Cholesterol Journal Articles

Record 7261 to 7280

In vivo metabolism of alpha-tocopherol in lipoproteins and liver: studies on rabbits in response to acute cholesterol loading
Fragoso, Y. D. and A. J. Brown (1998), Sao Paulo Med J 116(4): 1753-9.
Abstract: OBJECTIVE: To investigate the transport of alpha-tocopherol in lipoproteins of rabbits under normal diet and under acute loading of cholesterol. DESIGN: Two New Zealand White rabbits were fed 14C-alpha-tocopherol acetate in a single oral dose and the recovery of radiolabel in lipoproteins and plasma was monitored. Low density lipoprotein (LDL) from these animals was obtained and labeled with 3H cholesteryl ester. Three other rabbits were injected with this double-labeled LDL in the native form; while three other animals received this LDL in the acetylated form. RESULTS: Plasma clearance, liver uptake and levels of radiolabel in high density lipoprotein (HDL) of animals injected with 14C3Hacetyl LDL were significantly higher than those in animals injected with 14C3Hnative LDL. Larger particles of HDL, rich in apolipoprotein E (apoE) carried significantly higher levels of both labels in rabbits injected with acetylated LDL. CONCLUSION: These results provide evidence for in vivo mechanisms of "reverse alpha-tocopherol transport", analogous to "reverse cholesterol transport".

In vivo metabolism of apo A-I and apo A-II in subjects with apo A-I(Lys107-->0) associated with reduced HDL cholesterol and Lp(AI w AII) deficiency
Tilly-Kiesi, M., C. J. Packard, et al. (1997), Atherosclerosis 128(2): 213-22.
Abstract: Apolipoprotein A-I (apo A-I) and apolipoprotein A-II (apo A-II) represent 80 90% of the protein content of high density lipoproteins (HDL). Previously we have identified a Finnish family with an apo A-I variant (Lys107-->0) associated with reduced plasma HDL cholesterol level and decreased lipoprotein (Lp)(AI w AII) concentration compared to unaffected family members. To determine the in vivo metabolism of apo A-I and apo A-II in the carriers of apo A-I (Lys107-->0) variant we radioiodinated normal apo A-I with 125I and apo A-II with 131I and compared the kinetic data of two heterozygous apo A-I(Lysl07-->0) patients (HDL cholesterol leves 0.31 and 0.69 mmol/l) to that of eight normolipidemic, healthy control subjects. Plasma radioactivity curves of 125I-labelled normal apo A-I of the patients demonstrated accelerated clearance of apo A-I compared to control subjects. In the two patients the fractional catabolic rates (FCR) of apo A-I were 0.347/day and 0.213/day, respectively, while the mean FCR of apo A-I of the control subjects was 0.151 +/- 0.041/day. Similarly, the plasma decay curves of the 131I-labelled apo A-II showed more rapid clearance of apo A-II in the two patients than in control subjects. The FCR of apo A-II in the two patients were 0.470/day and 0.234/day, while the mean FCR of apo A-II in control subjects was 0.154 +/- 0.029/day. The calculated production rates of apo A-I were similar in patients and in control subjects, and the production rates of apo A-II were significantly higher in patients than in control subjects. Our results show that the Lp(AI w AII) deficiency in patients with the apo A-I(Lys107-->0) is associated with increased fractional catabolic rates of normal apo A-I and apo A-II, while the production rates of these apolipoproteins are normal (apo A-I) or slightly increased (apo A-II).

In vivo metabolism-based discovery of a potent cholesterol absorption inhibitor, SCH58235, in the rat and rhesus monkey through the identification of the active metabolites of SCH48461
Van Heek, M., C. F. France, et al. (1997), J Pharmacol Exp Ther 283(1): 157-63.
Abstract: SCH48461 is a selective and highly potent inhibitor of cholesterol absorption. In rats, SCH48461 is rapidly and completely metabolized in the first pass through the body. To compare the activity of the metabolites of SCH48461 with SCH48461 itself, an intestinally cannulated, bile duct-cannulated rat model for cholesterol absorption was developed. SCH48461 inhibited the absorption of cholesterol by 70%, whereas bile containing the metabolites of SCH48461 (henceforth, "metabolite bile") inhibited the absorption by greater than 95%. Very little of the recovered radioactive dose of SCH48461 was located in the intestinal lumen (7%) or wall (4%), whereas 85% appeared in bile. However, in rats treated with metabolite bile, 62% of the dose remained in the lumen, 13% was associated with the wall and only 24% reappeared in bile, which suggests that the activity of the metabolite bile may be related to its higher retention in the intestinal wall. Rats treated with metabolite bile had 64% and 84% less drug-related radioactivity in their plasma and livers, respectively, compared with animals treated with SCH48461, which indicates that the metabolites are systemically less available than SCH48461. The metabolites in bile were separated by high-performance liquid chromatography; the most active fraction in the bile duct-cannulated rat model was identified by mass spectrometry as the glucuronide of the C4-phenol of SCH48461. The other fractions had moderate or no activity. Through the identification of the most active biliary metabolites of SCH48461 in the rat, we have discovered SCH58235, a novel cholesterol absorption inhibitor which is 400 times more potent than SCH48461 in the cholesterol-fed rhesus monkey.

In vivo modulation of HDL phospholipid has opposing effects on SR-BI- and ABCA1-mediated cholesterol efflux
Yancey, P. G., M. A. Kawashiri, et al. (2004), J Lipid Res 45(2): 337-46.
Abstract: The effects of in vivo modulation of HDL phospholipid (PL) on scavenger receptor class BI (SR-BI)- and ATP binding cassette transporter 1 (ABCA1)-mediated efflux were examined by overexpressing either endothelial lipase (EL) or phosphatidylserine phospholipase (PS-PLA1) in human apolipoprotein A-I (apoA-I) transgenic mice. Overexpression of EL led to large reductions in the serum PL/apoA-I ratio (-60%), total cholesterol (TC; -89%), and HDL cholesterol (-91%). Relative to the serum before overexpression of EL, the efflux potential of the serum via SR-BI decreased by 90% and ABCA1-mediated efflux increased by 63%. In contrast to overexpression of EL, overexpression of PS-PLA1 led to increases in the PL/apoA-I ratio (88%), TC (78%), HDL cholesterol (57%), and HDL size. The efflux potential of the serum increased by 60% via SR-BI and decreased by 57% via ABCA1. There were significant positive correlations between SR-BI-mediated efflux and a number of serum parameters, including PL/apoA-I ratio, PL, TC, free cholesterol (FC), and HDL cholesterol. In striking contrast, the same correlations were seen with ABCA1-mediated efflux, but the relationships were inverse. In summary, in vivo modulation of HDL PL content affects ABCA1- and SR-BI-mediated efflux in a reciprocal manner. These findings indicate that the type of lipase acting on HDL in vivo will determine which FC efflux pathway the HDL serves. Additionally, the extent of lipolysis will determine the efficiency of FC removal via this pathway.

In vivo oxidised cholesterol in atherosclerosis
Stalenhoef, A. F., H. A. Kleinveld, et al. (1993), Atherosclerosis 98(1): 113-4.

In vivo quantification of cholesterol content in human carotid arteries by quantitative gamma-camera imaging after injection of autologous low density lipoproteins (LDL)
Virgolini, I., J. O'Grady, et al. (1992), Int J Rad Appl Instrum B 19(2): 245-50.
Abstract: Low density lipoproteins (LDL) were isolated by immunoaffinity chromatography from 18 patients (31-70 years) suffering from primary hypercholesterolemia with angiographically proven atherosclerosis of either one or both carotid arteries. LDL were labeled with 123I (1 mCi/mg LDL) by the iodine monochloride method followed by purification with dialysis and immediately reinjected thereafter. Gamma-camera serial controls over carotid regions allowed visual detection of uptake of the radiocompound uptake in 12 out of the 18 patients. The lipid entry ratio (LER; counts over the vascular region/pixel as compared to the contralateral side after background subtraction) confirmed the visual findings. Whole body images performed until 20 h after reinjection showed 3 different kinetic types of LDL-influx into the vessel wall: decreasing (type I), increasing and then decreasing (type II) and continuously increasing (type III) with time. Four patients underwent endarterectomy within 2-7 weeks after gamma-camera imaging. Histological control revealed an extensive amount of "foam cells" in tissue samples derived during surgery and an absence of endothelial lining in samples belonging to patients with type II kinetics.

In vivo regulation of hepatic lipase activity and mRNA levels by diets which modify cholesterol influx to the liver
Benhizia, F., D. Lagrange, et al. (1994), Biochim Biophys Acta 1211(2): 181-8.
Abstract: The aim of this study was to assess whether diets enriched in cholesterol, sodium cholate and drugs known to modify liver cholesterol biosynthesis can modulate hepatic lipase (H-TGL) expression and activity in vivo. Female lean Zucker rats, known to be good responders to cholesterol, were fed for 7 days with a control C diet or the C diet supplemented (w/w) with either 2% cholesterol, 0.5% sodium cholate, 2% cholestyramine or simvastatin (0.1%) added to the cholestyramine diet or given by gavage (10 mg/rat) for 3 days. H-TGL activity decreased by 34% with cholesterol, and by 27% when both cholesterol and cholate were administered to the rats. Under these conditions, H-TGL mRNA decreased by 34% and 87%, respectively. The sharp decrease in H-TGL expression was associated with a strong increase in cholesteryl ester in total liver and in the liver microsome fraction. H-TGL activity decreased by 33% with cholestyramine and the mRNA level decreased by 47%. Simvastatin lowered H-TGL activity by 55% when added to the cholestyramine diet, probably because of a reduction in food intake. When administrated by gavage, simvastatin increased both the H-TGL activity (by 28%) and mRNA (by 23%). These variations may be linked to the availability of mevalonate-derived sterol and non-sterol products.

In vivo regulation of low-density lipoprotein receptor and apolipoprotein B gene expressions by dietary fat and cholesterol in inbred strains of mice
Srivastava, R. A., S. Jiao, et al. (1991), Biochim Biophys Acta 1086(1): 29-43.
Abstract: Two proteins that may be important in the hypercholesterolemia and atherosclerosis produced by dietary fat and/or cholesterol are apoB and the LDL-receptor. We evaluated the molecular and genetic regulation of these two proteins by two important components of atherogenic diets: dietary fatty acids and dietary cholesterol. The control diet (C) contained 5% corn oil; the high cholesterol (HC) diets, 5% corn oil plus 0.5% or 2% cholesterol; the high fat diet (HF) 1% corn oil and 20% hydrogenated coconut oil; the fat plus cholesterol diets (HF/C) were the same as HF diet plus either 0.5% or 2% cholesterol. Ten strains of inbred mice were fed the C and HF/C (2% cholesterol) diets. Three strains; C3H, C57BL and SWR, were studied in greater detail. In them the effects of dietary fat and cholesterol were assessed separately and together. These three strains were fed all six diets. Lipoprotein profiles of plasma and indexes of lipoprotein composition were obtained by gel filtration chromatography and in selected strains by gradient ultracentrifugation. Relative rates of transcription of LDL-receptor mRNA and apoB mRNA were measured in purified mouse liver nuclei and levels of LDL-receptor mRNA and apoB mRNA in liver and intestine were quantified by RNA excess solution hybridization assays. The HF/C diet produced rises in plasma total-, VLDL- and LDL-cholesterol and apoB concentrations in the ten strains. VLDL and LDL became cholesterol-enriched and the proportion of total cholesterol transported in VLDL and LDL rose at the expense of HDL. This general pattern of HF/C diet-induced changes was similar in all strains, but there were marked quantitative differences between strains with respect to lipid and lipoprotein concentrations, and compositions and the distribution of cholesterol on both the HC and HF/C diets. The strain-related differences were not due to differences in absorption of dietary cholesterol because, for any given diet, hepatic cholesterol levels increased to the same extent in all strains. Nor were the strain-related differences related to alleles of the apoB gene as determined by RFLP analyses. In the three strains, hepatic LDL-receptor mRNA transcription was suppressed by all diets. But, LDL-receptor mRNA levels in both intestine and liver were suppressed only by the HC and HF/C diets and not by the HF diet. Thus, dietary cholesterol decreased LDL-receptor mRNA levels by mechanisms operating at the transcriptional level, while dietary fatty acids, in addition to inhibiting transcription also appeared to enhance mRNA stability.(ABSTRACT TRUNCATED AT 400 WORDS)

Inaccuracy of calculated LDL-cholesterol in type 2 diabetes: consequences for patient risk classification and therapeutic decisions
Wagner, A. M., J. L. Sanchez-Quesada, et al. (2000), Clin Chem 46(11): 1830-2.

Inactive lipoprotein lipase (LPL) alone increases selective cholesterol ester uptake in vivo, whereas in the presence of active LPL it also increases triglyceride hydrolysis and whole particle lipoprotein uptake
Merkel, M., J. Heeren, et al. (2002), J Biol Chem 277(9): 7405-11.
Abstract: We have previously shown that transgenic expression of catalytically inactive lipoprotein lipase (LPL) in muscle (Mck-N-LPL) enhances triglyceride hydrolysis as well as whole particle lipoprotein and selective cholesterol ester uptake. In the current study, we have examined whether these functions can be performed by inactive LPL alone or require the presence of active LPL expressed in the same tissue. To study inactive LPL in the presence of active LPL in the same tissue, the Mck-N-LPL transgene was bred onto the heterozygous LPL-deficient (LPL1) background. At 18 h of age, Mck-N-LPL reduced triglycerides by 35% and markedly increased muscle lipid droplets. In adult mice, it reduced triglycerides by 40% and increased lipoprotein particle uptake into muscle by 60% and cholesterol ester uptake by 110%. To study inactive LPL alone, the Mck-N-LPL transgene was bred onto the LPL-deficient (LPL0) background. These mice die at approximately 24 h of age. At 18 h of age, in the absence of active LPL, inactive LPL expression did not diminish triglycerides nor did it result in the accumulation of muscle lipid droplets. To study inactive LPL in the absence of active LPL in the same tissue in adult animals, the Mck-N-LPL transgene was bred onto mice that only expressed active LPL in the heart (LPL0/He-LPL). In this case, Mck-N-LPL did not reduce triglycerides or increase the uptake of lipoprotein particles but did increase muscle uptake of chylomicron and very low density lipoprotein cholesterol ester by 40%. Thus, in the presence of active LPL in the same tissue, inactive LPL augments triglyceride hydrolysis and increases whole particle triglyceride-rich lipoprotein and selective cholesterol ester uptake. In the absence of active LPL in the same tissue, inactive LPL only mediates selective cholesterol ester uptake.

Inborn errors of cholesterol biosynthesis
Kelley, R. I. (2000), Adv Pediatr 47: 1-53.
Abstract: Disorders of cholesterol biosynthesis have recently emerged as important errors of metabolism that collectively have taught us many new genetic and biochemical lessons. Whereas most metabolic diseases are characterized by exclusively or largely postnatal biochemical toxicities or deficiencies, disorders of cholesterol biosynthesis are notable for their severe effects on prenatal development. The remarkable embryonic consequences of abnormal cholesterol biosynthesis are exemplified by Smith-Lemli-Opitz syndrome (SLOS), a well-known multiple congenital anomaly syndrome only recently discovered to be caused by a deficiency in the last step in cholesterol biosynthesis. Equally surprising has been the discovery that primary defects of cholesterol biosynthesis cause several different forms of congenital skeletal dysplasia, most notably X-linked dominant chondrodysplasia punctata, or Conradi-Hunermann syndrome. Yet another sterol disorder, desmosterolosis, caused by defective activity of desmosterol reductase, combines a severe osteosclerotic skeletal dysplasia with multiple embryonic malformations similar to those of SLOS. The discovery of the biochemical basis of these diverse genetic disorders has provided not only accurate biochemical methods for their diagnosis and prenatal diagnosis, but also new insights into the biochemistry of vertebrate embryonic development. Among the lessons we have learned from the study of inborn errors of cholesterol biosynthesis, one of the most important is that the abnormal cholesterol metabolism of SLOS impairs the function of "Sonic hedgehog" and other related embryonic "signaling proteins" that help determine the vertebrate body plan during the earliest weeks of embryonic development. Most significant clinically has been the realization that many of the postnatal clinical problems of patients with SLOS are direct consequences of the inability to synthesize the large amounts of cholesterol needed for growth and for the synthesis of compounds derived from cholesterol, such as steroid hormones. In addition to the important finding that supplementary cholesterol eliminates or ameliorates many of the feeding and growth problems of SLOS, the discovery that the autistic behaviors of children with SLOS can be reduced or even eliminated by treatment with supplementary dietary cholesterol has been one of the most startling. Moreover, clinical and basic research on prenatal cholesterol nutrition in SLOS and various animal model systems has delineated a previously unrecognized system for the delivery of low-density lipoprotein cholesterol from the mother to the developing embryo. The many discoveries engendered by these experiments of nature argue that there are heretofore unrecognized beneficial effects of cholesterol, especially in children, and that we should consider very carefully possible adverse effects that the popular war against cholesterol may have on the prenatal and postnatal development of children.

Incidence of cholesterol embolisms in 70 atheromatous patients hospitalized for cardiovascular evaluation
Launay, J., P. Y. Baudouy, et al. (1992), Rev Med Interne 13(4): 268-72.
Abstract: Cholesterol crystal embolization must be considered in all atheromatous patients hospitalized for cardiovascular evaluation. Because this is a difficult and often belated diagnosis, between June 1989 and June 1990 a prospective study was conducted on 70 patients. Clinical monitoring, including examination of the fundus oculi, was performed before, and on the 5th day of cardiovascular investigations. The incidence of systemic emboli (12.8%) detected in this way corresponds to that reported in rare published series. Funduscopy is a simple, rapid and little expensive examination which should improve the investigative procedures and point to the best treatment.

Incidence of new atherothrombotic brain infarction in older persons with prior myocardial infarction and serum low-density lipoprotein cholesterol >or=125 mg/dl treated with statins versus no lipid-lowering drug
Aronow, W. S., C. Ahn, et al. (2002), J Gerontol A Biol Sci Med Sci 57(5): M333-5.
Abstract: BACKGROUND: We report the incidence of new atherothrombotic brain infarction (ABI) in older men and women with prior myocardial infarction and a serum low-density lipoprotein (LDL) cholesterol of >or=125 mg/dl treated with statins and with no lipid-lowering drug. METHODS: The incidence of new ABI was investigated in an observational prospective study of 1410 men and women, mean age 81 +/- 9 years, with prior myocardial infarction and a serum LDL cholesterol of >or=125 mg/dl treated with statins (679 persons or 48%) and with no lipid-lowering drug (731 persons or 52%). Follow-up was 36 +/- 21 months. RESULTS: At follow-up, the stepwise Cox regression model showed that significant independent predictors of new ABI were age (risk ratio = 1.04 for a 1-year increase in age), cigarette smoking (risk ratio = 3.5), hypertension (risk ratio = 3.1), diabetes mellitus (risk ratio = 2.3), initial serum LDL cholesterol (risk ratio = 1.01 for each 1 mg/dl increase), initial serum high-density lipoprotein cholesterol (risk ratio = 0.97 for each 1 mg/dl increase), prior stroke (risk ratio = 2.5), and use of statins (risk ratio = 0.40). The Cochran-Armitage test showed a trend in the reduction of new ABI in persons treated with statins as the level of serum LDL cholesterol decreased (p <.0001). CONCLUSIONS: Use of statins caused a 60%, significant, independent reduction in new ABI in older men and women with prior myocardial infarction and a serum LDL cholesterol of >or=125 mg/dl.

Incidence of new coronary events in older persons with prior myocardial infarction and serum low-density lipoprotein cholesterol > or = 125 mg/dl treated with statins versus no lipid-lowering drug
Aronow, W. S. and C. Ahn (2002), Am J Cardiol 89(1): 67-9.

Including walnuts in a low-fat/modified-fat diet improves HDL cholesterol-to-total cholesterol ratios in patients with type 2 diabetes
Tapsell, L. C., L. J. Gillen, et al. (2004), Diabetes Care 27(12): 2777-83.
Abstract: OBJECTIVE: The aim of this study was to examine the effect of a moderate-fat diet inclusive of walnuts on blood lipid profiles in patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: This was a parallel randomized controlled trial comparing three dietary advice groups each with 30% energy as fat: low fat, modified low fat, and modified low fat inclusive of 30 g of walnuts per day. Fifty-eight men and women, mean age 59.3 +/- 8.1 years, started the trial. Dietary advice was given at baseline with monthly follow-up and fortnightly phone calls for support. Body weight, percent body fat, blood lipids, HbA1c, total antioxidant capacity, and erythrocyte fatty acid levels were measured at 0, 3, and 6 months. Data were assessed by repeated-measures ANOVA with an intention-to-treat model. RESULTS: The walnut group achieved a significantly greater increase in HDL cholesterol-to-total cholesterol ratio (P=0.049) and HDL (P=0.046) than the two other treatment groups. A 10% reduction in LDL cholesterol was also achieved in the walnut group, reflecting a significant effect by group (P=0.032) and time (P=0.036). There were no significant differences between groups for changes in body weight, percent body fat, total antioxidant capacity, or HbA1c levels. The higher dietary polyunsaturated fat-to-saturated fat ratio and intakes of omega-3 fatty acids in the walnut group were confirmed by erythrocyte biomarkers of dietary intake. CONCLUSIONS: Structured "whole of diet" advice that included 30 g of walnuts/day delivering substantial amounts of polyunsaturated fatty acid improved the lipid profile of patients with type 2 diabetes.

Inclusion of a legume in a saturated fat-rich diet affects the cholesterol status but not the expression of triiodothyronine and retinoic acid receptors in rat liver
Bonilla, S., C. Noel-Suberville, et al. (1998), Ann Nutr Metab 42(5): 297-303.
Abstract: In a previous study, we showed that a high-fat diet, rich in saturated fatty acids and cholesterol, induced hypercholesterolemia and, in rat liver, a decreased expression of TR and RAR, nuclear receptors which are transcription factors for genes involved in cell growth, differentiation and cellular homeostasis. The aim of this study was to determine whether hypercholesterolemia plays a role in the onset of this decreased expression. Rats were fed a high-fat diet, rich in saturated fatty acids and cholesterol, for 3 weeks and then received in addition Vicia faba for 2 weeks. The inclusion of the legume induced a decrease in hypercholesterolemia (in agreement with numerous data) but did not affect the underexpression of TR or RAR (expression evaluated as the maximum binding capacity of receptors and as the abundance of mRNA of these receptors). Thus, it is suggested that, at least in this experimental model, hypercholesterolemia plays a minor role in the decreased expression of nuclear receptors in rat liver.

Inclusion of cholesterol in DOTAP transfection complexes increases the delivery of DNA to cells in vitro in the presence of serum
Crook, K., B. J. Stevenson, et al. (1998), Gene Ther 5(1): 137-43.
Abstract: The contrast between the relative efficiency of transfection by cationic lipid reagents in vitro and that in vivo is well recognised. One suggested reason for this is the presence of competing polyanionic surfaces in blood and other biological fluids, and even in vitro transfections have to be performed in low-serum medium. In this study we have shown that by preparing cationic lipid reagents based on DOTAP with cholesterol as a second constituent of the bilayer we can achieve significant levels of in vitro transfection in serum concentrations of up to 80% (DOTAP alone did not transfect at all in these conditions). In an effort to explain the behaviour of DOTAP/cholesterol mixes under these conditions, we examined the effect of serum on the transfection complex. We could detect protein bound to each type of cationic lipid complex, but there was no difference in the amount nor in the type of protein bound. DNA within either type of complex which were incubated with increasing amounts of serum remained resistant to digestion with DNase I, and there was no reduction in the condensation of the DNA as measured by ethidium bromide fluorescence. Finally, we measured the attachment and uptake into cells by the different complexes in the presence of serum and showed that more DOTAP-cholesterol than DOTAP complexes attach to and are taken up by cells in the presence of serum. We suggest that improved cell binding and uptake may be the main mechanism by which cholesterol acts to maintain transfection in the presence of serum.

Incorporating soy protein into a low-fat, low-cholesterol diet
Dunn, A. V. (2000), Cleve Clin J Med 67(10): 767-72.
Abstract: The US Food and Drug Administration recommends including four servings of at least 6.25 g each (25 g/day) of soy protein into a diet low in saturated fat and cholesterol to reduce the risk of heart disease. Patients are more likely to comply with this dietary change if they have their physician's support. The author discusses how the clinician can help patients incorporate soy protein into a low-cholesterol, low-fat diet. A meta-analysis found that soy protein consumption achieved an average 9.3% decrease in total cholesterol, a 12.9% decrease in low-density lipoprotein (LDL) cholesterol, and a 10.5% decrease in triglycerides. Soy pills and supplements such as isoflavone are not recommended. The cholesterol-lowering benefit has only been observed when the intact soy protein is used. Soy milk can be used in place of milk in coffee or over breakfast cereal, as well as in milkshakes and other blended drinks. Soy milk can be substituted for milk in many recipes.

Incorporation of amino acids into liver and serum proteins during prolonged administration to animals of ethanol and cholesterol
Bozhko, G., V. S. Chursina, et al. (1990), Ukr Biokhim Zh 62(1): 30-4.
Abstract: The synthesis of soluble liver proteins and amino acid incorporation into blood serum proteins were studied in guinea pigs which were daily administered ethanol and cholesterol during 3 months. 9 fractions obtained by electrophoresis in polyacrylamide gel were analyzed. It has been found that ethanol and cholesterol in the liver suppress the synthesis of 4 out of 9 recorded protein fractions. In the serum the ethanol effect against a background of the cholesterol administration is characterized by a sharp decrease of specific radioactivity of albumins while the quantity of the protein fraction is unchanged. These results together with the data available in literature on the ethanol suppression of proteolysis suppose that the joint effect of ethanol and cholesterol is accompanied by a decrease in the blood serum albumin decomposition.

Incorporation of cholesterol in sphingomyelin- phosphatidylcholine vesicles has profound effects on detergent-induced phase transitions
Moschetta, A., P. M. Frederik, et al. (2002), J Lipid Res 43(7): 1046-53.
Abstract: Vesicle <--> micelle transitions are important phenomena during bile formation and intestinal lipid processing. The hepatocyte canalicular membrane outer leaflet contains appreciable amounts of phosphatidylcholine (PC) and sphingomyelin (SM), and both phospholipids are found in the human diet. Dietary SM enrichment inhibits intestinal cholesterol absorption. We therefore studied detergent-induced vesicle --> micelle transitions in SM-PC vesicles. Phase transitions were evaluated by spectrophotometry and cryotransmission electron microscopy (cryo-TEM) after addition of taurocholate (3-7 mM) to SM-PC vesicles (4 mM phospholipid, SM/PC 40%/60%, without or with 1.6 mM cholesterol). After addition of excess (5-7 mM) taurocholate, SM-PC vesicles were more sensitive to micellization than PC vesicles. As shown by sequential cryo-TEM, addition of equimolar (4 mM) taurocholate to SM-PC vesicles induced formation of open vesicles, then (at the absorbance peak) fusion of bilayer fragments into large open structures (around 200 nm diameter) coexisting with some multilamellar or fused vesicles and thread-like micelles and, finally, transformation into an uniform picture with long thread-like micelles. Incorporation of cholesterol in the SM/PC bilayer changed initial vesicular shape from spherical into ellipsoid and profoundly increased detergent resistance. Disk-like micelles and multilamellar vesicles, and then extremely large vesicular structures, were observed by sequential cryo-TEM under these circumstances, with persistently increased absorbance values by spectrophotometry. These findings may be relevant for bile formation and intestinal lipid processing. Inhibition of intestinal cholesterol absorption by dietary SM enrichment may relate to high resistance against bile salt-induced micellization of intestinal lipids in presence of the sphingolipid.

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