| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Nef increases the synthesis of and transports cholesterol to lipid rafts and HIV-1 progeny virions Zheng, Y. H., A. Plemenitas, et al. (2003), Proc Natl Acad Sci U S A 100(14): 8460-5. Abstract: HIV buds from lipid rafts and requires cholesterol for its egress from and entry into cells. Viral accessory protein Nef plays a major role in this process. In this study, it not only increased the biosynthesis of lipid rafts and viral particles with newly synthesized cholesterol, but also enriched them. Furthermore, via the consensus cholesterol recognition motif at its C terminus, Nef bound cholesterol. When this sequence was mutated, Nef became unable to transport newly synthesized cholesterol into lipid rafts and viral particles. Interestingly, although its levels in lipid rafts were not affected, this mutant Nef protein was poorly incorporated into viral particles, and viral infectivity decreased dramatically. Thus, Nef also transports newly synthesized cholesterol to the site of viral budding. As such, it provides essential building blocks for the formation of viruses that replicate optimally in the host. |
| Nef induces multiple genes involved in cholesterol synthesis and uptake in human immunodeficiency virus type 1-infected T cells van 't Wout, A. B., J. V. Swain, et al. (2005), J Virol 79(15): 10053-8. Abstract: Several recent reports indicate that cholesterol might play an important role in human immunodeficiency virus type 1 (HIV-1) replication. We investigated the effects of HIV-1 infection on cholesterol biosynthesis and uptake using microarrays. HIV-1 increased gene expression of cholesterol genes in both transformed T-cell lines and primary CD4(+) T cells. Consistent with our microarray data, (14)C-labeled mevalonate and acetate incorporation was increased in HIV-1-infected cells. Our data also demonstrate that changes in cholesterol biosynthesis and uptake are only observed in the presence of functional Nef, suggesting that increased cholesterol synthesis may contribute to Nef-mediated enhancement of virion infectivity and viral replication. |
| Negative relationships between growth in height and levels of cholesterol in puberty: a 3-year follow-up study Kouda, K., H. Nakamura, et al. (2003), Int J Epidemiol 32(6): 1105-10. Abstract: BACKGROUND: Previously, there were only a few reports on the negative relationship between pubertal growth in height and levels of serum lipid in boys. Detailed information on both genders is needed. METHODS: We investigated the relationship between pubertal growth in height and serum lipid. Subjects were 1442 boys and 1350 girls followed up from age 10-11 years (the fifth grade level of elementary school) to age 13-14 years (the second year of junior high school). Anthropometric variables and serum lipids were measured by the same protocol at both ages. RESULTS: From cross-sectional analysis, at both ages negative relationships between total cholesterol levels and height were found in both genders. On longitudinal analysis, height at age 10-11 years was one of the factors predicting the level of total cholesterol at age 13-14 years. In addition, negative relationships between increase in height and change in serum lipids (total cholesterol and high density lipoprotein cholesterol) over the 3-year period were obtained in both genders. Thus, pubertal children who experience a large increase in height tended to show a decrease in serum lipids, and children who experience a small increase in height tended to show an increase in serum lipids. CONCLUSION: In both genders, total cholesterol level in pubertal children is negatively associated with height. Height velocity is inversely associated with dynamic changes in serum lipids during puberty. |
| Neither raw nor retrograded resistant starch lowers fasting serum cholesterol concentrations in healthy normolipidemic subjects Heijnen, M. L., J. M. van Amelsvoort, et al. (1996), Am J Clin Nutr 64(3): 312-8. Abstract: The question addressed was whether dietary resistant starch would lower serum cholesterol and triacylglycerol concentrations in healthy normolipidemic subjects. In a randomized single-blind 3 x 3 Latin-square study with corrections for any carryover effects, 27 males and 30 females consumed supplements containing glucose or resistant starch (RS) from raw high-amylose cornstarch (RS2) or from retrograded high-amylose cornstarch (RS3). The RS2 and RS3 supplements provided 30 g RS/d. Each type of supplement was consumed in addition to the habitual diet for 3 wk. At the end of each 3-wk period, fasting blood samples and a 24-h food-consumption recall were obtained from each subject. The subjects collected 24-h urine samples for lithium determination, which was added to the supplements to check compliance. Mean lithium recovery was 97% and did not differ between supplements. The mean composition of the background diet was similar when the three supplements were taken. Body weight remained constant throughout the study. There were no significant differences in the fasting concentrations of serum total, high-density-lipoprotein (HDL), and low-density-lipoprotein (LDL) cholesterol; triacylglycerols, or 3 alpha-hydroxy bile acids after consumption of glucose, RS2, or RS3. Evidence is presented that the lack of effect of RS2 and RS3 on serum lipid concentrations cannot be explained by insufficient statistical power, a low dose, or a short duration of treatment. The subjects reported softer stools and more gastrointestinal symptoms after supplementation with RS than after glucose. Neither the RS2 nor the RS3 supplements lowered serum lipid concentrations in healthy, normolipidemic men and women. |
| Neonatal genetically lean and obese pigs respond differently to dietary cholesterol Patterson, B. W., W. W. Wong, et al. (1992), J Nutr 122(9): 1830-9. Abstract: The impact of cholesterol exposure in early life on later cholesterol metabolism is not clearly understood. Sixteen newborn genetically lean and obese pigs were fed 0 or 5.0 g cholesterol/kg diet (0 or 0.5%) (liquid diets for 12 d, dry diets thereafter) for 33 d, after which they were all fed 10.0 g cholesterol/kg diet (1.0%) for 23 d. All animals were killed on d 56 and whole-body protein, fat and water were determined on the ground carcass. Dietary cholesterol had no consistent effect on growth rates or body composition. Mean fat content of lean pigs was 15.1% compared with 22.7% for obese pigs; corresponding values were 14.8 and 14.4% for protein and 65.5 and 58.3% for water. Concentrations of plasma total cholesterol, HDL cholesterol and apolipoproteins B and A-1 were increased by 0.5% dietary cholesterol in obese but not in lean piglets, although dietary cholesterol caused HDL and LDL size distribution profiles to shift toward larger-sized components in both strains. Plasma total cholesterol and apolipoprotein B concentrations rose two- to eightfold in all groups after the 1% cholesterol diet was consumed; these changes were accompanied by shifts in LDL and HDL size distribution profiles towards larger-sized components. With 1.0% cholesterol in the diet of all groups, HDL cholesterol concentration increased by approximately 50% in both groups of lean pigs and in obese pigs previously fed cholesterol, but did not increase further in obese pigs previously fed 0.5% cholesterol. The magnitude of the hypercholesterolemic response in lean pigs was blunted by previous exposure to 0.5% dietary cholesterol, but the response was accentuated in obese animals that had been previously exposed to 0.5% dietary cholesterol. These data provide evidence that genetic differences between obese and lean pigs affect their serum lipoprotein responses to high cholesterol intake. |
| Neonatal hypoxia-ischemia reduces ganglioside, phospholipid and cholesterol contents in the rat hippocampus Ramirez, M. R., F. Muraro, et al. (2003), Neurosci Res 46(3): 339-47. Abstract: Hypoxia-ischemia is a common cause of neonatal brain damage producing serious impact on cerebral maturation. This report demonstrates that rats submitted to hypoxia-ischemia present a marked decrease in hippocampal gangliosides, phospholipids and cholesterol contents as from 7 days after the injury. Although chromatographic profiles of the different ganglioside species (GM1, GD1a, GD1b, and GT1b) from the hippocampus of hypoxic-ischemic hippocampi groups (HI) were apparently unaffected, as compared with controls, there were quantitative absolute reductions in HI. The phospholipid patterns were altered in HI as from the 14th to the 30th day after the injury, where phosphatidylcholine (PC) quantities were higher than phosphatidylethanolamine (PE); additionally, the cardiolipin band was detected only in hippocampi of control adult rats. In general, the absolute quantities of phospholipids were lower in HI than in correspondent controls since 7th day after the injury. Considering that reported effects were maintained, we suggest they express a late biochemical response triggered by the neonatal hypoxic-ischemic episode; the consequences would be cell death and a delay on brain development, expressed by a reduction on synaptogenesis and myelinogenesis processes. |
| Nephrocalcinosis and hyperlipidemia in rats fed a cholesterol- and fat-rich diet: association with hyperoxaluria, altered kidney and bone minerals, and renal tissue phospholipid-calcium interaction Schmiedl, A., P. O. Schwille, et al. (2000), Urol Res 28(6): 404-15. Abstract: To determine whether an "atherogenic" diet (excess of cholesterol and neutral fat) induces pathological calcification in various organs, including the kidney, and abnormal oxalate metabolism, 24 male Sprague-Dawley rats were fed either normal lab chow (controls, n = 12) or the cholesterol- and fat-rich experimental diet (CH-F, n = 12) for 111 +/- 3 days. CH-F rats developed dyslipidemia high blood levels of triglycerides, total, low-density lipoprotein (LDL)-, very low-density lipoprotein (VLDL)-, high-density lipoprotein (HDL)-bound cholesterol, total phospholipids, elevated serum total alkaline phosphatase and lactate dehydrogenase (LDH) levels, in the absence of changes in overall renal function, extracellular mineral homeostasis serum protein-corrected total calcium, magnesium, parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (1,25(OH)2D), plasma glycolate and oxalate levels. There was a redistribution of bone calcium and enhanced exchange of this within the extraosseous space, which was accompanied by significant bone calcium loss, but normal bone histomorphometry. Liver oxalate levels, if expressed per unit of defatted (DF) dry liver, were three times higher than in the controls. Urinary glycolate, oxalate, calcium and total protein excretion levels were elevated, the latter showing an excess of proteins > 100 kD and a deficit of proteins > 30-50 kD. Urinary calcium oxalate supersaturation was increased, and calcium phosphate supersaturation was unchanged. There were dramatically increased (by number, circumference, and area) renal calcium phosphate calcifications in the cortico-medullary region, but calcium oxalate deposits were not detectable. Electron microscopy (EM) and elemental analysis revealed intratubular calcium phosphate, apparently needle-like hydroxyapatite. Immunohistochemistry of renal tissue calcifications revealed co-localization of phospholipids and calcium phosphate. It is concluded that rats fed the CH-F diet exhibited: (1) a spectrum of metabolic abnormalities, the more prominent being dyslipidemia, hyperoxaluria, hypercalciuria, dysproteinuria, loss of bone calcium, and calcium phosphate nephrocalcinosis (NC); and (2) an interaction between calcium phosphate and phospholipids at the kidney level. The biological significance of these findings for the etiology of idiopathic calcium urolithiasis in humans is uncertain, but the presented animal model may be helpful when designing clinical studies. |
| Nephrosclerosis, glycohemoglobin, cholesterol, and smoking in subjects dying of coronary heart disease Tracy, R. E., G. T. Malcom, et al. (1994), Mod Pathol 7(3): 301-9. Abstract: Subjects dying of coronary heart disease (CHD) were compared with subjects in a control (basal) group in two series of forensic autopsies. Serum cholesterol assessed in postmortem heart blood was significantly greater in the CHD than in the basal group. CHD subjects were smokers more often than basal subjects, as determined from postmortem serum thiocyanate levels, but the statistical significance is ambiguous (P < 0.06). After exclusion of overt diabetics, a stepwise increase in the percentage of subjects with CHD was observed throughout the normal range for glycohemoglobin. Fibroplasia of small renal arteries, the most reliable postmortem proxy for hypertension, did not differ between CHD and basal groups. These results suggest that young (mean age 49.2 yr) black and white men and women classified from autopsy findings as having CHD as cause of death are often not hypertensive, but instead tend to be hyperlipidemic and glucose intolerant. A surprising result was that arteriolar hyalinization and arterial fibroplasia of the renal cortex often failed to parallel each other between groups of subjects. This was true in comparisons between black and white, male and female, blood cholesterol and glycohemoglobin groupings, and between CHD and basal subjects. This outcome suggests that hyalinization of renal arterioles is an especially reliable marker for CHD and that this association may not be mediated entirely through high blood pressure. |
| Nerve regeneration and cholesterol reutilization occur in the absence of apolipoproteins E and A-I in mice Goodrum, J. F., T. W. Bouldin, et al. (1995), J Neurochem 64(1): 408-16. Abstract: Apolipoproteins have been implicated in the salvage and reutilization of myelin cholesterol during Wallerian degeneration and the subsequent nerve regeneration. Current evidence suggests that myelin cholesterol complexes with apolipoproteins E and A-I to form lipoproteins that are taken up via low-density lipoprotein receptors on myelinating Schwann cells. We recently reported, however, that apolipoprotein E is not required for nerve regeneration or reutilization of myelin cholesterol. We have now investigated nerve regeneration and the reutilization of cholesterol in mutant mice deficient in both apolipoproteins E and A-I. Morphologic examination of nerves 4 and 12 weeks after crush injury revealed that regeneration proceeded at a normal rate in the absence of these apolipoproteins. Autoradiography of regenerating nerves indicated that prelabeled myelin lipid was reutilized in the regenerating myelin. 3-Hydroxy-3-methylglutaryl-CoA reductase, the rate-limiting enzyme in cholesterol synthesis, was down-regulated in the regenerating nerves, indicative of cholesterol uptake via lipoproteins. Prelabeled myelin cholesterol was present in lipoprotein fractions isolated from crushed nerves of mutant mice. These data suggest that there is considerable redundancy in the process of cholesterol reutilization within nerve, and that apolipoproteins other than apolipoproteins E and A-I may be involved in the recycling of myelin cholesterol. |
| Net flux of nonesterified fatty acids, cholesterol, triacylglycerol, and glycerol across the portal-drained viscera and liver of pregnant ewes Freetly, H. C. and C. L. Ferrell (2000), J Anim Sci 78(5): 1380-8. Abstract: The objective of this study was to determine the pattern of nutrient flux across portal-drained viscera (PDV) and liver in ewes with varying numbers of fetuses. Catheters were placed in the hepatic portal vein, a branch of the hepatic vein, a mesenteric vein, and the abdominal aorta of each ewe. Plasma flow and net cholesterol, nonesterified fatty acids (NEFA), and glycerol release across the PDV and liver were determined prior to exposure to rams. Ewes were subsequently mated. Two ewes were not pregnant, six ewes gave birth to singles, and 11 ewes gave birth to twins. Additional measurements were taken 103, 82, 61, 39, 19, and 6 d before parturition. There was a net PDV uptake of nonesterified cholesterol in the nonpregnant ewes and a net release in the ewes with singles and twins. Net nonesterified cholesterol hepatic release did not differ with days from parturition (P =.77). There was a net hepatic release of nonesterified cholesterol in the ewes with twins and a net hepatic uptake in the ewes with singles and in nonpregnant ewes (P =.03). There was a net PDV release of NEFA; however, it did not differ with litter size (P =.59) or days from parturition (P =.63). Hepatic NEFA uptake increased with litter size (P =.03) and increased as gestation progressed (P =.006). There was an interaction (P =.04) between litter size and days from parturition for net PDV glycerol release. Net PDV glycerol release in the nonpregnant ewes decreased over time, but release in pregnant ewes tended to increase over time. Hepatic glycerol uptake increased with litter size and increased as gestation progressed. There was a net PDV uptake of triacylglycerol, but it did not differ with litter size (P =.11) or with days from parturition (P =.06). There was a net hepatic release of triacylglycerol, but it did not differ with litter size (P =.59) or with days from parturition (P =.67). Liver utilization of glycerol and NEFA as substrates for metabolism increases as pregnancy progresses. In the nonpregnant ewe, the combined contribution of glycerol and NEFA carbon accounted for 10% of the carbon taken up by the liver, and in ewes pregnant with twins, the combined contribution accounted for 42% of the carbon uptake 19 d before parturition. In conclusion, these data demonstrate NEFA are an important metabolite when determining carbon balance across the liver and their relative contribution to carbon balance increases as pregnancy progresses. |
| Net transport of cholesterol from cells of the human EA.hy 926 endothelial cell line to high density lipoproteins Kilsdonk, E. P., A. N. Dorsman, et al. (1993), Experientia 49(6-7): 561-6. Abstract: EA.hy 926 cells, a human endothelial cell line, show characteristics of differentiated endothelial cells. The cells express saturable binding of apo E-free 125I-high density lipoprotein3 (HDL3). Bmax increased from 71 to 226 ng HDL3 bound/mg cell protein after cholesterol loading of the confluent endothelial cells with cationized low density lipoprotein (LDL). The affinity did not change after cholesterol enrichment (Kd was 37 micrograms HDL3 protein/ml for control cells and 31 micrograms/ml for loaded cells). Incubation of cholesterol-loaded EA.hy 926 cells with native HDL and LDL had different effects on cellular cholesterol levels. Incubation with HDL decreased both esterified and unesterified cellular cholesterol, but LDL did not change total cellular cholesterol. However, LDL tended to increase cellular cholesteryl esters, with a concomitant decrease of unesterified cellular cholesterol. Incubation of endothelial cells with both HDL and LDL also resulted in decreased total cellular cholesterol levels. These data show that cationized LDL-loaded human endothelial EA.hy 926 cells can be used to study the net transport of cellular cholesterol to HDL, the first step in reverse cholesterol transport. |
| Neurobiology of cholesterol and violent behavior Friedman, E. H. (1995), Arch Intern Med 155(5): 543-4. |
| Neurobiology. Cholesterol--making or breaking the synapse Barres, B. A. and S. J. Smith (2001), Science 294(5545): 1296-7. |
| Neurodegenerative disorders and cholesterol Michikawa, M. (2004), Curr Alzheimer Res 1(4): 271-5. Abstract: It has been suggested that a high serum cholesterol level is a risk factor for Alzheimer's disease (AD), that treatment with cholesterol-lowering drugs (statins) reduces the frequency of AD development, and that the polymorpholism of genes encoding proteins regulating cholesterol metabolism is associated with the frequency of AD development. However, the mechanism by which high serum cholesterol level leads to AD, still remains unclarified. Several recent studies have shown the results challenging the above notions. Here another notion is proposed, that is, a low high-density lipoprotein (HDL) level in serum and cerebro-spinal fluid (CSF) is a risk factor for the development of AD; moreover, the possibility that AD and Niemann-Pick type C disease share a common cascade, by which altered cholesterol metabolism leads to neurodegeneration (tauopathy) is discussed. In this review, the association between cholesterol and AD pathogenesis is discussed from different viewpoints and several basic issues are delineated and addressed to fully understand the mechanisms underlying this relationship. |
| Neurological development of 5-year-old children receiving a low-saturated fat, low-cholesterol diet since infancy: A randomized controlled trial Rask-Nissila, L., E. Jokinen, et al. (2000), Jama 284(8): 993-1000. Abstract: CONTEXT: Early childhood introduction of nutritional habits aimed at atherosclerosis prevention is compatible with normal growth, but its effect on neurological development is unknown. OBJECTIVE: To analyze how parental counseling aimed at keeping children's diets low in saturated fat and cholesterol influences neurodevelopment during the first 5 years of life. DESIGN: Randomized controlled trial conducted between February 1990 and November 1996. SETTING: Outpatient clinic of a university department in Turku, Finland. PARTICIPANTS: A total of 1062 seven-month-old infants and their parents, recruited at well-baby clinics between 1990 and 1992. At age 5 years, 496 children still living in the city of Turku were available to participate in neurodevelopmental testing. INTERVENTION: Participants were randomly assigned to receive individualized counseling aimed at limiting the child's fat intake to 30% to 35% of daily energy, with a saturated:monounsaturated:polyunsaturated fatty acid ratio of 1:1:1 and a cholesterol intake of less than 200 mg/d (n = 540) or usual health education (control group, n = 522). MAIN OUTCOME MEASURES: Nutrient intake, serum lipid concentrations, and neurological development at 5 years, among children in the intervention vs control groups. RESULTS: Absolute and relative intakes of fat, saturated fatty acids, and cholesterol among children in the intervention group were markedly less than the respective values of control children. Mean (SD) percentages of daily energy at age 5 years for the intervention vs control groups were as follows: for total fat, 30.6% (4.5%) vs 33.4% (4.4%) (P<. 001); and for saturated fat, 11.7% (2.3%) vs 14.5% (2.4%) (P<.001). Mean intakes of cholesterol were 164.2 mg (60.1 mg) and 192.5 mg (71. 9 mg) (P<.001) for the intervention and control groups, respectively. Serum cholesterol concentrations were continuously 3% to 5% lower in children in the intervention group than in children in the control group. At age 5 years, mean (SD) serum cholesterol concentration of the intervention group was 4.27 (0.63) mmol/L (165 24 mg/dL) and of the control group, 4.41 (0.74) mmol/L (170 29 mg/dL) (P =.04). Neurological development of children in the intervention group was at least as good as that of children in the control group. Relative risks for children in the intervention group to fail tests of speech and language skills, gross motor functioning plus perception, and visual motor skills were 0.95 (90% confidence interval CI, 0.60-1.49), 0.95 (90% CI, 0.58-1.55), and 0.65 (90% CI, 0.39-1.08), respectively (P =.85.86, and.16, respectively, vs control children). CONCLUSION: Our data indicate that repeated child-targeted dietary counseling of parents during the first 5 years of a child's life lessens age-associated increases in children's serum cholesterol and is compatible with normal neurological development. JAMA. 2000;284:993-1000 |
| Neuronal membrane cholesterol loss enhances amyloid peptide generation Abad-Rodriguez, J., M. D. Ledesma, et al. (2004), J Cell Biol 167(5): 953-60. Abstract: Recent experimental and clinical retrospective studies support the view that reduction of brain cholesterol protects against Alzheimer's disease (AD). However, genetic and pharmacological evidence indicates that low brain cholesterol leads to neurodegeneration. This apparent contradiction prompted us to analyze the role of neuronal cholesterol in amyloid peptide generation in experimental systems that closely resemble physiological and pathological situations. We show that, in the hippocampus of control human and transgenic mice, only a small pool of endogenous APP and its beta-secretase, BACE 1, are found in the same membrane environment. Much higher levels of BACE 1-APP colocalization is found in hippocampal membranes from AD patients or in rodent hippocampal neurons with a moderate reduction of membrane cholesterol. Their increased colocalization is associated with elevated production of amyloid peptide. These results suggest that loss of neuronal membrane cholesterol contributes to excessive amyloidogenesis in AD and pave the way for the identification of the cause of cholesterol loss and for the development of specific therapeutic strategies. |
| Neurons in Niemann-Pick disease type C accumulate gangliosides as well as unesterified cholesterol and undergo dendritic and axonal alterations Zervas, M., K. Dobrenis, et al. (2001), J Neuropathol Exp Neurol 60(1): 49-64. Abstract: Niemann-Pick disease type C (NPC) is a lethal neurologic storage disorder of children most often caused by a defect in the protein NPC1. To better understand the disease we thoroughly characterized the cellular and morphological alterations occurring in murine, feline, and human NPC. Using immunocytochemistry and filipin histochemistry we show that both gangliosides and unesterified cholesterol are differentially stored in neurons of the cerebral cortex, cerebellum, and hippocampus, as well as in liver. Double fluorescence labeling revealed that GM2 ganglioside and unesterified cholesterol were partially co-localized in vesicular structures, and triple fluorescence labeling utilizing a LAMP-1 antibody identified many of these organelles as part of the late endosomal/lysosomal pathway. These observations, coupled with the proposed role of NPC1 in intracellular cholesterol movement, suggest that GM3 and GM2 gangliosides as well as unesterified cholesterol may be retrogradely cleared from late endosomes/lysosomes by an NPC1-dependent mechanism. Cellular consequences of the NPC metabolic defect as shown by parvalbumin immunocytochemistry and rapid Golgi staining, respectively, revealed characteristic axonal spheroids on GABAergic neurons and ectopic dendritogenesis that followed a species-specific gradient of: mouse < feline < human. These studies suggest that the homeostatic regulation of gangliosides and cholesterol in neurons is mediated by NPC1 and that perturbations in this mechanism cause a complex neuronal storage disorder. |
| Neuropeptide Y and serum cholesterol Uusitupa, M. I., M. K. Karvonen, et al. (1999), Duodecim 115(3): 241-2. |
| Neuropeptide Y: a novel link between the neuroendocrine system and cholesterol metabolism Uusitupa, M. I., M. K. Karvonen, et al. (1998), Ann Med 30(6): 508-10. Abstract: High serum total and low-density lipoprotein (LDL) cholesterol levels constitute the main risk factor for atherosclerotic vascular diseases. Both genetic and environmental factors are involved in the regulation of serum cholesterol levels. Neuropeptide Y (NPY), which is widely expressed in both the central and peripheral nervous systems, is known to regulate food intake and energy balance but its role in cholesterol metabolism has remained almost untouched in former literature. A newly discovered association between a leucine(7)-to-proline(7) polymorphism (Pro(7)) in the signal peptide of NPY and a high cholesterol level may provide new ideas for the genetic regulation of cholesterol metabolism. The presence of the Pro(7) in NPY results in serum total cholesterol levels 0.6-1.4 mmol/L higher compared with subjects without this gene variant. The Pro(7) in NPY was detected in 14% of Finns but only in 6% of Dutchmen, and its impact on serum cholesterol concentration seems to be stronger in obese than in normal-weight subjects. At least among Finns, the Pro(7) in NPY is one of the strongest genetic factors identified thus far affecting serum cholesterol levels. |
| Neuroprotective effects of statins may not be related to total and low-density lipoprotein cholesterol lowering George, S. J., A. J. Dhond, et al. (2002), Am J Cardiol 90(11): 1237-9. |