Increased plasma cholesterol levels are listed between the major atherosclerosis risk factors. The final plasma cholesterol levels result from the interplay between the genetic and environmental (diet, physical activity) factors. Little is known, how dietary factor influence epigenetics. We have analyzed, if an over-generation feeding of rat with cholesterol influences total liver-DNA methylation, and if total liver-DNA methylation differ between the different rat strains (Prague hereditary hypercholesterolemic rats, Prague hereditary hypertriglyceridemic rats and Wistar Kyoto rats). The animals were feed with high fat (additional 5 % over normal capacity) high cholesterol (2 %) diet for 14 days. DNA methylation in the liver tissue in different generations was analyzed using the liquid chromatography coupled with tandem mass spectrometry. We have not observed any significant changes in total liver-DNA methylation over the 9 generations of animals feed by fat/cholesterol enriched diet. Additionally, there were no differences in DNA methylation between different rat strains. In animal model, the dietary changes (hypercholesterolemic diet) not significantly influence the total DNA methylation status within the liver.

• MeSH
• cholesterol dietní aplikace a dávkování   škodlivé účinky   MeSH
• dieta s vysokým obsahem tuků * škodlivé účinky   MeSH
• hypercholesterolemie chemicky indukované   genetika   metabolismus   MeSH
• játra metabolismus   MeSH
• krysa rodu Rattus MeSH
• metylace DNA genetika   MeSH
• potkani Wistar MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• cholesterol dietní MeSH

INTRODUCTION: The aim of study was to evaluate impact of long-term dietary cholesterol overload on the cholesterol homeostasis and liver regeneration. MATERIAL AND METHODS: Serum lipid parameters, 14C-cholesterol incorporation, liver DNA synthesis and protein expression was determined in partially hepatectomized (PH) rats fed with a standard (SLD) or hypercholesterolemic (CHOL) diet. RESULTS: 29-day intake of CHOL diet before PH produced increase in serum total cholesterol, LDL lipoprotein, and triglyceride concentration. PH provoked decrease in serum total cholesterol and triglyceride concentration in both groups. PH was associated with increase in serum ALT activity more pronounced in CHOL animals. Hepatic DNA synthesis was increased after PH in both groups, but lower in CHOL. Hypercholesterolemic diet reduced the absorption of radiolabelled cholesterol in intestine and then activity in blood and liver. The 14C-cholesterol hepatic activities tend to increase after PH in both groups. CHOL diet produced up-regulation of Acyl-CoA:cholesterol acyltransferase-2 protein expression. PH was associated with increase of LDL receptor and Acyl-CoA:cholesterol acyltransferase-2 protein expression in both dietary groups. DISCUSSION: Liver regeneration after PH is negatively influenced by CHOL diet. The increased uptake of cholesterol in the liver after PH associated with up-regulation of LDL receptor protein expression suggests preferential use of extrahepatic cholesterol by the liver.

• Klíčová slova
• ACAT-2, LDL receptor, cholesterol, liver, partial hepatectomy, rat,
• MeSH
• cholesterol dietní farmakologie   MeSH
• cholesterolacyltransferasa účinky léků   metabolismus   MeSH
• DNA účinky léků   metabolismus   MeSH
• hepatektomie MeSH
• játra účinky léků   metabolismus   patologie   MeSH
• krysa rodu Rattus MeSH
• lipoproteiny LDL účinky léků   metabolismus   MeSH
• potkani Wistar MeSH
• radioizotopy uhlíku MeSH
• regenerace jater účinky léků   MeSH
• sterol-O-acyltransferasa 2 MeSH
• triglyceridy metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• Carbon-14 MeSH Prohlížeč
• cholesterol dietní MeSH
• cholesterolacyltransferasa MeSH
• DNA MeSH
• lipoproteiny LDL MeSH
• radioizotopy uhlíku MeSH
• triglyceridy MeSH

Spontaneously Diabetic Torii (SDT) fatty rats, a new obese diabetic model, reportedly presented with features of non-alcoholic steatohepatitis (NASH) after 32 weeks of age. We tried to accelerate the onset of NASH in SDT fatty rats using dietary cholesterol loading and noticed changes in the blood choline level which is expected to be a NASH biomarker. Body weight and biochemical parameters were measured from 8 to 24 weeks of age. At 16, 20, 24 weeks, pathophysiological analysis of the livers were performed. Hepatic lipids, lipid peroxides, and the expression of mRNA related to triglyceride (TG) synthesis, inflammation, and fibrosis were evaluated at 24 weeks. Hepatic fibrosis was observed in SDT fatty rats fed cholesterol-enriched diets (SDT fatty-Cho) from 16 weeks. Furthermore, hepatic lipids and lipid peroxide were significantly higher in SDT fatty-Cho than SDT fatty rats fed normal diets at 24 weeks. Hepatic mRNA expression related to TG secretion decreased in SDT fatty-Cho, and the mRNA expression related to inflammation and fibrosis increased in SDT fatty-Cho at 24 weeks. Furthermore, SDT fatty-Cho presented with increased plasma choline, similar to human NASH. There were no significant changes in the effects of feeding a cholesterol-enriched diet in Sprague-Dawley rats. SDT fatty-Cho has the potential to become a valuable animal model for NASH associated with type 2 diabetes and obesity.

• MeSH
• cholesterol dietní aplikace a dávkování   škodlivé účinky   MeSH
• diabetes mellitus 2. typu krev   patofyziologie   MeSH
• krysa rodu Rattus MeSH
• nealkoholová steatóza jater krev   etiologie   patofyziologie   MeSH
• potkani Sprague-Dawley MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• cholesterol dietní MeSH

UNLABELLED: Recently, thousands of papers brought knowledge about effects of nutrients on cellular level, in experimental animals and in human experiments on one side, the results of epidemiological studies on the other side have suggested the nutrients and foods for healthy diet and nutrients and foods, which should be consumed only in limited amount. Among foods, which should be avoided, those with higher content of trans-fatty acids. Their daily intake should not exceed 1 % of total energy intake. Similar should be limited saturated fatty acid, added sugar and salt. On the contrary, the intake of monounsaturated and polyunsaturated fatty acids in foods should be basic part of fat intake. In these conditions the amount of consumed fat could create up to 35 % of all daily energy intake. Beneficial carbohydrates are those with low glycemic index, i.e. whole grain and brown rice products and legumes. The intake of salt is necessary to limit fewer than 6 g per day and alcohol intake should not exceed 10 g per day in women and 20 g per day in men. The recommendation in last years do not limit cholesterol daily intake. The food of animal origin with high content of saturated fatty acids, i.e. meat and milk products parallel contains also cholesterol. On the other hand, the oils of vegetable origin mostly from tropical oils, which contents high amount of saturated fatty acids represents the risk? On the contrary eggs and shellfish contents high amount of cholesterol and very low amounts of saturated fatty acids. Therefore, there is no reason for their strict limitation in the diet. KEY WORDS: carbohydrate - diabetes - dietary recommendation - energy intake - fat - healthy diet - iron - cholesterol - protein.

• MeSH
• cholesterol dietní MeSH
• diabetická dieta * MeSH
• dietní tuky MeSH
• dospělí MeSH
• lidé MeSH
• mastné kyseliny MeSH
• nenasycené mastné kyseliny MeSH
• nutriční nároky * MeSH
• rizikové faktory MeSH
• stravovací zvyklosti * MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• cholesterol dietní MeSH
• dietní tuky MeSH
• mastné kyseliny MeSH
• nenasycené mastné kyseliny MeSH

BACKGROUND: Cardiovascular disease (CVD) represents a leading cause of mortality worldwide, especially in the elderly. Lowering the number of CVD deaths requires preventive strategies targeted on the elderly. OBJECTIVE: The objective was to generate evidence on the association between WHO dietary recommendations and mortality from CVD, coronary artery disease (CAD), and stroke in the elderly aged ≥60 y. DESIGN: We analyzed data from 10 prospective cohort studies from Europe and the United States comprising a total sample of 281,874 men and women free from chronic diseases at baseline. Components of the Healthy Diet Indicator (HDI) included saturated fatty acids, polyunsaturated fatty acids, mono- and disaccharides, protein, cholesterol, dietary fiber, and fruit and vegetables. Cohort-specific HRs adjusted for sex, education, smoking, physical activity, and energy and alcohol intakes were pooled by using a random-effects model. RESULTS: During 3,322,768 person-years of follow-up, 12,492 people died of CVD. An increase of 10 HDI points (complete adherence to an additional WHO guideline) was, on average, not associated with CVD mortality (HR: 0.94; 95% CI: 0.86, 1.03), CAD mortality (HR: 0.99; 95% CI: 0.85, 1.14), or stroke mortality (HR: 0.95; 95% CI: 0.88, 1.03). However, after stratification of the data by geographic region, adherence to the HDI was associated with reduced CVD mortality in the southern European cohorts (HR: 0.87; 95% CI: 0.79, 0.96; I(2) = 0%) and in the US cohort (HR: 0.85; 95% CI: 0.83, 0.87; I(2) = not applicable). CONCLUSION: Overall, greater adherence to the WHO dietary guidelines was not significantly associated with CVD mortality, but the results varied across regions. Clear inverse associations were observed in elderly populations in southern Europe and the United States.

• Klíčová slova
• CHANCES, aging, cardiovascular disease, cohort, meta-analysis,
• MeSH
• adherence pacienta MeSH
• cholesterol dietní aplikace a dávkování   MeSH
• chronická nemoc MeSH
• dieta normy   MeSH
• dietní proteiny aplikace a dávkování   MeSH
• dietní sacharidy aplikace a dávkování   MeSH
• etnicita MeSH
• hodnocení stavu výživy MeSH
• kardiovaskulární nemoci mortalita   prevence a kontrola   MeSH
• lidé středního věku MeSH
• lidé MeSH
• mastné kyseliny aplikace a dávkování   MeSH
• metaanalýza jako téma MeSH
• nenasycené mastné kyseliny MeSH
• ovoce MeSH
• potravní vláknina aplikace a dávkování   MeSH
• prospektivní studie MeSH
• senioři MeSH
• Světová zdravotnická organizace MeSH
• výživová politika * MeSH
• zelenina MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Extramural MeSH
• Geografické názvy
• Evropa epidemiologie   MeSH
• Spojené státy americké epidemiologie   MeSH
• Názvy látek
• cholesterol dietní MeSH
• dietní proteiny MeSH
• dietní sacharidy MeSH
• mastné kyseliny MeSH
• nenasycené mastné kyseliny MeSH
• potravní vláknina MeSH

To understand the pathogenesis of hypercholesterolemia in Prague hereditary hypercholesterolemic (PHHC) rat, we analyzed the response of hepatic transcriptome to dietary cholesterol in PHHC and control Wistar rats. Male PHHC and Wistar rats were fed chow (C), 5 % fat (palm kernel oil) (CF) or 1 % cholesterol + 5 % fat (CHOL) diet for three weeks. Hepatic transcriptome was analyzed using Affymetrix GeneChip arrays. No differences were found in the effect of both control diets (C and CF) on lipid metabolism and gene expression of 6500 genes. Therefore, these data were pooled for further analysis. Dietary cholesterol induced accumulation of cholesterol and triacylglycerols in the liver in both strains and hypercholesterolemia in PHHC rats. However, there were no differences in response of hepatic transcriptome to CHOL diet. On the other hand, several genes were found to be differently expressed between both strains independently of the diet. Two of those genes, Apof and Aldh1a7, were studied in more detail, and their role in pathogenesis of hypercholesterolemia in PHHC rats could not been corroborated. In conclusion, the hypercholesterolemia in PHHC rats is due to physiological response of hepatic transcriptome to dietary cholesterol in different genetic background.

• MeSH
• cholesterol dietní škodlivé účinky   metabolismus   MeSH
• hypercholesterolemie genetika   metabolismus   MeSH
• játra metabolismus   MeSH
• krysa rodu Rattus MeSH
• molekulární sekvence - údaje MeSH
• potkani Wistar MeSH
• sekvence nukleotidů MeSH
• transkriptom genetika   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• cholesterol dietní MeSH

OBJECTIVES: The aim of this study was to investigate whether rosuvastatin affects expression and activity of rat CYP2C6. This cytochrome P450 is considered to be a counterpart of human CYP2C9, which metabolizes many drugs, including diclofenac, ibuprofen or warfarin. DESIGN: Male hereditary hypertriglyceridemic (HHTg) rats were fed standard laboratory diet (STD) or high cholesterol diet (HCD: STD + 1% of cholesterol w/w + 10% of lard fat w/w) for 21 days. A third group of rats were fed high a cholesterol diet with rosuvastatin added (0.03% w/w). Expression of CYP2C6 was measured in liver samples using real-time PCR (mRNA level) and Western blotting (protein level). Formation of diclofenac metabolites (typical enzyme activity of CYP2C6) was analyzed using HPLC with UV detection. RESULTS: Administration of rosuvastatin to HHTg rats resulted in significantly increased mRNA expression and enzyme activity in HCD-fed animals; changes of CYP2C6 protein were non-significant. These results suggest that CYP2C6 expression and activity are positively affected by rosuvastatin in hereditary hypertriglyceridemic rats after intake of HCD. CONCLUSION: The results presented open the possibility that in humans, rosuvastatin may affect the metabolism of many drugs by influencing expression and activity of CYP2C6 (counterpart of human CYP2C9). Further studies are needed to elucidate the effects of this statin on CYP2C9 in humans.

• MeSH
• aromatické hydroxylasy antagonisté a inhibitory   metabolismus   MeSH
• cholesterol dietní farmakologie   MeSH
• cytochrom P450 CYP2C9 MeSH
• fluorbenzeny farmakologie   MeSH
• genetická transkripce účinky léků   MeSH
• hyperlipoproteinemie typ IV farmakoterapie   genetika   metabolismus   MeSH
• jaterní mikrozomy účinky léků   enzymologie   MeSH
• krysa rodu Rattus MeSH
• lidé MeSH
• messenger RNA metabolismus   MeSH
• mutantní kmeny potkanů MeSH
• potkani Wistar MeSH
• pyrimidiny farmakologie   MeSH
• regulace genové exprese enzymů účinky léků   MeSH
• rodina 2 cytochromů P450 MeSH
• rosuvastatin kalcium MeSH
• statiny farmakologie   MeSH
• steroid-21-hydroxylasa antagonisté a inhibitory   genetika   metabolismus   MeSH
• sulfonamidy farmakologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• lidé MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• aromatické hydroxylasy MeSH
• cholesterol dietní MeSH
• Cyp2c6v1 protein, rat MeSH Prohlížeč
• CYP2C9 protein, human MeSH Prohlížeč
• cytochrom P450 CYP2C9 MeSH
• fluorbenzeny MeSH
• messenger RNA MeSH
• pyrimidiny MeSH
• rodina 2 cytochromů P450 MeSH
• rosuvastatin kalcium MeSH
• statiny MeSH
• steroid-21-hydroxylasa MeSH
• sulfonamidy MeSH

Endoglin (a type III TGF-β receptor) is able to modulate ligand binding and signaling by association with the TGF-β type I receptors (ALK-1 and ALK-5). In this study, we hypothesized whether atorvastatin treatment affects endoglin/ALK-1/p-Smad1/VEGF expression in the aorta and endoglin levels in serum in ApoE/LDLR double knockout mice. ApoE/LDLR double knockout mice were fed with a diet containing either 1% of cholesterol (CHOL) or cholesterol with atorvastatin (ATV) at a dose of 50mg/kg/day. Biochemical analysis of cholesterol levels and ELISA analysis of endoglin levels in serum, lesion area size, immunohistochemistry and Western blot analysis in mice aorta were performed. Atorvastatin treatment resulted in a significant decrease of total, VLDL and LDL cholesterol, atherosclerotic lesion size and endoglin serum levels in comparison with CHOL mice. On the other hand, atorvastatin treatment significantly increased the expressions of endoglin by 1431%, ALK-1 by 310%, p-Smad1 by 135% and VEGF by 62% in aorta when compared to CHOL mice. In conclusion, it has been demonstrated that atorvastatin increases endoglin/ALK-1/p-Smad1/VEGF expression in aorta and decreases the size of atherosclerotic lesions, suggesting that activation of this endothelial-protective pathway might support the antiatherogenic effects of atorvastatin. Moreover, atorvastatin concurrently decreased serum levels of endoglin suggesting that monitoring of endoglin levels in blood might represent an important marker of the progression and/or treatment of atherosclerosis.

• MeSH
• aktivinové receptory typu I metabolismus   MeSH
• aktivinové receptory typu II MeSH
• apolipoproteiny E genetika   MeSH
• aterosklerotický plát chemicky indukované   metabolismus   patologie   prevence a kontrola   MeSH
• ateroskleróza krev   chemicky indukované   metabolismus   patologie   prevence a kontrola   MeSH
• atorvastatin MeSH
• biomarkery farmakologické krev   metabolismus   MeSH
• cholesterol dietní farmakologie   MeSH
• cholesterol krev   MeSH
• endoglin MeSH
• fosforylace účinky léků   MeSH
• HDL-cholesterol krev   MeSH
• intracelulární signální peptidy a proteiny krev   metabolismus   MeSH
• krev účinky léků   MeSH
• kyseliny heptylové farmakologie   terapeutické užití   MeSH
• LDL-cholesterol krev   MeSH
• LDL-receptory genetika   MeSH
• myši inbrední C57BL MeSH
• myši knockoutované MeSH
• myši MeSH
• protein Smad1 metabolismus   MeSH
• pyrroly farmakologie   terapeutické užití   MeSH
• Valsalvův sinus metabolismus   patologie   MeSH
• vaskulární endoteliální růstový faktor A metabolismus   MeSH
• VLDL-cholesterol krev   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• Acvrl1 protein, mouse MeSH Prohlížeč
• aktivinové receptory typu I MeSH
• aktivinové receptory typu II MeSH
• apolipoproteiny E MeSH
• atorvastatin MeSH
• biomarkery farmakologické MeSH
• cholesterol dietní MeSH
• cholesterol MeSH
• endoglin MeSH
• Eng protein, mouse MeSH Prohlížeč
• HDL-cholesterol MeSH
• intracelulární signální peptidy a proteiny MeSH
• kyseliny heptylové MeSH
• LDL-cholesterol MeSH
• LDL-receptory MeSH
• protein Smad1 MeSH
• pyrroly MeSH
• Smad1 protein, mouse MeSH Prohlížeč
• vascular endothelial growth factor A, mouse MeSH Prohlížeč
• vaskulární endoteliální růstový faktor A MeSH
• VLDL-cholesterol MeSH

BACKGROUND: The aim of the study was to evaluate whether cholesterol-rich diet affects transforming growth factor-β-RIII (endoglin) levels in blood and 2 endoglin-related pathways in the aorta of ApoE/LDLR double knockout mice. METHODS AND RESULTS: Mice were fed either chow diet (CHOW) (n=8) or by 1% cholesterol-rich diet (CHOL) (n=8). Biochemical analysis of cholesterol and endoglin levels in blood, lesion size area, immunohistochemistry and Western blot analysis in mice aortas were performed. Biochemical analysis showed that cholesterol-rich diet resulted in a significant increase of cholesterol and endoglin levels in serum, and increased plaque size in the aorta. In addition, a cholesterol-rich diet significantly decreased the expressions of endoglin by 92%, activin receptor-like kinase (ALK)-1 by 71%, p-Smad2 by 21%, and vascular endothelial growth factor (VEGF) by 37% when compared to CHOW mice, but ALK-5, p-Smad1, and endothelial nitric oxide synthase were not significantly affected. CONCLUSIONS: Hypercholesterolemia increases endoglin levels in blood and simultaneously decreases its expression in aorta, together with atherosclerosis protective markers p-Smad2 and VEGF, followed by increased plaque size. Inhibition of endoglin signaling might be one of the mechanisms responsible for the promoting of endothelial dysfunction and atherogenesis. Moreover, the monitoring of endoglin serum levels might represent an attractive blood marker of progression of disease; however, the precise source and role of endoglin in blood serum remains to be elucidated.

• MeSH
• aktivinové receptory typu I metabolismus   MeSH
• aktivinové receptory typu II MeSH
• aktivinové receptory metabolismus   MeSH
• aorta metabolismus   patologie   MeSH
• apolipoproteiny E nedostatek   genetika   metabolismus   MeSH
• aterosklerotický plát metabolismus   patologie   MeSH
• ateroskleróza metabolismus   patologie   MeSH
• biologické markery krev   MeSH
• cholesterol dietní farmakologie   MeSH
• cholesterol krev   MeSH
• endoglin MeSH
• intracelulární signální peptidy a proteiny krev   MeSH
• LDL-receptory nedostatek   genetika   metabolismus   MeSH
• modely nemocí na zvířatech MeSH
• myši knockoutované MeSH
• myši MeSH
• protein Smad1 metabolismus   MeSH
• protein Smad2 metabolismus   MeSH
• protein-serin-threoninkinasy metabolismus   MeSH
• receptory transformujícího růstového faktoru beta metabolismus   MeSH
• signální transdukce účinky léků   fyziologie   MeSH
• synthasa oxidu dusnatého, typ III metabolismus   MeSH
• TGF-beta receptor I. typu MeSH
• vaskulární endoteliální růstový faktor A metabolismus   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• Acvrl1 protein, mouse MeSH Prohlížeč
• aktivinové receptory typu I MeSH
• aktivinové receptory typu II MeSH
• aktivinové receptory MeSH
• apolipoproteiny E MeSH
• biologické markery MeSH
• cholesterol dietní MeSH
• cholesterol MeSH
• endoglin MeSH
• Eng protein, mouse MeSH Prohlížeč
• intracelulární signální peptidy a proteiny MeSH
• LDL-receptory MeSH
• protein Smad1 MeSH
• protein Smad2 MeSH
• protein-serin-threoninkinasy MeSH
• receptory transformujícího růstového faktoru beta MeSH
• Smad1 protein, mouse MeSH Prohlížeč
• Smad2 protein, mouse MeSH Prohlížeč
• synthasa oxidu dusnatého, typ III MeSH
• TGF-beta receptor I. typu MeSH
• Tgfbr1 protein, mouse MeSH Prohlížeč
• vaskulární endoteliální růstový faktor A MeSH

AIM: The aim of our work was to determine the influence of intestinal bacteria on the development of atherosclerotic lesions using apolipoprotein E (ApoE)-deficient knockout mice. METHODS: The experiments were performed on ApoE-/--deficient mouse strain C57BL/6, bred under germ-free (GF) conditions for two generations or under conventional conditions with defined microflora (CV). The mice were fed a standard low cholesterol diet or cholesterol-rich diet for 3-4 months. We studied the development of advanced lesions in the thoracic and abdominal aorta by histological, morphometric and immunohistological methods. RESULTS: Conventionally reared ApoE-/- mice (containing no pathogenic intestinal microbiota) and fed a standard low cholesterol diet in contrast to a high cholesterol diet did not develop atherosclerotic aortic plaques. In contrast, ApoE-/- mice reared under germfree conditions for 2 generations and fed a low cholesterol diet exhibited atherosclerotic plaques in the aorta. Characteristic lipid deposition with foam cells and macrophages was found in their arterial walls. CONCLUSION: In contrast to the absence of atherosclerotic plaques in conventionally reared ApoE-deficient mice, germ-free ApoE-/- mice consuming the same low cholesterol standard diet developed atherosclerotic plaques in the aorta. Differences in atherosclerotic plaques between GF and CV ApoE-/- mice are not so apparent when mice are fed a high cholesterol diet. Our findings thus document the protective effect of microbiota (commensal bacteria) on atherosclerosis development.

• MeSH
• aorta abdominalis metabolismus   patologie   MeSH
• aorta thoracica metabolismus   patologie   MeSH
• apolipoproteiny E fyziologie   MeSH
• ateroskleróza etiologie   metabolismus   prevence a kontrola   MeSH
• cholesterol dietní aplikace a dávkování   MeSH
• cholesterol krev   MeSH
• gnotobiologické modely MeSH
• messenger RNA genetika   MeSH
• metagenom * MeSH
• modely nemocí na zvířatech MeSH
• myši inbrední C57BL MeSH
• myši knockoutované MeSH
• myši MeSH
• polymerázová řetězová reakce s reverzní transkripcí MeSH
• střevní sliznice mikrobiologie   MeSH
• western blotting MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• apolipoproteiny E MeSH
• cholesterol dietní MeSH
• cholesterol MeSH
• messenger RNA MeSH