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41 results on '"Mymin, David"'

1. Progress and perspectives in plant sterol and plant stanol research.

Author

Jones, Peter JH, Shamloo, Maryam, MacKay, Dylan S, Rideout, Todd C, Myrie, Semone B, Plat, Jogchum, Roullet, Jean-Baptiste, Baer, David J, Calkins, Kara L, Davis, Harry R, Barton Duell, P, Ginsberg, Henry, Gylling, Helena, Jenkins, David, Lütjohann, Dieter, Moghadasian, Mohammad, Moreau, Robert A, Mymin, David, Ostlund, Richard E, Ras, Rouyanne T, Ochoa Reparaz, Javier, Trautwein, Elke A, Turley, Stephen, Vanmierlo, Tim, and Weingärtner, Oliver

Subjects
Cardiovascular, Complementary and Integrative Health, Nutrition, Good Health and Well Being, Anticholesteremic Agents, Canada, Cardiovascular Diseases, Cholesterol, Cholesterol, LDL, Congresses as Topic, Diet, Humans, Hypercholesterolemia, Intestinal Diseases, Lipid Metabolism, Inborn Errors, Phytosterols, cholesterol, nutrition, plant sterols, plant stanols, sitosterolemia, Medical and Health Sciences, Psychology and Cognitive Sciences, Nutrition & Dietetics
Abstract

Current evidence indicates that foods with added plant sterols or stanols can lower serum levels of low-density lipoprotein cholesterol. This review summarizes the recent findings and deliberations of 31 experts in the field who participated in a scientific meeting in Winnipeg, Canada, on the health effects of plant sterols and stanols. Participants discussed issues including, but not limited to, the health benefits of plant sterols and stanols beyond cholesterol lowering, the role of plant sterols and stanols as adjuncts to diet and drugs, and the challenges involved in measuring plant sterols and stanols in biological samples. Variations in interindividual responses to plant sterols and stanols, as well as the personalization of lipid-lowering therapies, were addressed. Finally, the clinical aspects and treatment of sitosterolemia were reviewed. Although plant sterols and stanols continue to offer an efficacious and convenient dietary approach to cholesterol management, long-term clinical trials investigating the endpoints of cardiovascular disease are still lacking.

Published
2018

9. Hyperhomocysteinemia induces hepatic cholesterol biosynthesis and lipid accumulation via activation of transcription factors

Author

Woo, Connie W.H., Siow, Yaw L., Pierce, Grant N., Choy, Patrick C., Minuk, Gerald Y., Mymin, David, and O., Karmin

Subjects
Cholesterol -- Health aspects, Cardiovascular diseases -- Care and treatment, Cyclic adenylic acid -- Research, Protein kinases -- Research, Biological sciences
Abstract

Hyperhomocysteinemia is an independent risk factor for cardiovascular disorders. Elevated plasma homocysteine (Hcy) concentration is associated with other cardiovascular risk factors. We previously reported that Hcy stimulated cholesterol biosynthesis in HepG2 cells. In the present study, we investigated the underlying mechanisms of Hcy-induced hepatic cholesterol biosynthesis in an animal model. Hyperhomocysteinemia was induced in Sprague-Dawley rats by feeding a high-methionine diet for 4 wk. The mRNA expression and the enzyme activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase were significantly increased in livers of hyperhomocysteinemic rats. There were marked hepatic lipid accumulation and an elevation of plasma cholesterol concentration in hyperhomocysteinemic rats. Three transcription factors, namely, sterol regulatory element-binding protein-2 (SREBP-2), cAMP response element-binding protein (CREBL and nuclear factor Y (NF-Y) were activated in livers of hyperhomocysteinemic rats. Upon Hey treatment of hepatocytes, there was a significant increase in HMG-CoA reductase mRNA expression in these cells. The activation of SREBP-2, CREB, and NF-Y preceded the increase in HMG-CoA reductase expression in Hcy-treated cells. Pretreatment of hepatocytes with inhibitors for transcription factors not only blocked the activation of SREBP-2, CREB, and NF-Y but also attenuated Hey-induced HMG-CoA reductase mRNA expression. These results suggested that hyperhomocysteinemia-induced activation of SREBP-2, CREB, and NF-Y was responsible for increased cholesterol biosynthesis by transcriptionally regulating HMG-CoA reductase expression in the liver leading to hepatic lipid accumulation and subsequently hypercholesterolemia. In conclusion, the stimulatory effect of Hcy on hepatic cholesterol biosynthesis may represent an important mechanism for hepatic lipid accumulation and cardiovascular disorder associated with hyperhomocysteinemia. homocysteine; 3-hydroxy-3-methylglutaryl coenzyme A reductase; cAMP response element-binding protein; sterol regulatory element-binding protein-2; nuclear factor Y

Published
2005

27. Hyperhomocy steinemia induces hepatic cholesterol bio synthesis and lipid accumulation via activation of transcription factors.

Author

Woo, Connie W. H., Siow, Yaw L., Pierce, Grant N., Choy, Patrick C., Minuk, Gerald Y., Mymin, David, and O, Karmin

Subjects
HOMOCYSTEINE, SULFUR amino acids, LIPIDS, CARDIOVASCULAR diseases, ISOPENTENOIDS
Abstract

Hyperhomocysteinemia is an independent risk factor for cardiovascular disorders. Elevated plasma homocysteine (Hey) concentration is associated with other cardiovascular risk factors. We previously reported that Hcy stimulated cholesterol biosynthesis in HepG2 cells. In the present study, we investigated the underlying mechanisms of Hcy-induced hepatic cholesterol biosynthesis in an animal model. Hyperhomocys- teinemia was induced in Sprague-Dawley rats by feeding a high- methionine diet for 4 wk. The mRNA expression and the enzyme activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase were significantly increased in livers of hyperhomocysteinemic rats. There were marked hepatic lipid accumulation and an elevation of plasma cholesterol concentration in hyperhomocysteinemic rats. Three transcription factors, namely, sterol regulatory element-binding protein-2 (SREBP-2), cAMP response element-binding protein (CREB), and nuclear factor Y (NF-Y) were activated in livers of hyperhomocysteinemic rats. Upon Hcy treatment of hepatocytes, there was a significant increase in HMG-CoA reductase mRNA expression in these cells. The activation of SREBP-2, CREB, and NF-Y preceded the increase in HMG-CoA reductase expression in Hey-treated cells. Pretreatment of hepatocytes with inhibitors for transcription factors not only blocked the activation of SREBP-2, CREB, and NF-Y but also attenuated Hcy-induced HMG-CoA reductase mRNA expression. These results suggested that hyperhomocys- teinemia-induced activation of SREBP-2, CREB, and NF-Y was responsible for increased cholesterol biosynthesis by transcriptionally regulating HMG-CoA reductase expression in. the liver leading to hepatic lipid accumulation and subsequently hypercholesterolemia. In conclusion, the stimulatory effect of Hcy on hepatic cholesterol biosynthesis may represent an important mechanism for hepatic lipid accumulation and cardiovascular disorder associated with hyperhomocysteinemia. [ABSTRACT FROM AUTHOR]

Published
2005
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36. Moderate Exercise and High-Density Lipoprotein-Cholesterol: Observations During a Cardiac Rehabilitation Program

Author

Streja, Dan and Mymin, David

Abstract

The effects of a 13-week moderate exercise program on fasting plasma insulin, lipids, and lipoprotein cholesterol concentrations were studied in 32 sedentary, middle-aged men with coronary artery disease. The preponderant component of the exercise program was walking or slow jogging. There was no significant change in the systolic blood pressure and pulse rate product response to a standard exercise load. The high-density lipoprotein-cholesterol (HDL-C) level increased, and the fasting plasma insulin concentration decreased. There were no significant changes in plasma triglycerides or low-density lipoprotein cholesterol levels. In sedentary subjects with coronary artery disease, a modest increase in activity can result in an increase in the HDL-C level and a decrease in the plasma insulin concentration. These changes occurred in the absence of variations in diet, smoking habits, adiposity, or plasma triglyceride concentrations and did not require a cardiovascular training effect.(JAMA 242:2190-2192, 1979)

Published
1979
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37. Second Look at Coronary Angiography: The Evolution of Coronary Artery Disease

Author

Mark, Richard J., Lansdown, Edward L., Mymin, David, and Jackson, Donald

Abstract

Twenty-eight patients who had two or more coronary angiograms with no intervening surgical procedure were studied in order to evaluate natural progression of coronary artery disease. Various clinical and laboratory data were examined to determine if any of these factors would be helpful in predicting which patients would have an accelerated progression in their coronary lesions. In the criteria studied, no correlation was found. However, we found that progression can occur in as short an interval as five weeks, and that it does not always correlate with symptoms.

Published
1973
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40. Progress and perspectives in plant sterol and plant stanol research

Author

Rouyanne T. Ras, P. Barton Duell, Semone B. Myrie, Jean Baptiste Roullet, Robert A. Moreau, Peter B. Jones, Jogchum Plat, David Mymin, Stephen D. Turley, Richard E. Ostlund, David J. Baer, Elke A. Trautwein, Oliver Weingärtner, Kara L. Calkins, Helena Gylling, Javier Ochoa Reparaz, Dieter Lütjohann, Henry N. Ginsberg, Mohammad Moghadasian, Todd C Rideout, Tim Vanmierlo, Harry R. Davis, David J.A. Jenkins, Dylan S. MacKay, Maryam Shamloo, Jones, Peter J. H., Shamloo, Maryam, MacKay, Dylan S., Rideout, Todd C., Myrie, Semone B., Plat, Jogchum, Roullet, Jean-Baptiste, Baer, David J., Calkins, Kara L., Davis, Harry R., Duell, P. Barton, Ginsberg, Henry, Gylling, Helena, Jenkins, David, Luetjohann, Dieter, Moghadasian, Mohammad, Moreau, Robert A., Mymin, David, Ostlund, Richard E., Jr., Ras, Rouyanne T., Reparaz, Javier Ochoa, Trautwein, Elke A., Turley, Stephen, VANMIERLO, Tim, and Weingaetner, Oliver

Subjects
0301 basic medicine, Medicine (miscellaneous), Blood lipids, 030204 cardiovascular system & hematology, LDL-CHOLESTEROL, Cardiovascular, Medical and Health Sciences, plant sterols, 0302 clinical medicine, Medicine, Cholesterol management, Lipoprotein cholesterol, Nutrition and Dietetics, biology, Traditional medicine, NON-CHOLESTEROL STEROLS, Inborn Errors, Anticholesteremic Agents, Phytosterols, food and beverages, Lead Article, Plant sterol, HMG-COA REDUCTASE, nutrition, Cardiovascular Diseases, HMG-CoA reductase, SERUM-LIPIDS, lipids (amino acids, peptides, and proteins), Sitosterolemia, plant stanols, Canada, Hypercholesterolemia, ENDOTHELIAL FUNCTION, sitosterolemia, Lipid Metabolism, Inborn Errors, LDL, 03 medical and health sciences, Complementary and Integrative Health, Humans, CORONARY-HEART-DISEASE, Nutrition & Dietetics, business.industry, BLOOD-BRAIN-BARRIER, Psychology and Cognitive Sciences, fungi, CENTRAL-NERVOUS-SYSTEM, cholesterol, Cholesterol, LDL, Congresses as Topic, Lipid Metabolism, medicine.disease, Diet, Intestinal Diseases, HIGH-RISK, Good Health and Well Being, 030104 developmental biology, Plant stanol ester, biology.protein, business, VASCULAR FUNCTION, Plant sterols
Abstract

Current evidence indicates that foods with added plant sterols or stanols can lower serum levels of low-density lipoprotein cholesterol. This review summarizes the recent findings and deliberations of 31 experts in the field who participated in a scientific meeting in Winnipeg, Canada, on the health effects of plant sterols and stanols. Participants discussed issues including, but not limited to, the health benefits of plant sterols and stanols beyond cholesterol lowering, the role of plant sterols and stanols as adjuncts to diet and drugs, and the challenges involved in measuring plant sterols and stanols in biological samples. Variations in interindividual responses to plant sterols and stanols, as well as the personalization of lipid-lowering therapies, were addressed. Finally, the clinical aspects and treatment of sitosterolemia were reviewed. Although plant sterols and stanols continue to offer an efficacious and convenient dietary approach to cholesterol management, long-term clinical trials investigating the endpoints of cardiovascular disease are still lacking. International Plant Sterol and Stanol Association (IPSSA); National Center for Complementary and Integrative Health (NCCIH); National Center for Advancing Translational Sciences [IR13AT009270-01]

Published
2018

41. Sitosterolemia

Author

Myrie SB, Steiner RD, Mymin D, Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJH, Gripp KW, Mirzaa GM, and Amemiya A

Abstract

Clinical Characteristics: Sitosterolemia is characterized by: Hypercholesterolemia (especially in children) which (1) shows an unexpected significant lowering of plasma cholesterol level in response to low-fat diet modification or to bile acid sequestrant therapy; or (2) does not respond to statin therapy; Tendon xanthomas or tuberous (i.e., planar) xanthomas that can occur in childhood and in unusual locations (heels, knees, elbows, and buttocks); Premature atherosclerosis, which can lead to angina, aortic valve involvement, myocardial infarction, and sudden death; Hemolytic anemia, abnormally shaped erythrocytes (stomatocytes), and large platelets (macrothrombocytopenia). On occasion, the abnormal hematologic findings may be the initial presentation or the only clinical feature of this disorder. Arthritis, arthralgias, and splenomegaly may sometimes be seen and one study has concluded that "idiopathic" liver disease could be undiagnosed sitosterolemia. The clinical spectrum of sitosterolemia is probably not fully appreciated due to underdiagnosis and the fact that the phenotype in infants is likely to be highly dependent on diet., Diagnosis/testing: In an individual with sitosterolemia, increased plasma concentrations of plant sterols (especially sitosterol, campesterol, and stigmasterol) are observed – if the diet includes plant-derived food, which contain plant sterols – once the plant sterols have accumulated in the body. The diagnosis of sitosterolemia is established in a proband with greatly increased plant sterol concentrations in plasma and/or by identification of biallelic pathogenic variants in ABCG5 and/or ABCG8 ., Management: Treatment of manifestations: Treatment should begin at the time of diagnosis, though there is little experience treating children younger than age two years. Treatment can decrease plasma concentrations of cholesterol and sitosterol by 10% to 50%. Often existing xanthomas regress. Treatment recommendations include a diet low in shellfish sterols and plant sterols (vegetable oils, margarine, nuts, seeds, avocados, and chocolate) and use of the sterol absorption inhibitor, ezetimibe. In those with an incomplete response to ezetimibe, use of a bile acid sequestrant such as cholestryramine may be considered. Partial ileal bypass surgery may be considered as a last resort for those with poor response to maximal therapies. If arthritis, arthralgias, anemia, thrombocytopenia, and/or splenomegaly require treatment, the first step is management of the sitosterolemia, followed by routine symptomatic management. Surveillance: Begin monitoring at the time of diagnosis on an annual basis: plasma concentrations of plant sterols (primarily beta-sitosterol and campesterol) and cholesterol; the size, number, and distribution of xanthomas; and CBC and platelet count, and liver transaminases (for elevation). In persons with long-standing untreated sitosterolemia, noninvasive imaging is used to exclude coronary and carotid plaque as well as valvular atherosclerotic manifestations. Agents/circumstances to avoid: Margarines and other products containing stanols (e.g., campestanol and sitostanol) that are recommended for use by persons with hypercholesterolemia are contraindicated as they can exacerbate plant stanol accumulation. Evaluation of relatives at risk: Early diagnosis of at-risk relatives either through measurement of plasma concentrations of plant sterols or through molecular genetic testing (if the family-specific pathogenic variants are known) allows early institution of treatment and surveillance to optimize outcome. Pregnancy management: There are no adequate and well-controlled studies of ezetimibe in pregnant women; ezetimibe can be used during pregnancy only if the potential benefits justifiy the risk to the fetus. Since no studies have been published on the fetal effects of ezetimibe, it should be used with caution during pregnancy., Genetic Counseling: Sitosterolemia is inherited in an autosomal recessive manner. At conception, each sib of an affected individual has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier. Heterozygotes (carriers) are asymptomatic but may occasionally have a mildly elevated concentration of sitosterol. Once the sitosterolemia-causing pathogenic variants have been identified in an affected family member, carrier testing for at-risk family members, prenatal testing for pregnancies at increased risk, and preimplantation genetic testing are possible., (Copyright © 1993-2021, University of Washington, Seattle. GeneReviews is a registered trademark of the University of Washington, Seattle. All rights reserved.)

Published
1993

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