| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Regulation of sterol regulatory element-binding proteins in hamster intestine by changes in cholesterol flux Field, F. J., E. Born, et al. (2001), J Biol Chem 276(20): 17576-83. Abstract: A control chow diet or diets containing 1% cholesterol (cholesterol-enriched) or 4% cholestyramine and 0.15% lovastatin (cholesterol-depletion) were fed to hamsters for 2 weeks. Sterol regulatory element-binding protein (SREBP)-1a, SREBP-1c, SREBP-2, 3-hydroxy-3-methylglutaryl-coenzyme A reductase, 3-hydroxy-3-methylglutaryl-coenzyme A synthase, and LDL receptor mRNA levels and SREBP-1 and -2 protein expression were estimated in villus cell populations from duodenum, jejunum, and ileum. SREBP-1a was a minor transcript in hamster intestine, and its gene expression was not altered by changes in dietary cholesterol flux. In contrast, SREBP-1c gene expression was increased by dietary cholesterol and decreased by cholesterol depletion. mRNA levels for SREBP-2 and the other sterol-responsive genes were increased in intestines of animals on the cholesterol depletion diet but minimally suppressed if at all, by the diet enriched in cholesterol. In general, the amount of the precursor form of SREBP-1 was higher in cells of the upper villus and lower in cells of the lower villus. SREBP-2 precursor was higher in cells of the lower villus and lower in cells of the upper villus. Protein expression of precursor correlated with the location of gene expression for SREBPs. The amount of precursor mass of SREBP-2 was not altered by cholesterol feeding but was increased by cholesterol depletion. The mature form of SREBP-2 was in very low abundance and difficult to detect in intestines of animals fed control chow or cholesterol. It was readily detectable and increased in intestines of animals on the cholesterol-depletion diet. The diets did not significantly alter the amount of precursor or mature forms of SREBP-1. Cholesterol feeding had no effect on cholesterol or fatty acid synthesis, whereas synthesis of these lipids was increased in intestines of hamsters on the cholesterol-depleted diet. These results suggest that SREBP-1a has little or no role in regulating intestinal cholesterol synthesis. It is postulated that under basal conditions, SREBP-1c regulates intestinal fatty acid synthesis and SREBP-2 regulates cholesterol synthesis. Following marked changes in cholesterol flux across the intestine, SREBP-2 assumes the role of SREBP-1 and regulates both cholesterol and fatty acid synthesis in intestine. |
| Regulation of the activities of thrombin and plasmin by cholesterol sulfate as a physiological inhibitor in human plasma Iwamori, M., Y. Iwamori, et al. (1999), J Biochem (Tokyo) 125(3): 594-601. Abstract: Thrombin and plasmin, both of which are serine proteases in the plasma of vertebrates, play essential roles in blood clotting and fibrinolysis, respectively, and regulation of their activities is important to suppress the excessive reactions within the vascular network and to prevent tissue injury. Along with the peptidic inhibitors belonging to the serpin family, we found that cholesterol sulfate (CS), which is present at the concentration of 2.0+/-1.2 nmol/ml in human plasma, was a potent inhibitor of both plasma thrombin and plasmin. Thrombin, as determined both using a chromogenic substrate and the natural substrate, fibrinogen, was inactivated upon reaction with CS in a dose-dependent manner, but not in the presence of the structurally related steroid sulfates, I3SO3-GalCer and II3NAalpha-LacCer, suggesting that both the sulfate group and the hydrophobic side chain of CS are necessary for the inhibitory activity of CS. Preincubation of thrombin with CS at 37 degrees C for 10 min was required to achieve maximum inhibition, and virtually complete inhibition was achieved at a molar ratio of CS to thrombin of 18:1. CS-treated thrombin had the same Km and a lower Vmax than the original enzyme, and a higher molecular weight. The molecular weight and activity of the original enzyme were not observed on the attempted separation of the CS-treated enzyme by gel permeation chromatography and native PAGE, indicating that the inactivation of thrombin by CS is irreversible. In contrast, CS was readily liberated from the enzyme by SDS-PAGE, suggesting that hydrophobic interactions are involved in the CS-mediated inactivation of thrombin. When acidic lipids were reacted with thrombin after dissolving them in DMSO, I3SO3-GalCer, steroid sulfates and II3NAalpha-LacCer, as well as CS, but not SDS and sodium taurocholate, exhibited inhibitory activity, probably due to micellar formation facilitating interaction between thrombin and negatively charged lipids. On the other hand, plasmin, as determined using a chromogenic substrate, was more susceptible to acidic lipids than thrombin. CS, I3SO3-GalCer and II3NAalpha-LacCer, all of which are present in serum, inhibited the activity of plasmin in aqueous media, as well as in DMSO-mediated lipid solutions. Thus, acidic lipids in plasma were demonstrated to possess regulatory activity as endogenous detergents toward both enzymes for blood clotting and fibrinolysis. |
| Regulation of the Ca2+-inhibitable adenylyl cyclase type VI by capacitative Ca2+ entry requires localization in cholesterol-rich domains Fagan, K. A., K. E. Smith, et al. (2000), J Biol Chem 275(34): 26530-7. Abstract: The endogenous Ca(2+)-inhibitable adenylyl cyclase type VI of C6-2B glioma cells is regulated only by capacitative Ca(2+) entry and not by a substantial elevation of Ca(2+)(i) from either intracellular stores or via ionophore-mediated Ca(2+) entry (Chiono, M., Mahey, R., Tate, G., and Cooper, D. M. F. (1995) J. Biol. Chem. 270, 1149-1155; Fagan, K. A., Mons, N., and Cooper, D. M. F. (1998) J. Biol. Chem. 273, 9297-9305). The present studies explored the role of cholesterol-rich domains in maintaining this functional association. The cholesterol-binding agent, filipin, profoundly inhibited adenylyl cyclase activity. Depletion of plasma membrane cholesterol with methyl-beta-cyclodextrin did not affect forskolin-stimulated adenylyl cyclase activity and did not affect capacitative Ca(2+) entry. However, cholesterol depletion completely ablated the regulation of adenylyl cyclase by capacitative Ca(2+) entry. Repletion of cholesterol restored the sensitivity of adenylyl cyclase to capacitative Ca(2+) entry. Adenylyl cyclase catalytic activity and immunoreactivity were extracted into buoyant caveolar fractions with Triton X-100. The presence of adenylyl cyclase in such structures was eliminated by depletion of plasma membrane cholesterol. Altogether, these data lead us to conclude that adenylyl cyclase must occur in cholesterol-rich domains to be susceptible to regulation by capacitative Ca(2+) entry. These findings are the first indication of regulatory significance for the localization of adenylyl cyclase in caveolae. |
| Regulation of the cholesterol efflux gene, ABCA1 Wade, D. P. and J. S. Owen (2001), Lancet 357(9251): 161-3. |
| Regulation of the cholesterol ester cycle and progesterone synthesis by juvenile hormone in MA-10 Leydig tumor cells Vladusic, E. A., O. P. Pignataro, et al. (1995), J Steroid Biochem Mol Biol 52(1): 83-90. Abstract: We had previously reported that juvenile hormone III (JH III) and the JH analogue 2-(4-phenoxy phenoxy)-ethoxytetrahydropyran exert inhibitory effects on progesterone synthesis by blocking cAMP production in hCG-stimulated MA-10 Leydig tumor cells. In the present study, the effects of JH analogue upon the biosynthetic pathway of progesterone synthesis have been examined. Our results demonstrated that JH analogue inhibited progesterone production even in the presence of 20-hydroxycholesterol or 25-hydroxycholesterol. Furthermore, although JH analogue inhibited pregnenolone production in hCG-stimulated MA-10 cells the activity of the 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) was unaffected. These data suggest that JH analogue might inhibit the steroidogenic pathway in Leydig tumor cells by inhibiting the activity of the cholesterol side chain cleavage (CSCC) enzymatic complex. The JH analogue was also evaluated for inhibitory actions on cholesterol availability. An important effect of this compound was the interference with the cellular process of plasma membrane cholesterol internalization. Moreover, JH analogue inhibited not only the use of cholesterol ester for steroid biosynthesis under Bt2cAMP stimulation, but also the cholesterol ester hydrolase (CEH) activity in MA-10 Leydig tumor cells. |
| Regulation of the cholesterol side-chain cleavage cytochrome P-450 and adrenodoxin mRNAs in cultured choriocarcinoma cells Ritvos, O. and R. Voutilainen (1992), Mol Cell Endocrinol 84(3): 195-202. Abstract: Cytochrome P-450scc (P-450scc) catalyzes the cholesterol side-chain cleavage reaction, a rate-limiting enzymatic step for progesterone synthesis in trophoblastic and other steroidogenic cells. Adrenodoxin is the iron/sulfur protein donating electrons to P-450scc during this reaction. We examined the effects of cholera toxin (CT), an activator of adenylate cyclase, and 12-O-tetradecanoylphorbol acetate (TPA), a phorbol ester protein kinase C activator, on the levels of mRNAs encoding P-450scc and adrenodoxin in JEG-3 choriocarcinoma cells. CT induced in a concentration- and time-dependent manner P-450scc and adrenodoxin mRNA levels to 8-fold and 1.5-fold above that of control, respectively. TPA also increased P-450scc and adrenodoxin mRNA levels about 3-fold and 1.5-fold above that of control, respectively. Epidermal growth factor (EGF) was found to weakly induce P-450scc mRNA accumulation with a maximal 20% stimulation above basal levels. The effects of CT and TPA were apparently additive on both mRNAs. The protein synthesis inhibitor cycloheximide diminished basal, CT-, TPA-, and EGF-stimulated P-450scc mRNA accumulation whereas the opposite was observed for the adrenodoxin mRNA. Insulin-like growth factor I (IGF-I) appeared to have no effect on either mRNA. These data indicate that: (1) the accumulation of P-450scc and adrenodoxin mRNAs is mainly controlled by the cyclic adenosine 3',5'-monophosphate (cAMP)-dependent pathway but their stimulation by TPA- and EGF-induced signals may also play a weaker synergistic role; (2) the protein synthesis inhibitor cycloheximide inhibits basal, CT-, TPA- and EGF-stimulated P-450scc mRNA levels while it increases the expression of adrenodoxin mRNA suggesting that in the malignant trophoblasts these two enzyme mRNAs are differentially controlled. |
| Regulation of the hamster cholesterol 7 alpha-hydroxylase gene (CYP7A): prevalence of negative over positive transcriptional control De Fabiani, E., M. Crestani, et al. (1996), Biochem Biophys Res Commun 226(3): 663-71. Abstract: Cholesterol 7 alpha-hydroxylase plays a crucial role in cholesterol homeostasis. We investigated the regulation of this enzyme in the hamster, a suitable animal model for studying cholesterol metabolism. DNase I hypersensitivity assay revealed the presence of a hypersensitive region in the proximal promoter. Both negative (bile acids, phorbol esters and insulin) and positive (glucocorticoid hormones) effects were mediated through sequences in the region 318 bp upstream of the ATG codon. All-trans-retinoic acid, cAMP, and LDL did not affect transcriptional activity. These findings show that the hamster cholesterol 7 alpha-hydroxylase gene undergoes a predominant negative regulation, as opposed to the rat CYP7A homologous gene. |
| Regulation of the human cholesterol 7alpha-hydroxylase gene (CYP7A1) by thyroid hormone in transgenic mice Drover, V. A. and L. B. Agellon (2004), Endocrinology 145(2): 574-81. Abstract: Thyroid hormones exert significant changes in the metabolism of bile acids. However, in humans, the effect of thyroid hormone on cholesterol 7alpha-hydroxylase (cyp7a), the rate- controlling enzyme in the classical bile acid biosynthetic pathway, remains poorly understood and has been difficult to study directly in vivo. Previous studies from our laboratory have shown that the activity of the human cholesterol 7alpha-hydroxylase gene promoter is repressed by T(3) in cultured cells. Accordingly, we hypothesized that T(3) would negatively regulate human CYP7A1 gene expression in vivo. We tested this hypothesis by inducing hypo- and hyperthyroidism in transgenic mice expressing the human CYP7A1 gene. Hypothyroidism did not affect the abundance of human cyp7a mRNA in transgenic mice. In hyperthyroid male mice, human cyp7a mRNA abundance was decreased. No significant change in cyp7a mRNA abundance was observed in hyperthyroid female mice. Gender differences in the amount of cholesterol and bile acids in gallbladder bile were also observed. The data indicate that thyroid hormone can repress the human CYP7A1 gene in transgenic mice, but this effect is dependent on gender in this in vivo model. |
| Regulation of the last two enzymatic reactions in cholesterol biosynthesis in rats: effects of BM 15.766, cholesterol, cholic acid, lovastatin, and their combinations Honda, A., S. Shefer, et al. (1996), Hepatology 24(2): 435-9. Abstract: The Smith-Lemli-Opitz syndrome is a common inherited birth disorder caused by markedly reduced 7-dehydrocholesterol delta 7-reductase activity, the final enzyme in the cholesterol biosynthetic pathway. BM 15.766 (4-2-1-(4-chlorocinnamyl)piperazin-4-ylethyl-benzoic acid) inhibits 7-dehydrocholesterol delta 7-reductase activity, reduces plasma cholesterol levels, and increases 7-dehydrocholesterol levels to reproduce the biochemical abnormalities of the syndrome in rats. Cholesterol, cholic acid, and lovastatin, alone or in combinations, were fed to rats given BM 15.766, and hepatic activities of the last two enzymes in the cholesterol biosynthetic pathway, lathosterol 5-dehydrogenase and 7-dehydrocholesterol delta 7-reductase, were measured. After feeding BM 15.766, hepatic 7-dehydrocholesterol delta 7-reductase activity decreased by 77% while lathosterol 5-dehydrogenase activity tended to increase, so that the ratio of 5-dehydrogenase to delta 7-reductase activities increased from 0.33 to 2.8. In BM 15.766-fed rats, treatment with cholesterol suppressed both 5-dehydrogenase and delta 7-reductase activities by 76% and 66%, respectively, and decreased the 5-dehydrogenase: delta 7-reductase activities ratio from 2.8 to 2.2. In contrast, treatment with cholic acid and BM 15.766 further inhibited delta 7-reductase activity by 67% without changing significantly the 5-dehydrogenase activity that had increased the ratio to 5.5. Combining BM 15.766 with lovastatin increased 5-dehydrogenase activity fivefold but did not change delta 7-reductase activity, raising the ratio to 14.3. In BM 15.766-treated rats, the first and last two enzymatic reactions in the cholesterol biosynthetic pathway catalyzed by 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, lathosterol 5-dehydrogenase, and 7-dehydrocholesterol delta 7-reductase are down-regulated by cholesterol. Thus, only cholesterol and not cholic acid or lovastatin could reduce elevated plasma 7-dehydrocholesterol levels induced by BM 15.766. |
| Regulation of the SHP-2 tyrosine phosphatase by a novel cholesterol- and cell confluence-dependent mechanism Burkart, A., B. Samii, et al. (2003), J Biol Chem 278(20): 18360-7. Abstract: Endothelial cells approaching confluence exhibit marked decreases in tyrosine phosphorylation of receptor tyrosine kinases and adherens junctions proteins, required for cell cycle arrest and adherens junctions stability. Recently, we demonstrated a close correlation in endothelial cells between membrane cholesterol and tyrosine phosphorylation of adherens junctions proteins. Here, we probe the mechanistic basis for this correlation. We find that as endothelial cells reach confluence, the tyrosine phosphatase SHP-2 is recruited to a low-density membrane fraction in a cholesterol-dependent manner. Binding of SHP-2 to this fraction was not abolished by phenyl phosphate, strongly suggesting that this binding was mediated by other regions of SHP-2 beside its SH2 domains. Annexin II, previously implicated in cholesterol trafficking, was associated in a complex with SHP-2, and both proteins localized to adhesion bands in confluent endothelial monolayers. These studies reveal a novel, cholesterol-dependent mechanism for the recruitment of signaling proteins to specific plasma membrane domains via their interactions with annexin II. |
| Regulation of the threshold for lipoprotein-induced acyl-CoA:cholesterol O-acyltransferase stimulation in macrophages by cellular sphingomyelin content Okwu, A. K., X. X. Xu, et al. (1994), J Lipid Res 35(4): 644-55. Abstract: Macrophage acyl-CoA:cholesterol O-acyltransferase (ACAT), a key enzyme in atheroma foam cell formation, is stimulated by lipoproteins only after a "threshold" amount of cholesterol has accumulated in the cell. The present study explores the hypothesis that cellular sphingomyelin, by increasing the capacity of the cell to accommodate excess cholesterol, can influence the threshold of ACAT stimulation by lipoproteins. When the sphingomyelin content of macrophages was increased by either incubation with exogenous sphingomyelin or ceramide (a stimulator of endogenous sphingomyelin synthesis), the ability of acetyl-LDL to stimulate whole-cell ACAT activity was substantially reduced despite similar lipoprotein uptake and total cholesterol accumulation as in control cells. When the sphingomyelin content of macrophages was decreased by sphingomyelinase treatment, the ability of acetyl-LDL to stimulate whole-cell ACAT activity was enhanced despite no change in lipoprotein uptake. Importantly, microsomes isolated from control, sphingomyelin-, or sphingomyelinase-treated macrophages showed no difference in ACAT activity when assayed in vitro in the presence of exogenous cholesterol, suggesting that these treatments affected cholesterol trafficking. Lastly, a corollary of the hypothesis, that cells might adapt to a large increase in free cholesterol by increasing their sphingomyelin content, was supported by showing that the sphingomyelin content of macrophages increased 2.6-fold when the cells were induced to accumulate free cholesterol by incubation with acetyl-LDL plus an ACAT inhibitor. Thus, the sphingomyelin content of macrophages can influence the threshold at which ACAT is stimulated by lipoprotein delivery of cholesterol, and the cholesterol content of macrophages can influence the sphingomyelin content of the cell. These findings are consistent with a model in which cellular sphingomyelin plays an important role in accommodating pools of cellular cholesterol that result from the uptake of atherogenic lipoproteins by macrophages. |
| Regulation of vascular endothelial growth factor receptor-2 activity by caveolin-1 and plasma membrane cholesterol Labrecque, L., I. Royal, et al. (2003), Mol Biol Cell 14(1): 334-47. Abstract: The stimulation of vascular endothelial growth factor receptor-2 (VEGFR-2) by tumor-derived VEGF represents a key event in the initiation of angiogenesis. In this work, we report that VEGFR-2 is localized in endothelial caveolae, associated with caveolin-1, and that this complex is rapidly dissociated upon stimulation with VEGF. The kinetics of caveolin-1 dissociation correlated with those of VEGF-dependent VEGFR-2 tyrosine phosphorylation, suggesting that caveolin-1 acts as a negative regulator of VEGF R-2 activity. Interestingly, we observed that in an overexpression system in which VEGFR-2 is constitutively active, caveolin-1 overexpression inhibits VEGFR-2 activity but allows VEGFR-2 to undergo VEGF-dependent activation, suggesting that caveolin-1 can confer ligand dependency to a receptor system. Removal of caveolin and VEGFR-2 from caveolae by cholesterol depletion resulted in an increase in both basal and VEGF-induced phosphorylation of VEGFR-2, but led to the inhibition of VEGF-induced ERK activation and endothelial cell migration, suggesting that localization of VEGFR-2 to these domains is crucial for VEGF-mediated signaling. Dissociation of the VEGFR-2/caveolin-1 complex by VEGF or cyclodextrin led to a PP2-sensitive phosphorylation of caveolin-1 on tyrosine 14, suggesting the participation of Src family kinases in this process. Overall, these results suggest that caveolin-1 plays multiple roles in the VEGF-induced signaling cascade. |
| Regulatory effect of sense line diet on cholesterol and body weight in mice fed a high-fat diet An, H. J., H. S. Chung, et al. (2004), Ann Nutr Metab 48(6): 398-403. Abstract: BACKGROUND/AIMS: Sense line diet (SLD) is a newly developed dietary functional food that is composed of a lot of herbs. The function of SLD is to help control weight. Although it is reported that each herb has effects on lipid metabolism and obesity, these effects are not the same as SLD. The aim of this study was therefore to investigate whether SLD combined with high fat (HF) diet can influence body weight and fat accumulation. METHODS: An experiment was conducted with 40 C57BL/6J mice with an initial body weight of about 16 g. Body weight was recorded every week, plasma levels of triglyceride, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol were analyzed at the end of the study. RESULTS: Weight increases in the 10 or 20% SLD group were significantly less than in the HF diet group (p < 0.05). Plasma triglyceride and LDL cholesterol levels were decreased by 52.1 and 34.2% in the 10% SLD group and 15.4 and 15.4% in the 20% SLD group, respectively, compared to the high-fat diet group. HDL cholesterol level was increased by 7.8% in the 10% SLD and by 54.9% in the 20% SLD group. CONCLUSIONS: Our findings indicate that SLD may be beneficial in the regulation of high-fat-diet-induced blood circulatory disorders as well as overweight. |
| Regulatory function of glucose and insulin on high-density lipoprotein cholesterol in normolipidemic subjects Ghiselli, G., G. B. Bon, et al. (1994), Metabolism 43(11): 1332-7. Abstract: A decreased plasma concentration of high-density lipoprotein (HDL) cholesterol is associated with a higher incidence of coronary artery disease in populations. Therefore, there is intense investigation into the mechanisms responsible for the regulation of HDL cholesterol concentration in plasma. Insulin has a potent effect on HDL cholesterol, but it is unclear whether this is mediated by the primary effect insulin has on plasma triglycerides (TG). In this study, the question of the relationship between glucose, insulin, and HDL cholesterol has been addressed by investigating a cohort of nondiabetic normolipidemic men living in the Venice, Italy, area. One hundred twenty-eight men aged 30 to 69 years were initially recruited. The following parameters were measured: fasting plasma cholesterol, TG, HDL cholesterol, glucose, and insulin. One hundred seventeen of these subjects underwent an oral glucose tolerance test (OGTT), and the glucose and insulin responses were assessed. The final statistical analysis was performed on 98 nondiabetic individuals with plasma lipid levels within the 75th percentile for cholesterol and TG concentrations of the general population of the same age. The insulin response was a positive independent variable for plasma TG (P <.005) and HDL cholesterol (P <.005). On the other hand, HDL cholesterol was negatively associated with plasma TG. This relationship remained significant (P <.0001) also after controlling for age, body mass index (BMI), and glucose- and insulin-related measurements. Consistent with these results, both a stepwise variable selection analysis and a stratification analysis of the data indicated that the plasma TG concentration is the major determinant of HDL cholesterol level.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Related factors of meeting National Cholesterol Education Program-recommended goals with atorvastatin Yoshitomi, Y., T. Tsujibayashi, et al. (2003), J Atheroscler Thromb 10(1): 19-24. Abstract: The aim of this study was to observe the efficacy of atorvastatin and the related factors of meeting the National Cholesterol Education Program (NCEP)-recommended low-density lipoprotein (LDL) cholesterol levels in patients with hypercholesterolemia. A total of 107 patients were treated with atorvastatin 10 mg/day for 12 weeks. Eighty % of the patients achieved the target goals. There was a significant difference in the initial body mass index (BMI) between patients achieving the target goals and those not achieving the target goals (p < 0.05). In multiple stepwise logistic regression analysis, initial BMI and complications correlated with reaching the NCEP-recommended target goals (p < 0.05). A great number of patients treated with atorvastatin, including those previously poorly controlled with other therapies, reached the target goals at the starting dose 10 mg/day. BMI may be a useful index of achieving the NCEP-recommended target goals with atorvastatin. |
| Relation among body condition score, milk production, and serum urea nitrogen and cholesterol concentrations in high-producing Holstein dairy cows in early lactation Ruegg, P. L., W. J. Goodger, et al. (1992), Am J Vet Res 53(1): 5-9. Abstract: Body condition scoring (using a 5-point scale with quarter-point divisions) was performed on 66 Holstein dairy cows that began their second or later lactation in August, September, or October 1988. Body condition was scored, beginning on postpartum day 4(+/- 1) and subsequently at postpartum days (+/- 1) 18, 32, 46, 60, 73, and 87. Blood samples were obtained on the same dates. Kilograms of milk produced per cow was measured daily. Body condition score and changes in body condition score were evaluated in relation to daily milk production, cumulative 80-day milk yield, and serum urea nitrogen and cholesterol concentrations. Average daily milk production during week 1 was indicative of cumulative 80-day production, but not of 305-day milk yields. Cows that calved with body condition score greater than or equal to 3.50 did not differ in average daily milk production, cumulative 80-day milk yield, or 305-day milk yield, compared with cows that calved with body condition score less than 3.50. Cows that calved with body condition score greater than or equal to 3.50 lost more condition than did cows that calved with body condition score less than 3.50. Body condition score at calving and amount of body condition loss interacted with the rate of change in daily milk production. Serum urea nitrogen concentration did not differ for cows grouped by cumulative 80-day milk production or for cows grouped by amount of condition loss. Serum cholesterol values were higher than previously reported values and increased directly with milk production. Serum cholesterol values were inversely related to condition loss but changes in cholesterol concentration were not related to condition loss. |
| Relation among body condition score, serum urea nitrogen and cholesterol concentrations, and reproductive performance in high-producing Holstein dairy cows in early lactation Ruegg, P. L., W. J. Goodger, et al. (1992), Am J Vet Res 53(1): 10-4. Abstract: Body condition scoring (using a 5-point scale with quarter-point divisions) was performed on 66 Holstein dairy cows that began their second or later lactation in August, September, or October 1988. Cows' body condition was scored beginning on postpartum day 4 (+/- 1) and subsequently at postpartum days (+/- 1) 18, 32, 46, 60, 73 and 87. Blood samples were obtained on the same dates. Reproductive health examinations were conducted by 1 of 2 veterinarians beginning at postpartum day 21. Reproductive performance was evaluated in relation to body condition score and serum urea nitrogen and cholesterol concentrations. Number of days to first recorded signs of estrus and first breeding were not related to body condition score at calving, amount of condition loss, cumulative 80-day milk yield, or 305-day fat corrected milk yield. Cows that calved with body condition score greater than or equal to 3.50 required more days to conceive. Cows losing greater than 0.75 points of condition had longer days of conception. Body condition score at calving and amount of condition lost were not related to services per conception or diagnosis of follicular cyst. Cumulative 80-day milk yield was not related to days to conception or services per conception. Cows that produced greater than or equal to the mean 305-day milk yield required more services and had longer days to conception than cows that produced less than the mean 305-day milk yield.(ABSTRACT TRUNCATED AT 250 WORDS) |
| Relation between 25-hydroxyvitamin D3, apolipoprotein A-I, and high density lipoprotein cholesterol Auwerx, J., R. Bouillon, et al. (1992), Arterioscler Thromb 12(6): 671-4. Abstract: In a survey of cardiovascular risk factors in 185 men and 173 women of a Belgian population group, an independent and highly significant positive correlation was found between the serum concentrations of 25-hydroxyvitamin D3 and apolipoprotein A-I (p less than 0.001 in both sexes). 25-Hydroxyvitamin D3 also showed a positive correlation with high density lipoprotein cholesterol levels (p less than 0.05 in men and p less than 0.005 in women). This relation was independent of a possible effect of 25-hydroxyvitamin D3 on serum calcium. Taking the biological variation of 25-hydroxyvitamin D3 levels (+/- 2 SD = 25 ng/ml) into account, these findings could explain variations in the levels of apolipoprotein A-I of 15 mg/100 ml and of high density lipoprotein cholesterol of 4 mg/100 ml. |
| Relation between cholesterol ester transfer protein activities and lipoprotein cholesterol in patients with hypercholesterolemia and combined hyperlipidemia Tato, F., G. L. Vega, et al. (1995), Arterioscler Thromb Vasc Biol 15(1): 112-20. Abstract: Cholesterol ester transfer protein (CETP) promotes the transfer of cholesterol esters among different lipoprotein classes-high-density lipoproteins (HDL), very-low-density lipoproteins, intermediate-density lipoproteins, and low-density lipoproteins (LDL). The current study was carried out to determine whether CETP activities are correlated with lipoprotein cholesterol levels in a large number of patients having elevated LDL cholesterol and normal triglycerides (hypercholesterolemia) and elevated LDL cholesterol and high triglycerides (combined hyperlipidemia). Compared with 50 normolipidemic male patients, 113 hypercholesterolemic patients had a 42% higher mean activity of CETP, and approximately 60% of these patients had CETP activities outside the normal range. A similar elevation of CETP was observed in 47 patients with combined hyperlipidemia. Furthermore, in those with combined hyperlipidemia, CETP activities were highly correlated with LDL cholesterol, non-HDL cholesterol, and non-HDL/HDL ratios. Similar high correlations were obtained by combining normotriglyceridemic patients with and without elevated LDL cholesterol. Since patients with elevated LDL cholesterol had a significantly lower mean level of HDL cholesterol, a high CETP activity also was related to a reduced HDL cholesterol level. Our results are consistent with this concept, although they do not constitute final proof that high CETP activities contribute to elevated cholesterol concentrations and reduced HDL cholesterol levels in patients with hypercholesterolemia and in those with combined hyperlipidemia. |
| Relation between cholesterol levels, statins and Alzheimer's disease in the human population Austen, B., G. Christodoulou, et al. (2002), J Nutr Health Aging 6(6): 377-82. Abstract: This review paper discusses potential relationships between Cholesterol levels, the therapeutic use of Statins and the risk of Alzheimer s Disease. Comparisons have also been made between the Western populations and Oriental populations. Epidemiological studies have shown that statins, which reduce the levels of plasma cholesterol by inhibiting the enzyme 3 hydroxy-3methylglutaryl-coenzyme A (HMGCoA) reductase, reduce the risk of Alzheimer s disease by up to 70%. Further research is required to determine whether cholesterol levels have a direct, causative, or indirect relationship with Alzheimer disease. Also, it is not clear why some statins reduce the prevalence of AD and others do not. Statins may have an affect on other AD risk factors, or act by mechanisms which are independent of their effects on cholesterol levels? |