| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Cholesterol biosynthesis from lanosterol: molecular cloning, chromosomal localization, functional expression and liver-specific gene regulation of rat sterol delta8-isomerase, a cholesterogenic enzyme with multiple functions Bae, S., J. Seong, et al. (2001), Biochem J 353(Pt 3): 689-99. Abstract: Sterol Delta(8)-isomerase (SI) (EC 5.3.3.5), also known as emopamil binding protein or sigma receptor, catalyses the conversion of the 8-ene isomer into the 7-ene isomer in the cholesterol biosynthetic pathway in mammals. Recently, mutations of SI have been found to be associated with Conradi-Hunermann syndrome in humans. To investigate the in vitro and in vivo modes of molecular regulation of SI and its role in cholesterol biosynthesis in mammals, we isolated a full-length cDNA encoding rat SI. The deduced amino-acid sequence of rat SI predicts a 230-residue protein (26737 Da) with 87% and 80% amino-acid identity to mouse and human counterparts. The rat SI gene was mapped to chromosome 12q1.2 using fluorescence in situ hybridization (FISH). The biological function of the cloned rat SI cDNA was verified by overexpressing recombinant Myc-SI in Saccharomyces cerevisiae. It showed a characteristic pattern of inhibition on exposure to trans-2-4-(1,2-diphenylbuten-1-yl)phenoxy-N,N-dimethylethylamine (tamoxifen; IC(50)=11.2 microM) and 3beta-2-(diethylamino)ethoxyandrost-5-en-17-one (U18666A; IC(50)=4.2 microM), two well known potent inhibitors of SI. Northern-blot analysis of 3-week-old rats compared with 2-year-old rats showed that SI mRNA expression in both age groups was restricted to liver, where a 70% reduction in mRNA levels was observed in 2-year-old rats. The FISH studies revealed ubiquitous expression of SI mRNA in rat hepatocytes. The in vitro studies showed that the SI mRNA was highly suppressed by 25-hydroxycholesterol in H4IIE cells. Treatment of H4IIE cells grown in medium supplemented with fetal bovine serum with tamoxifen for 24 h resulted in a dose-dependent induction of SI mRNA, with a concomitant suppression of sterol regulatory element binding protein-1 mRNA. Interestingly, this effect was not seen in emopamil-treated cells. The in vivo experiments also indicate that both mRNA expression and enzymic activity of SI in liver were induced approx. 3-fold in rats fed 5% (w/w) cholestyramine plus 0.1% (w/w) lovastatin in normal chow for 2 weeks. With this newly cloned rat SI cDNA, it becomes possible to gain molecular understanding of previously unknown and tamoxifen-mediated gene regulation of SI that is involved in cholesterol metabolism, ischaemia and genetic diseases. |
| Cholesterol biosynthesis from lanosterol: regulation and purification of rat hepatic sterol 14-reductase Kim, C. K., K. I. Jeon, et al. (1995), Biochim Biophys Acta 1259(1): 39-48. Abstract: We have previously characterized the membrane-bound sterol 14-reductase (14-reductase) that catalyzes anaerobically NADPH-dependent reduction of the 14-double bond of delta 8,14-diene or delta 7,14-diene sterols that are sterol intermediates in cholesterol biosynthesis in mammals (Paik et al. (1984) J. Biol. Chem. 259, 13413-13423). To elucidate the regulatory mechanism as well as molecular characteristics of the 14-reductase, we extended our investigation on the consequences of alteration of the enzymic activity under various physiological conditions. The enzymic activity of rat hepatic sterol 14-reductase was induced more than 11-fold by feeding 5% cholestyramine plus 0.1% lovastatin (the CL-diet) for 7 days but was severely suppressed by feeding 5% cholesterol or 0.01% AY-9944 (an inhibitor of 14-reductase) for the same period. The increase or decrease in the 14-reductase activity also parallels the same change in the cholesterol synthetic rate in hepatocytes from rats that had been fed either the CL-diet or 0.01% AY-9944. In vitro inhibition studies revealed that AY-9944 acts as a competitive inhibitor of the 14-reductase (Ki = 0.26 microM). A diurnal variation was observed for the 14-reductase with peak activity near the middle of the dark cycle (10 p.m.), which was abolished by administration of cycloheximide. With induced enzyme conditions 14-reductase has been further purified with chromatographic procedures to near homogeneity. Purified 14-reductase appears to be a M(r) = 70,000 protein that is composed of two equally-sized subunits having a M(r) = 38,000. All properties of the purified 14-reductase suggest that the solubilized enzyme is the principal 14-reductase of microsomes. Taken together, our results provide the first evidence in support of a previously unknown regulatory role for the 14-reductase in the overall cholesterol synthetic pathway. |
| Cholesterol biosynthesis from lanosterol: regulation and purification of rat hepatic sterol 8-isomerase Kang, M. K., C. K. Kim, et al. (1995), J Biochem (Tokyo) 117(4): 819-23. Abstract: The membrane bound sterol-8-isomerase (isomerase) catalyzes the anaerobic conversion of sterol-8-ene to the sterol-7-ene isomer in eucaryotes. To examine the regulatory mechanism as well as molecular characteristics of the isomerase we investigated the consequences of alteration of the enzymic activity under various diet conditions. Feeding 5% cholesterol or 0.1% AY-9944 for a minimum of 2 days caused more than a 70% decrease in microsomal isomerase activity. Feeding 5% cholestyramine plus 0.1% lovastatin (CL-diet) for 7 days led to approximately 4.0-fold induction of the isomerase activity. In addition, diurnal variation in the enzymic activity was observed with this diet. Induction of the isomerase activity by the CL-diet was quantitatively reflected in an increase in the cholesterol synthetic rate in isolated rat hepatocytes. The isomerase was highly purified from liver of rats fed the CL-diet, and its molecular mass was determined to be 21,000 Da by denaturing sodium dodecylsulfate gel electrophoresis. |
| Cholesterol biosynthesis in dermal fibroblasts from patients with metabolic disorders of peroxisomal origin Malle, E., K. Oettl, et al. (1995), Eur J Clin Invest 25(1): 59-67. Abstract: As peroxisomes possess some of the integral enzymes for cholesterol biosynthesis, the role of these organelles in cholesterol formation was studied in dermal fibroblasts with three types of peroxisomal defect: group I, characterized by the absence of intact peroxisomes (neonatal adrenoleukodystrophy, cerebrohepatorenal syndrome of Zellweger); group II, showing impaired activity of a single peroxisomal enzyme (X-linked adrenoleukodystrophy, adrenomyeloneuropathy); and group III, defective in more than one peroxisomal enzyme (rhizomelic chondrodysplasia punctata). Cells were incubated with three different radioactive precursors, namely 14C-octanoate, 14C-acetate, and 3H-mevalonate, and incorporation of these radiolabels into cholesterol was determined. All fibroblasts with peroxisomal defects were able to form cholesterol at concentrations comparable or higher than those in controls dependent on the radioactive substrate. Binding properties (KD) and bmax values) of LDL to fibroblasts with peroxisomal defects and downregulation of intracellular cholesterol biosynthesis were similar to those found in fibroblasts from normolipidaemic controls, but different to those observed in LDL-receptor negative fibroblasts. As our studies revealed that cholesterol biosynthesis is not impaired in fibroblasts from patients with metabolic disorders of peroxisomal origin, we conclude that peroxisomes play little or no role in the pathway of cholesterol synthesis beyond mevalonate. In earlier steps of the cholesterol synthesis pathway, peroxisomal and mitochondrial defects in parallel may alter cholesterol synthesis indirectly. |
| Cholesterol biosynthesis in normocholesterolemic patients after cholesterol removal by plasmapheresis Feillet, C., J. P. Cristol, et al. (1997), J Clin Apher 12(3): 110-5. Abstract: Plasmapheresis and low-density lipoprotein (LDL)-apheresis are recognized procedures for the treatment of hyperlipidemia resistant to diet and lipid-lowering drugs and provide information on cholesterol synthesis in hypercholesterolemic patients. However, cholesterol synthesis after acute cholesterol removal from plasma has never been investigated in normocholesterolemic patients. In this study, cholesterol synthesis was evaluated in three normocholesterolemic patients by determination of plasma lathosterol, lathosterol-to-cholesterol ratio, and plasma mevalonic acid. In a short-term kinetic study, samples were collected before and after plasmapheresis and every 6 hours during 24 hours. In the second part of the study, cholesterol synthesis was evaluated daily for 3 days. In normocholesterolemic patients, cholesterol returns to basal levels in 3 days. However, cholesterol removal did not result in a significant increase in lathosterol-to-cholesterol ratio or in plasma mevalonic acid, despite a slight increase in lathosterol. In contrast, when repeated plasma exchanges induced a dramatic hypocholesterolemia (< 1 mmol/liter), an acute but transient stimulation of cholesterol synthesis was observed (lathosterol/cholesterol ratio and MVA, respectively, increase from 8.2 to 22.3 and from 28 nmol/liter to 98 nmol/liter). This study shows that cholesterol synthesis is not stimulated by plasmapheresis in normocholesterolemic patients but is enhanced in dramatic hypocholesterolemic patients (< 1 mmol/liter). |
| Cholesterol biosynthesis in Zellweger syndrome: normal activity of mevalonate kinase, mevalonate-5'-pyrophosphate decarboxylase and IPP-isomerase in patients' fibroblasts but deficient mevalonate kinase activity in liver Wanders, R. J. and G. J. Romeijn (1996), J Inherit Metab Dis 19(2): 193-6. |
| Cholesterol biosynthesis inhibited by BM15.766 induces holoprosencephaly in the rat Kolf-Clauw, M., F. Chevy, et al. (1997), Teratology 56(3): 188-200. Abstract: To confirm that blocking 7-dehydrocholesterol delta 7 reductase (7DHC reductase), as observed in Smith-Lemli-Opitz syndrome (SLOS), induces craniofacial defects, we tested BM15.766, which blocks 7DHC reductase but is chemically unrelated to the holoprosencephaly-inducing teratogen AY9944. Rats were given BM15.766 either in methylcellulose from days (D) 1 through D11 (3 treated groups: protocol A) or in olive oil from D4 through D7 (300 mg/kg/d: protocol B). The sera were sampled on D0, D3, and D5 or D6, D10, D14, and D21 to measure cholesterol and dehydrocholesterols in all groups and steroid hormones in protocol B. D21 fetuses showed the holoprosencephaly spectrum of malformations and the treated dams low cholesterol and accumulation of 7DHC, 8DHC, and trienols, as in SLOS-affected children. In the 3 dosage groups the malformations were dose-related and enzymatic cholesterol decreased to a plateau. The DHC reached 25-44% of the total sterols in the dams. In protocol B, one-third of the BM15.766-treated fetuses presented facial malformations and almost two-thirds pituitary agenesis. On D10, cholesterol reached a minimum and the DHC a maximum while estradiol 17 beta and progesterone were lowered, the latter decreasing in correlation with cholesterolemia. A sterol profile similar to that previously observed after AY9944 associated with a similarly high incidence of pituitary agenesis confirmed that time-limited inhibition of 7DHC reductase induces holoprosencephaly and that pituitary agenesis is the minor form of holoprosencephaly. |
| Cholesterol biosynthesis inhibitory component from Zingiber officinale Roscoe Tanabe, M., Y. D. Chen, et al. (1993), Chem Pharm Bull (Tokyo) 41(4): 710-3. Abstract: We previously reported on the isolation and identification of (E)-8 beta,17-epoxylabd-12-ene-15,16-dial (ZT) from ginger (rhizome of Zingiber officinale Roscoe, Zingiberaceae). In this paper, the pharmacological effects of ZT are reported. The experimental mouse hypercholesterolemia induced by Triton WR-1339 was treated after oral administration of ZT. In homogenated rat liver with ZT, cholesterol biosynthesis was decreased. In addition, the same activity was observed in the homogenated rat liver which was resected after the oral administration of ZT. According to the results of general pharmacological screening, no remarkable activity of ZT was observed except for an inhibitory effect on the cholesterol biosynthesis. |
| Cholesterol biosynthesis is not defective in peroxisome biogenesis defective fibroblasts Hogenboom, S., R. J. Wanders, et al. (2003), Mol Genet Metab 80(3): 290-5. Abstract: To evaluate the presumed peroxisomal involvement in cholesterol/isoprenoid biosynthesis, we determined the protein levels and activities of five different enzymes of the presqualene segment of the cholesterol/isoprenoid biosynthetic pathway in primary skin fibroblasts of selected patients with a peroxisomal biogenesis disorder (PBD). These five enzymes all have been reported to be partly or exclusively peroxisomal and include HMG-CoA reductase, mevalonate kinase, phosphomevalonate kinase, mevalonate pyrophosphate decarboxylase, and isopentenyl pyrophosphate isomerase. To exclude that genetic differences, resulting in different defects in peroxisomal biogenesis, have differential effects on the activity of the cholesterol biosynthetic enzymes and on de novo cholesterol biosynthesis, we chose fibroblasts of patients with defined defects in one of four different PEX genes leading to Zellweger syndrome (PEX1, PEX5, PEX16 or PEX19). We found that all enzymes measured are at least as active in the peroxisome-deficient cells cultured in cholesterol-depleted medium as in identically cultured control cells. This indicates that if these presumed peroxisomal proteins are mislocalized to the cytosol they do not loose their activity, nor get degraded unlike most other authentic peroxisomal proteins. We also measured de novo cholesterol synthesis from radio-labeled acetate in all cell lines and found similar or even elevated rates for the PBD cells when compared to controls. Our results imply that functional peroxisomes are not a prerequisite for the functioning of enzymes involved in cholesterol/isoprenoid biosynthesis and as such raise doubts about the true involvement of peroxisomes therein. |
| Cholesterol biosynthesis regulation and protein changes in rat liver following treatment with fluvastatin Steiner, S., C. L. Gatlin, et al. (2001), Toxicol Lett 120(1-3): 369-77. Abstract: The enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase is a key regulator in cholesterol biosynthesis and HMG CoA reductase inhibitors (statins) have become a widely prescribed family of lipid lowering agents. Cholesterol synthesis occurs predominantly in liver which is the target organ of statins. We studied the effects of fluvastatin (Lescol), a member of the statin family, on hepatic protein regulation. Male F344 rats treated with 0.8 mg/kg per day fluvastatin or 24 mg/kg per day fluvastatin for 7 days showed treatment-related changes in 58 liver proteins (P<0.005). Major effects were evident in the cholesterol biosynthesis pathway including the induction of enzymes upstream and downstream of the target enzyme HMG CoA reductase. Treatment also triggered alterations in key enzymes of carbohydrate metabolism and was associated with changes in a heterogeneous set of cellular stress proteins involved in cytoskeletal structure, calcium homeostasis and protease activity. The latter set of protein alterations indicates that hepatotoxicity is associated with high-dose treatment. Based on the results it is suggested that HMG-CoA synthase and isopentenyl-diphosphate delta-isomerase may be explored as alternative drug targets and that the induction levels of these enzymes may serve as a measure of potency of individual statin drugs. It is proposed that efficacy and cellular stress markers discovered in this study may be used in a high throughput screen (HTS) assay format to compare efficiently and accurately the therapeutic windows of different members of the statin family. |
| Cholesterol biosynthesis, peroxisomes and peroxisomal disorders: mevalonate kinase is not only deficient in Zellweger syndrome but also in rhizomelic chondrodysplasia punctata Wanders, R. J. and G. J. Romeijn (1998), J Inherit Metab Dis 21(3): 309-12. |
| Cholesterol blood levels in children: comparison of a Munich screening to worldwide studies from 1980 to 1990 Kunze, D. (1992), J Am Coll Nutr 11 Suppl: 23S-27S. Abstract: Total cholesterol results of a screening of 134 Munich school children aged 6-11 years are described. In reviewing worldwide studies on blood lipids in children, in the last 10 years, I note a large variance in the so-called "normal" values, with mean levels of total cholesterol ranging from 148 to 214 mg%. Age-, sex-, and race-specific reference data for a population are needed. Only with these special data can one determine the point for intervention. With school health education programs, including medical screening examinations, the aim of primary prevention of coronary heart disease can be reached. |
| Cholesterol bonded phase as a separation medium in liquid chromatography. Evaluation of properties and applications Pesek, J. J., M. T. Matyska, et al. (2003), J Chromatogr A 986(2): 253-62. Abstract: An extensive survey of the properties and separation capabilities of a cholesterol bonded phase is reported. The intermediate hydrophobic/hydrophilic properties of the bonded cholesterol material allows this stationary phase to be used for both reversed-phase and aqueous normal-phase separations. Interesting high selectivity is reported for the structural isomers of some antibiotics. The cholesterol bonded material does not display "phase collapse" in high aqueous content mobile phases. Variable temperature studies demonstrate that substantial structural changes of the bonded moiety occur that might be used to control selectivity. Finally, separation of some enantiomers of compounds with a variety of chemical structures is reported under reversed-phase conditions indicating that the cholesterol material may be chiral stationary phase with a broad range of applicability. |
| Cholesterol bound to hemoglobin in normal human erythrocytes: a new form of cholesterol in circulation? Nikolic, M., D. Stanic, et al. (2004), Clin Biochem 37(1): 22-6. Abstract: OBJECTIVE: To study lipid fraction that is occasionally observed in red blood cell (RBC) hemolysate (supernatants from which membranes were separated). STUDY DESIGN: Plasma lipid profiles, cholesterol (Ch) and phospholipids (PL) in intact RBCs, RBC membranes and hemolysates were examined in young healthy male population in winter and summer. RESULTS: The RBC Ch and PL content was significantly higher than in membranes, both in winter and summer. The "excess" of cholesterol (associated with phospholipid) was bound to hemoglobin yielding Hb-lipid adduct (Hb-Ch), the pools in the RBC membrane remaining virtually unaltered. Levels of hemoglobin-lipid complex (Hb-Ch), which were significantly higher in winter than in summer (30% and 19% of the total Hb, respectively), positively correlated with plasma HDL cholesterol levels. CONCLUSION: To our knowledge, this is the first demonstration of cholesterol binding to Hb. The results suggest influence of plasma lipoprotein metabolism on the formation of Hb-Ch. |
| Cholesterol can be lowered in older persons. Should we care? Kaiser, F. E. and J. E. Morley (1990), J Am Geriatr Soc 38(1): 84-5. |
| Cholesterol carriers in human bile: are "lamellae" involved? Cohen, D. E., E. W. Kaler, et al. (1993), Hepatology 18(6): 1522-31. Abstract: Cholesterol, a highly insoluble molecule, is transported in bile by specialized lipid aggregates. On the basis of extensive correlations between laboratory-prepared model biles and surgically harvested native biles, it has become generally accepted that biliary cholesterol is solubilized by simple and mixed micelles, single bilayered (unilamellar) vesicles and, under certain conditions, multilamellar vesicles (liposomes or liquid crystals) all composed of bile salts, lecithin and cholesterol in different proportions. Current concepts suggest that in lithogenic biles multilamellar vesicles result from aggregation and fusion of unilamellar vesicles and are a principal source from which cholesterol precipitates to form gallstones. Recent reports now challenge the prevailing paradigm by proposing that the principal cholesterol-carrying particles in human biles are not micelles but are "lamellae" composed of stacked membrane-like bilayers of lipids. In this article, we provide a critical overview of the experiments that led to the established views of biliary cholesterol transport and to the newer lamellae hypothesis. The principal evidence for lamellae stems from negative-stain electron microscopy, an artifactprone technique when used to study lipid-rich fluids such as bile. We show that lamellar structures represent both the electron microscopic analog of multilamellar vesicles in supersaturated biles that presage the nucleation of cholesterol crystals and an electron microscopic artifact of fossilized mixed micelles that are in fact very tiny (2 to 4 nm in radius) by state-of-the-art noninvasive techniques. We argue further that the lamellae nomenclature improperly equates two fundamentally distinct physical-chemical mechanisms for cholesterol solubilization and dispersion in bile on the basis of identically appearing electron microscopic images. |
| Cholesterol catabolism in patients with acute myelogenous leukemia and hypocholesterolemia: suppressed levels of a circulating marker for bile acid synthesis Tatidis, L., S. Vitols, et al. (2001), Cancer Lett 170(2): 169-75. Abstract: Hypocholesterolemia is a frequent finding in patients with acute myelogenous leukemia (AML) and in other types of malignancies. Since bile acids are major excretion products of cholesterol, the hepatic degradation of cholesterol to bile acids was investigated in AML patients by analyzing a circulating marker for bile acid synthesis. In addition, plasma levels of a marker for cholesterol synthesis were determined. The plasma levels of 7alpha-hydroxy-4-cholesten-3-one, reflecting bile acid production, were markedly lower in patients with AML than in healthy controls. The median levels were 3.3 and 18.5ng/ml (P<0.0001) in the AML patients (n=29) and the healthy subjects (n=16), respectively. The plasma levels of 7-dehydrocholesterol, reflecting hepatic cholesterol synthesis, were similar for the AML patients and the controls. The results show that the conversion of cholesterol to bile acids was suppressed in AML patients, a phenomenon that may result in a decreased intestinal absorption of cholesterol and subsequent hypocholesterolemia. |
| Cholesterol cell content affects prolactin but not growth hormone release in GH4C1 cells Lasa, M., F. J. Perez-Caballero, et al. (1993), Endocrinology 132(4): 1701-6. Abstract: It is generally accepted that cholesterol affects dynamic membrane properties and the function of membrane bound proteins involved in secretion processes. In the present study we employed GH4C1 cells treated with human lipoprotein-deficient serum (h-LPDS), exogenous cholesterol and high density lipoprotein (HDL3) to investigate the role of cholesterol cell content on PRL and GH basal release. Incubation of GH4C1 cells with h-LPDS decreased free cholesterol content and cholesterol added to the media increased it. HDL3 did not act as a cholesterol acceptor in either cholesterol-depleted or cholesterol-loaded cells; however, in depleted cells HDL3 was a net donor, significantly increasing cell cholesterol. Control or cholesterol loaded cells incubated in media with h-LPDS increased their secretion of PRL in parallel with the loss of cell cholesterol. Conversely, the addition of either cholesterol or HDL3 to cholesterol depleted cells inhibited PRL release. However, GH secretion was not modified by changes in free cholesterol in any of these situations. In the experiments in which HDL3 was present, a highly positive correlation was found between cholesterol cell content at the end of the experiment and PRL secretion, no effect could be related to the amount of added HDL3, suggesting that the HDL3 had no specific effect on the secretion of PRL or GH. Our results indicate that cholesterol cell content is an important factor in the release of PRL but not of GH, and emphasize the differences in the basal regulation of the secretion of both hormones. |
| Cholesterol cell content modulates GTPase activity of G proteins in GH4C1 cell membranes Ropero, S., A. Chiloeches, et al. (2003), Cell Signal 15(1): 131-8. Abstract: Previous results from our laboratory showed that GH(4)C(1) cells with low-cholesterol cell content had increased adenylyl cyclase (AC) activity with a parallel increase in G protein alpha subunits associated to the plasma membrane. This effect was directly related to mevalonate availability. In the present report, we characterized the high-affinity GTPase activity present in GH(4)C(1) cell membranes and studied its regulation by cholesterol cell content. The high-affinity GTPase activity, measured as the gamma32PGTP hydrolysis rate, was both time-dependent and protein concentration-dependent. Cultured cells with lipoprotein-deficient serum (LPDS) showed decreased cholesterol cell content and decreased GTPase activity. The kinetic analysis, as interpreted by Lineweaver-Burk plots, indicated that low-cholesterol cell content had no effect on the apparent affinity for GTP, but resulted in a 47% decrease in the maximal velocity of the reaction. Addition of 25-hydroxycholesterol (25-HC), an inhibitor of the expression of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and synthetase to cells in LPDS, further decreased GTPase activity in a dose-dependent manner. This effect was reverted by exogenous cholesterol, but not by mevalonate. Studies with bacterial toxins revealed that neither cholera toxin (CTX) nor pertussis toxins (PTX) were able to revert the inhibition produced by low-cholesterol cell content. These results allowed us to postulate that cholesterol modulates GTPase activity in both Gs and Gi protein families. To analyse further the mechanism of modulation of GTPase activity by cholesterol cell content, 35SGTPgammaS binding in membranes of GH(4)C(1) cells was studied. Changes in cholesterol cell content did not have any effect on GTP binding. Data demonstrated that high-affinity GTPase activity in plasma membrane of GH(4)C(1) cells is direct stimulated by cholesterol cell content and not by mevalonate availability. This example provides a mechanism by which cholesterol cell content can modulate signal transduction mediating by G proteins. |
| Cholesterol changes in coronary patients after a short behavior modification program Sebregts, E. H., P. R. Falger, et al. (2003), Int J Behav Med 10(4): 315-30. Abstract: Serum cholesterol changes after an 8-week behavior modification program for patients with coronary artery disease (CAD) were studied in a randomized controlled clinical trial. Acute myocardial infarction (AMI) or coronary artery bypass grafting (CABG) patients were randomly assigned to the intervention (N = 94) or to usual care (N = 90). After 9 months' follow-up the intervention was effective in reducing total cholesterol and LDL cholesterol levels, particularly in patients with high baseline lipid levels. After correcting for changes in dose of statins during follow-up, effects were weakened, but for patients with high baseline cholesterol levels favorable effects remained. In these patients, the intervention group showed a decline of total cholesterol and LDL cholesterol levels of 20% and 29%, respectively, compared to a 12% and 19% reduction in the control group (p <.01). These effects could not be explained by changes in dietary fat consumption. An unexpected finding was a lower increase in HDL cholesterol in the intervention group than in the control group. |