المؤلفون: Bittencourt, Marcio, Generoso, Giuliano

المصدر: International Journal of Cardiovascular Sciences. December 2019 32(6)

مصطلحات موضوعية: Cardiovascular Diseases/ prevention and control, Lifestyle Physical, Activity, Weight Loss, Diet, Atherogenic, Cholesterol, Dietary

وصف الملف: text/html

الوصول الحر: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S2359-56472019000600635Test

المؤلفون: Norimitsu Ban, Tae Jun Lee, Abdoulaye Sene, Zhenyu Dong, Andrea Santeford, Jonathan B. Lin, Daniel S. Ory, Rajendra S. Apte

المصدر: Journal of Lipid Research, Vol 59, Iss 8, Pp 1414-1423 (2018)

مصطلحات موضوعية: ATP binding cassette transporter G1, cholesterol/dietary, cholesterol/efflux, eye/retina, neurons, aging, Biochemistry, QD415-436

الوصف: Photoreceptors have high intrinsic metabolic demand and are exquisitely sensitive to metabolic perturbation. In addition, they shed a large portion of their outer segment lipid membranes in a circadian manner, increasing the metabolic burden on the outer retina associated with the resynthesis of cell membranes and disposal of the cellular cargo. Here, we demonstrate that deletion of both ABCA1 and ABCG1 in rod photoreceptors leads to age-related accumulation of cholesterol metabolites in the outer retina, photoreceptor dysfunction, degeneration of rod outer segments, and ultimately blindness. A high-fat diet significantly accelerates rod neurodegeneration and vision loss, further highlighting the role of lipid homeostasis in regulating photoreceptor neurodegeneration and vision.

وصف الملف: electronic resource

العلاقة: http://www.sciencedirect.com/science/article/pii/S0022227520330522Test; https://doaj.org/toc/0022-2275Test

الوصول الحر: https://doaj.org/article/f37d5b70129147069a9c4ae9a8dbc85eTest

المؤلفون: Fan Zhang, Junhua Li, Cuihua Chang, Luping Gu, Wen Xiong, Yujie Su, Yanjun Yang

المصدر: Journal of Agricultural and Food Chemistry. 70:14977-14988

مصطلحات موضوعية: Cholesterol, Dietary, Cardiovascular Diseases, Health Status, Humans, General Chemistry, General Agricultural and Biological Sciences

الوصف: The public and scientists remain skeptical about egg consumption, given that cardiovascular diseases (CVDs) are the leading causes of death in worldwide. This review mainly explained the recurrence of contradictory conclusions about relationships between egg consumption and CVD risk and discussed effects of egg cholesterol intake on cholesterol homeostasis. Factors including individual health status and cholesterol sensitivity, dietary pattern, region, and race should be distinguished when understanding generalized conclusions. Identified compensatory mechanisms in response to dietary cholesterol and the resulting balance in cholesterol biosynthesis, absorption, and efflux supported the view that moderate egg consumption had no substantial overall impacts on cholesterol homeostasis in healthy people. Excessive cholesterol intake is not recommended in individuals with distempered metabolism. More than cholesterol metabolism, impacts of egg consumption as a part of overall diet on CVD risk should be considered from aspects of nutrient intake, lipid metabolism, and energy supply in the future.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dfa1d8e461e8465879d29da86423778cTest
https://doi.org/10.1021/acs.jafc.2c04634Test

المؤلفون: Michela Frascoli, Andrea Reboldi, Joonsoo Kang

المصدر: The Journal of Immunology. 209:645-653

مصطلحات موضوعية: Cholesterol, Dietary, Cholesterol, Immunology, Humans, Immunology and Allergy, Obesity, Oxysterols

الوصف: Obesity is considered the primary environmental factor associated with morbidity and severity of wide-ranging inflammatory disorders. The molecular mechanism linking high-fat or cholesterol diet to imbalances in immune responses, beyond the increased production of generic inflammatory factors, is just beginning to emerge. Diet cholesterol by-products are now known to regulate function and migration of diverse immune cell subsets in tissues. The hydroxylated metabolites of cholesterol oxysterols as central regulators of immune cell positioning in lymphoid and mucocutaneous tissues is the focus of this review. Dedicated immunocyte cell surface receptors sense spatially distributed oxysterol tissue depots to tune cell metabolism and function, to achieve the “right place at the right time” axiom of efficient tissue immunity.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e7e2b52c5dcb6e248a68c766078281c4Test
https://doi.org/10.4049/jimmunol.2200273Test

المؤلفون: Allison Y. Louie, Joseph Tingling, Evan Dray, Jamal Hussain, Daniel B. McKim, Kelly S. Swanson, Andrew J. Steelman

المصدر: The Journal of Immunology. 208:2523-2539

مصطلحات موضوعية: Cholesterol, Dietary, Mice, Inbred C57BL, Mice, Orthomyxoviridae Infections, Influenza A virus, Immunology, Animals, Cytokines, Immunology and Allergy, CD8-Positive T-Lymphocytes, Morbidity, Lung

الوصف: Influenza is a common cause of pneumonia-induced hospitalization and death, but how host factors function to influence disease susceptibility or severity has not been fully elucidated. Cellular cholesterol levels may affect the pathogenesis of influenza infection, as cholesterol is crucial for viral entry and replication, as well as immune cell proliferation and function. However, there is still conflicting evidence on the extent to which dietary cholesterol influences cholesterol metabolism. In this study, we examined the effects of a high-cholesterol diet in modulating the immune response to influenza A virus (IAV) infection in mice. Mice were fed a standard or a high-cholesterol diet for 5 wk before inoculation with mouse-adapted human IAV (Puerto Rico/8/1934), and tissues were collected at days 0, 4, 8, and 16 postinfection. Cholesterol-fed mice exhibited dyslipidemia characterized by increased levels of total serum cholesterol prior to infection and decreased triglycerides postinfection. Cholesterol-fed mice also displayed increased morbidity compared with control-fed mice, which was neither a result of immunosuppression nor changes in viral load. Instead, transcriptomic analysis of the lungs revealed that dietary cholesterol caused upregulation of genes involved in viral-response pathways and leukocyte trafficking, which coincided with increased numbers of cytokine-producing CD4+ and CD8+ T cells and infiltrating dendritic cells. Morbidity as determined by percent weight loss was highly correlated with numbers of cytokine-producing CD4+ and CD8+ T cells as well as granulocytes. Taken together, dietary cholesterol promoted IAV morbidity via exaggerated cellular immune responses that were independent of viral load.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::27423b806a9f8aa272c91d78c02c55f9Test
https://doi.org/10.4049/jimmunol.2100927Test

المؤلفون: Bin Zhao, Lu Gan, Barry I. Graubard, Satu Männistö, Demetrius Albanes, Jiaqi Huang

المصدر: Circulation

مصطلحات موضوعية: Cholesterol, Dietary, Male, Cholesterol, Cardiovascular Diseases, Risk Factors, Cause of Death, Eggs, Physiology (medical), Humans, Prospective Studies, Cardiology and Cardiovascular Medicine, Article, Diet

الوصف: Background: Despite substantial research highlighting the importance of exogenous dietary cholesterol intake and endogenous serum cholesterol level in human health, a thorough evaluation of the associations is lacking. Our study objective was to examine overall and cause-specific mortality in relation to dietary and serum cholesterol, as well as egg consumption, and conduct an updated meta-regression analysis of cohort studies. Methods: We conducted a prospective analysis of 27 078 men in the ATBC Study (Alpha-Tocopherol, Beta-Carotene Cancer Prevention). Multivariable-controlled cause-specific Cox proportional hazards regression models were used to calculate hazard ratios and 31-year absolute mortality risk differences. A systematic review and meta-analysis of cohort studies was also performed (PROSPERO [URL: https://www.crd.york.ac.uk/prosperoTest/ ; Unique identifier: CRD42021272756]). Results: Based on 482 316 person-years of follow-up, we identified 22 035 deaths, including 9110 deaths from cardiovascular disease (CVD). Greater dietary cholesterol and egg consumption were associated with increased risk of overall and CVD-related mortality. Hazard ratios for each additional 300 mg cholesterol intake per day were 1.10 and 1.13 for overall and CVD-related mortality, respectively; for each additional 50-g egg consumed daily, hazard ratios were 1.06 and 1.09, respectively, for overall and CVD-related mortality (all P valuesP 2 =80.1%). In the subgroup analysis of geographic regions ( P interaction =0.02), an increase of 50-g egg consumed daily was associated with a higher risk of CVD in US cohorts (pooled relative risk, 1.08 [95% CI, 1.02–1.14]) and appeared related to a higher CVD risk in European cohorts with borderline significance (pooled relative risk, 1.05), but was not associated with CVD risk in Asian cohorts. Conclusions: In this prospective cohort study and updated meta-analysis, greater dietary cholesterol and egg consumption were associated with increased risk of overall and CVD-related mortality. Our findings support restricted consumption of dietary cholesterol as a means to improve long-term health and longevity.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::72abe532f4937e7b92f966a87ab4cd9eTest
https://doi.org/10.1161/circulationaha.121.057642Test

المؤلفون: Geoffrey C. Farrell, Amilcar Morales, George N. Ioannou, Christopher E. Savard, Christian L. Horn

المصدر: Hepatology Communications, Vol 6, Iss 1, Pp 12-35 (2022)
Hepatology Communications

مصطلحات موضوعية: medicine.medical_specialty, Statin, medicine.drug_class, Review, RC799-869, digestive system, Cholesterol, Dietary, Ezetimibe, Non-alcoholic Fatty Liver Disease, Risk Factors, Fibrosis, Internal medicine, Nonalcoholic fatty liver disease, medicine, Animals, Homeostasis, Humans, Hepatology, business.industry, Anticholesteremic Agents, nutritional and metabolic diseases, Diseases of the digestive system. Gastroenterology, medicine.disease, digestive system diseases, Fatty Liver, Cholesterol, Endocrinology, Lipotoxicity, Hepatic stellate cell, lipids (amino acids, peptides, and proteins), Hydroxymethylglutaryl-CoA Reductase Inhibitors, Steatohepatitis, Hepatic fibrosis, business, medicine.drug

الوصف: The rising prevalence of nonalcoholic fatty liver disease (NAFLD) and NAFLD‐related cirrhosis in the United States and globally highlights the need to better understand the mechanisms causing progression of hepatic steatosis to fibrosing steatohepatitis and cirrhosis in a small proportion of patients with NAFLD. Accumulating evidence suggests that lipotoxicity mediated by hepatic free cholesterol (FC) overload is a mechanistic driver for necroinflammation and fibrosis, characteristic of nonalcoholic steatohepatitis (NASH), in many animal models and also in some patients with NASH. Diet, lifestyle, obesity, key genetic polymorphisms, and hyperinsulinemia secondary to insulin resistance are pivotal drivers leading to aberrant cholesterol signaling, which leads to accumulation of FC within hepatocytes. FC overload in hepatocytes can lead to ER stress, mitochondrial dysfunction, development of toxic oxysterols, and cholesterol crystallization in lipid droplets, which in turn lead to hepatocyte apoptosis, necrosis, or pyroptosis. Activation of Kupffer cells and hepatic stellate cells by hepatocyte signaling and cholesterol loading contributes to this inflammation and leads to hepatic fibrosis. Cholesterol accumulation in hepatocytes can be readily prevented or reversed by statins. Observational studies suggest that use of statins in NASH not only decreases the substantially increased cardiovascular risk, but may ameliorate liver pathology. Conclusion: Hepatic FC loading may result in cholesterol‐associated steatohepatitis and play an important role in the development and progression of NASH. Statins appear to provide significant benefit in preventing progression to NASH and NASH‐cirrhosis. Randomized controlled trials are needed to demonstrate whether statins or statin/ezetimibe combination can effectively reverse steatohepatitis and liver fibrosis in patients with NASH.
Free cholesterol accumulates in the liver in some patients with NAFLF and promotes the necroinflammation and fibrosis typical of NASH. Cholesterol‐associated steatohepatitis (CASH) plays an important role in the development and progression of NASH. Randomized controlled trials are needed to demonstrate whether statins or statin/ezetimibe combination can effectively reverse steatohepatitis and liver fibrosis in patients with NASH.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::686feba9ac6a8bba91002d73e5303d5aTest
https://doaj.org/article/4f097a96f8524768bc96ff42f332dc82Test

المؤلفون: Yan Liu, Xuan Yang, Fan Xiao, Fan Jie, Qinjun Zhang, Yuqi Liu, Hang Xiao, Baiyi Lu

المصدر: Comprehensive Reviews in Food Science and Food Safety. 21:738-779

مصطلحات موضوعية: Cholesterol, Dietary, Cholesterol, Food Handling, Phytochemicals, Humans, Oxidation-Reduction, Food Science

الوصف: Dietary cholesterol oxidation products (COPs) are heterogeneous compounds formed during the processing and storage of cholesterol-rich foods, such as seafood, meat, eggs, and dairy products. With the increased intake of COPs-rich foods, the concern about health implications of dietary COPs is rising. Dietary COPs may exert deleterious effects on human health to induce several inflammatory diseases including atherosclerosis, neurodegenerative diseases, and inflammatory bowel diseases. Thus, knowledge regarding the effects of processing and storage conditions leading to formation of COPs is needed to reduce the levels of COPs in foods. Efficient methodologies to determine COPs in foods are also essential. More importantly, the biological roles of dietary COPs in human health and effects of phytochemicals on dietary COPs-induced diseases need to be established. This review summarizes the recent information on dietary COPs including their formation in foods during their processing and storage, analytical methods of determination of COPs, metabolic fate, implications for human health, and beneficial interventions by phytochemicals. The formation of COPs is largely dependent on the heating temperature, storage time, and food matrices. Alteration of food processing and storage conditions is one of the potent strategies to restrict hazardous dietary COPs from forming, including maintaining relatively low temperatures, shorter processing or storage time, and the appropriate addition of antioxidants. Once absorbed into the circulation, dietary COPs can contribute to the progression of several inflammatory diseases, where the absorbed dietary COPs may induce inflammation, apoptosis, and autophagy in cells in the target organs or tissues. Improved intake of phytochemicals may be an effective strategy to reduce the hazardous effects of dietary COPs.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f93b8d838ff62d4e5ef81c91376d12d6Test
https://doi.org/10.1111/1541-4337.12880Test

المؤلفون: Marc K. Hellerstein, Edna Nyangau, Rachael Kim, Julia Han, Hussein Mohammed, Mohamad Dandan, Sabrina A Mann

المصدر: Arteriosclerosis, Thrombosis, and Vascular Biology. 41:2866-2876

مصطلحات موضوعية: Male, medicine.medical_specialty, Cholesterol, Dietary, Tandem Mass Spectrometry, Internal medicine, medicine, Animals, Homeostasis, RNA, Messenger, Receptor, Chemistry, PCSK9, Subtilisin, Protein turnover, Cholesterol, LDL, Proprotein convertase, Mice, Inbred C57BL, Endocrinology, Liver, Models, Animal, LDL receptor, Kexin, lipids (amino acids, peptides, and proteins), Proprotein Convertase 9, Cardiology and Cardiovascular Medicine, Low Density Lipoprotein Receptor-Related Protein-1, Chromatography, Liquid, Lipoprotein

الوصف: Objective: We measured the turnover rates of the LDLR (low-density lipoprotein receptor) and PCSK9 (proprotein convertase subtilisin/kexin type 9) in mice by metabolic labeling with heavy water and mass spectrometry. Approach and Results: In liver of mice fed high-cholesterol diets, LDLR mRNA levels and synthesis rates were markedly lower with complete suppression of cholesterol synthesis and higher cholesterol content, consistent with the Brown-Goldstein model of tissue cholesterol homeostasis. We observed markedly lower PCSK9 mRNA levels and synthesis rates in liver and lower concentrations and synthesis rates in plasma. Hepatic LDLR half-life (t½) was prolonged, consistent with an effect of reduced PCSK9, and resulted in no reduction in hepatic LDLR content despite reduced mRNA levels and LDLR synthesis rates. These changes in PCSK9 synthesis complement and expand the well-established model of tissue cholesterol homeostasis in mouse liver, in that reduced synthesis and levels of PCSK9 counterbalance lower LDLR synthesis by promoting less LDLR catabolism, thereby maintaining uptake of LDL cholesterol into liver despite high intracellular cholesterol concentrations. Conclusions: Lower hepatic synthesis and secretion of PCSK9, an SREBP2 (sterol response element binding protein) target gene, results in longer hepatic LDLR t½ in response to cholesterol feeding in mice in the face of high intracellular cholesterol content. PCSK9 modulation opposes the canonical lowering of LDLR mRNA and synthesis by cholesterol surplus and preserves LDLR levels. The physiological and therapeutic implications of these opposing control mechanisms over liver LDLR are of interest and may reflect subservience of hepatic cholesterol homeostasis to whole body cholesterol needs.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::864d6b6dad1002240dc03b771a1d0929Test
https://doi.org/10.1161/atvbaha.121.316764Test

المؤلفون: Kevin C. Maki, Mary R. Dicklin

المصدر: Journal of the American College of Cardiology. 81(1)

مصطلحات موضوعية: Cholesterol, Dietary, Lipoproteins, LDL, Dietary Supplements, Hypercholesterolemia, Cholesterol, HDL, Humans, Cholesterol, LDL, Cardiology and Cardiovascular Medicine

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0358e2210326a56abaff45cc38e05767Test
https://pubmed.ncbi.nlm.nih.gov/36599607Test