation at therapeutic doses and that this may account for its atheroprotective action. |
| Tamoxifen-induced decreases in total cholesterol with 2 weeks of treatment Love, R. R., C. C. Mamby, et al. (1993), J Natl Cancer Inst 85(16): 1344-5. |
| Tangier disease as a test of the reverse cholesterol transport hypothesis Tall, A. R. and N. Wang (2000), J Clin Invest 106(10): 1205-7. |
| Tangle-bearing neurons contain more free cholesterol than adjacent tangle-free neurons Distl, R., V. Meske, et al. (2001), Acta Neuropathol (Berl) 101(6): 547-54. Abstract: Neurofibrillary tangles are seen both in senile dementia of Alzheimer's disease and in juvenile dementia of Niemann-Pick type C disease. Apolipoprotein E is a main cholesterol transport molecule in brain. In Alzheimer's disease, possession of the apolipoprotein E epsilon4 allele is associated with an earlier onset in tangle formation and an increased tangle load. Niemann-Pick type C disease is a disorder with elevated intracellular levels of free cholesterol due to a genetic deficit in its transport. The link between tangle formation and cholesterol metabolism in both diseases suggests that alterations of intracellular free cholesterol levels could influence tangle formation. Using semiquantitative fluorescence microscopy with the free cholesterol probe filipin and analysing 939 neurons, we observed that mean levels of free cholesterol in tangle-bearing neurons were higher than those of adjacent tangle-free neurons. |
| Taq1B CETP polymorphism, plasma CETP, lipoproteins, apolipoproteins and sex differences in a Jewish population sample characterized by low HDL-cholesterol Kark, J. D., R. Sinnreich, et al. (2000), Atherosclerosis 151(2): 509-18. Abstract: Mean high-density lipoprotein cholesterol (HDL-C) concentrations are low in the Jewish population of Israel. With this in mind we assessed the association of the Taq1B CETP polymorphism, plasma CETP mass and plasma lipid, lipoprotein and apolipoprotein concentrations in a sample of 884 Jerusalem residents aged 28-32. The allele frequency (0.435 +/- 0.017(S.E.)) is similar to that reported elsewhere. There was a strong (apparently codominant) association of the Taq1 B allele with plasma CETP in both sexes, and an inverse association with HDL-C and apo A-1, significant in women and undiminished upon adjustment for plasma CETP. There was evidence in this population for an admixture of two plasma CETP distributions, with 9% belonging to a distribution with the higher mean, pointing to a possible major gene effect. Mean plasma CETP was higher in women than men. Plasma CETP was inversely associated with HDL-C in men but not in women (P< 0.05 for the sex difference, multivariate analysis), inversely related to the HDL-C/apo A-1 ratio in men and positively related in women (P < 0.005 for the sex difference), and was positively associated with total cholesterol (TC) and low-density lipoprotein cholesterol in both sexes, and with the TC/HDL-C ratio and apo B in men alone. The sex differences may reflect dissimilarities in the regulatory function of CETP in lipid exchange. The absence of an unusual allele frequency of the Taq1B CETP polymorphism and its relatively modest association with HDL-C argue against an important role for this or strongly linked sites in determining the low population levels of HDL-C in Israel. |
| Targeted disruption of the murine cholecystokinin-1 receptor promotes intestinal cholesterol absorption and susceptibility to cholesterol cholelithiasis Wang, D. Q., F. Schmitz, et al. (2004), J Clin Invest 114(4): 521-8. Abstract: Cholecystokinin (CCK) modulates contractility of the gallbladder, the sphincter of Oddi, and the stomach. These effects are mediated through activation of gastrointestinal smooth muscle as well as enteric neuron CCK-1 receptors (CCK-1Rs). To investigate the potential physiological and pathophysiological functions linked to CCK-1R-mediated signaling, we compared male WT and CCK-1R-deficient mice (129/SvEv). After 12 weeks on either a standard mouse chow or a lithogenic diet (containing 1% cholesterol, 0.5% cholic acid, and 15% dairy fat), small-intestinal transit time, intestinal cholesterol absorption, biliary cholesterol secretion, and cholesterol gallstone prevalence were compared in knockout versus WT animals. Analysis of mice on either the chow or the lithogenic diet revealed that CCK-1R(-/-) animals had larger gallbladder volumes (predisposing to bile stasis), significant retardation of small-intestinal transit times (resulting in increased cholesterol absorption), and increased biliary cholesterol secretion rates. The elevation in bile cholesterol, coupled with a tendency toward gallbladder stasis (due to the absence of CCK-induced contraction), facilitates nucleation, growth, and agglomeration of cholesterol monohydrate crystals; this sequence of events in turn results in a significantly higher prevalence of cholesterol gallstones in the CCK-1R-null mice. |
| Targeted disruption of the murine lecithin:cholesterol acyltransferase gene is associated with reductions in plasma paraoxonase and platelet-activating factor acetylhydrolase activities but not in apolipoprotein J concentration Forte, T. M., M. N. Oda, et al. (1999), J Lipid Res 40(7): 1276-83. Abstract: Lecithin:cholesteryl acyltransferase (LCAT) deficiency resulting from targeted disruption of the Lcat gene in the mouse is associated with dramatic decreases in HDL concentration and the accumulation of nascent HDL in the plasma. We examined whether LCAT deficiency in mice is associated with a concomitant decrease in two antioxidative enzymes, paraoxonase (PON) and platelet-activating factor acetylhydrolase (PAF-AH). In control Lcat (+/+) mice both these enzymes are transported on HDL. Compared to Lcat (+/+) mice, HDL-cholesterol is reduced 94% and apoA-I, 90%, in Lcat (-/-) mice; this reduction in HDL is paralleled by a 71% decrease in PAF-AH activity and in a 58% decrease in PON activity. Apolipoprotein J (apoJ) levels, rather than being decreased, were significantly (P = 0.01) higher (36%) in Lcat (-/-) than in Lcat (+/+) mice, and the apo J/PON ratio was 3-fold greater in Lcat (-/-) than in Lcat (+/+) animals. Even though apolipoprotein A-I (apoA-I) concentration and PON activity were drastically reduced, there was no reduction in apoA-I and PON liver mRNA levels suggesting that post-transcriptional events are responsible for the reduction of plasma PON and apoA-I levels. Fast protein liquid chromatography (FPLC) revealed that in Lcat (+/+) mice both PON and PAF-AH activity is associated with large, apoA-I-containing HDL particles (9.7 nm by non-denaturing gradient gel electrophoresis) while in Lcat (-/-) mice both enzymes are associated with small 8.2 nm particles.We conclude that the concomitant reduction in HDL and apoA-I concentrations and PON and PAF-AH activities is best explained by rapid clearance of the small HDL particles found in LCAT deficiency. |
| Targeted disruption of the murine mucin gene 1 decreases susceptibility to cholesterol gallstone formation Wang, H. H., N. H. Afdhal, et al. (2004), J Lipid Res 45(3): 438-47. Abstract: Gallbladder mucins play a critical role in the pathogenesis of cholesterol gallstones because of their ability to bind biliary lipids and accelerate cholesterol crystallization. Mucin secretion and accumulation in the gallbladder is determined by multiple mucin genes. To study whether mucin gene 1 (Muc1) influences susceptibility to cholesterol cholelithiasis, we investigated male Muc1-deficient (Muc1(-/-)) and wild-type mice fed a lithogenic diet containing 1% cholesterol and 0.5% cholic acid for 56 days. Gene expression of the gallbladder Muc1 and Muc5ac was significantly reduced in Muc1(-/-) mice in response to the lithogenic diet. Muc3 and Muc4 levels were upregulated and were similar between Muc1(-/-) and wild-type mice. Little or no Muc2 and Muc5b mRNAs were detected. Muc1(-/-) mice displayed significant decreases in total mucin secretion and accumulation in the gallbladder as well as retardation of crystallization, growth, and agglomeration of cholesterol monohydrate crystals. At 56 days of feeding, gallstone prevalence was decreased by 40% in Muc1(-/-) mice. However, cholesterol saturation indices of gallbladder bile, hepatic secretion of biliary lipids, and gallbladder size were comparable in Muc1(-/-) and wild-type mice. We conclude that decreased gallstone formation in mice with disrupted Muc1 gene results from reduced mucin secretion and accumulation in the gallbladder. |
| Targeted mutation reveals a central role for SR-BI in hepatic selective uptake of high density lipoprotein cholesterol Varban, M. L., F. Rinninger, et al. (1998), Proc Natl Acad Sci U S A 95(8): 4619-24. Abstract: Scavenger receptor BI (SR-BI) is a cell surface receptor that binds high density lipoproteins (HDL) and mediates selective uptake of HDL cholesteryl esters (CE) in transfected cells. To address the physiological role of SR-BI in HDL cholesterol homeostasis, mice were generated bearing an SR-BI promoter mutation that resulted in decreased expression of the receptor in homozygous mutant (designated SR-BI att) mice. Hepatic expression of the receptor was reduced by 53% with a corresponding increase in total plasma cholesterol levels of 50-70% in SR-BI att mice, attributable almost exclusively to elevated plasma HDL. In addition to increased HDL-CE, HDL phospholipids and apo A-1 levels were elevated, and there was an increase in HDL particle size in mutant mice. Metabolic studies using HDL bearing nondegradable radiolabels in both the protein and lipid components demonstrated that reducing hepatic SR-BI expression by half was associated with a decrease of 47% in selective uptake of CE by the liver, and a corresponding reduction of 53% in selective removal of HDL-CE from plasma. Taken together, these findings strongly support a pivotal role for hepatic SR-BI expression in regulating plasma HDL levels and indicate that SR-BI is the major molecule mediating selective CE uptake by the liver. The inverse correlation between plasma HDL levels and atherosclerosis further suggests that SR-BI may influence the development of coronary artery disease. |
| Targeting HDL-mediated cellular cholesterol efflux for the treatment and prevention of atherosclerosis Francis, G. A. and R. J. Perry (1999), Clin Chim Acta 286(1-2): 219-30. Abstract: The hallmark of the atherosclerotic lesion is the overaccumulation of cholesterol in arterial wall cells. As no pathway exists for the degradation of cholesterol in peripheral cells, a mechanism is necessary to prevent its accumulation to toxic levels in these cells and to allow its delivery to the liver for excretion in bile. Promoting this reverse cholesterol transport pathway is believed to be the main cardioprotective action of high density lipoprotein (HDL). The rate-limiting step in this pathway is likely the initial removal of cholesterol from peripheral cells by HDL. The pathway HDL utilizes for inducing efflux of excess cellular cholesterol represents an important and as-yet untapped mechanism to employ for the treatment and prevention of atherosclerotic vascular disease. This review summarizes the potential cardioprotective actions of HDL, the mechanisms of HDL-mediated cellular cholesterol efflux, and evidence that the specific pathway of cholesterol removal by HDL may be enhanced and used as a novel target in the therapy of atherosclerosis. |
| Targeting low high-density lipoprotein cholesterol for therapy: lessons from the Veterans Affairs High-density Lipoprotein Intervention Trial Robins, S. J. (2001), Am J Cardiol 88(12A): 19N-23N. Abstract: Results of the Veterans Affairs High-Density Lipoprotein Intervention Trial (VA-HIT) showed that therapy with the fibric acid gemfibrozil significantly reduced the incidence of coronary artery disease events in men with known coronary artery disease and a low level of high-density lipoprotein cholesterol (HDL-C). Coronary artery disease event reduction was inversely related to levels of HDL-C achieved with gemfibrozil and, even at relatively low concentrations of HDL-C, coronary artery disease event reduction with gemfibrozil was significantly greater than with placebo. Subjects with a low HDL-C level who were recruited for VA-HIT had a high prevalence of features of the metabolic syndrome with obesity, type 2 diabetes, and hyperinsulinemia. These individuals especially benefited from gemfibrozil, and thus, fibrate therapy may have an increasing role in reducing coronary artery disease risk in a setting of an increasing worldwide prevalence of obesity and diabetes. |
| Taurine and cholesterol supplementation in the term infant: responses of growth and metabolism Rassin, D. K., N. C. Raiha, et al. (1990), JPEN J Parenter Enteral Nutr 14(4): 392-7. Abstract: The effects of taurine and of cholesterol supplementation to a whey-protein-predominant formula fed ad libitum on the growth and biochemical responses of term infants were studied. The responses of these infants were compared to those of infants fed formula without a supplement and infants that were breastfed. These infants were followed for 12 weeks. No effect of cholesterol was observed on any of the measurements and no effect of taurine was observed on any of the biochemical measures with the exception that taurine concentrations in plasma and urine (reduced in infants fed formula alone) were corrected to concentrations observed in breastfed infants. Taurine supplementation had no effect on the rate of weight gain or on linear growth over the complete course of the study. Thus, taurine supplementation of formulas returns plasma and urine concentrations of this amino acid to those found in human milk-fed infants. However, these data indicate that the supplementation of formulas with taurine has no benefit with respect to growth. |