Research Topics
Species | H VlassaraSummaryAffiliation: Mount Sinai School of Medicine Country: USA Publications
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Publications
Diet-derived advanced glycation end products are major contributors to the body's AGE pool and induce inflammation in healthy subjectsJaime Uribarri
Division of Nephrology, Deparment of Medicine, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA
Ann N Y Acad Sci 1043:461-6. 2005..Together with previous evidence from diabetics and renal failure patients, these data suggest that dietary AGEs may play an important role in the causation of chronic diseases associated with underlying inflammation...
Oral glycotoxins determine the effects of calorie restriction on oxidant stress, age-related diseases, and lifespanWeijing Cai
Department of Geriatrics, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA
Am J Pathol 173:327-36. 2008..Therefore, the beneficial effects of a CR diet may be partly related to reduced oxidant intake, a principal determinant of oxidant status in aging mice, rather than decreased energy intake...
Managing chronic inflammation in the aging diabetic patient with CKD by diet or sevelamer carbonate: a modern paradigm shiftH Vlassara
Division of Experimental Diabetes and Aging, Department of Geriatrics and Palliative Care, Mount Sinai School of Medicine, 1 Gustave Levy Place, NY 10029, USA
J Gerontol A Biol Sci Med Sci 67:1410-6. 2012..If larger and longer studies confirm the hypothesis that one or both of these interventions reduce progression of CKD, it could represent a new paradigm in the management of complications in the type 2 diabetes patient with CKD...- The role of advanced glycation end products in the development of atherosclerosisMelpomeni Peppa
Division of Experimental Diabetes and Aging, The Mount Sinai School of Medicine, One Gustave Levy Place, Box 1640, New York, NY 10029, USA
Curr Diab Rep 4:31-6. 2004..An increased understanding of the mechanisms of formation and interaction of AGEs has allowed the development of several potential anti-AGE approaches... - Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathyHelen Vlassara
Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
Proc Natl Acad Sci U S A 99:15596-601. 2002..05). Thus in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury. Restriction of dietary AGEs suppresses these effects... - Glycoxidation and diabetic complications: modern lessons and a warning?Helen Vlassara
Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY, USA
Rev Endocr Metab Disord 5:181-8. 2004 - Glycotoxins in the diet promote diabetes and diabetic complicationsHelen Vlassara
Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, Box 1640, One Gustave Levy Place, New York, NY 10029, USA
Curr Diab Rep 7:235-41. 2007..This beneficial outcome requires only a 50% decrease in dietary AGEs, making this necessary intervention practical and inexpensive... - Glycoxidation: the menace of diabetes and agingHelen Vlassara
Division of Experimental Diabetes and Aging, Box 1640, Mount Sinai School of Medicine, One East 100th Street, New York, NY 10029, USA
Mt Sinai J Med 70:232-41. 2003..AGE toxicity may be averted by promising dietary and pharmacological strategies which are currently being investigated... - Advanced glycation end product homeostasis: exogenous oxidants and innate defensesHelen Vlassara
Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
Ann N Y Acad Sci 1126:46-52. 2008..In both humans and mice, there was an inverse correlation between the AGER1 to RAGE ratio and the levels of OS... - Protection against loss of innate defenses in adulthood by low advanced glycation end products (AGE) intake: role of the antiinflammatory AGE receptor-1Helen Vlassara
Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, New York 10029, USA
J Clin Endocrinol Metab 94:4483-91. 2009..Whereas AGE receptor-1 (AGER1) reduces OS/infl in animals, this has not been assessed in normal humans... - Diabetes and advanced glycation endproductsH Vlassara
Department of Geriatrics, Mount Sinai School of Medicine, NY 10029, USA
J Intern Med 251:87-101. 2002..The final disposal of AGE depends on renal clearance. Promising pharmacologic strategies to prevent AGE formation, reduce AGE toxicity, and/or inactivate AGE are under investigation... - Identifying advanced glycation end products as a major source of oxidants in aging: implications for the management and/or prevention of reduced renal function in elderly personsHelen Vlassara
Division of Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
Semin Nephrol 29:594-603. 2009..These data suggest that the changes in renal function in normal aging may be subject to control and this subject deserves renewed attention... - The AGE-receptor in the pathogenesis of diabetic complicationsH Vlassara
Mount Sinai School of Medicine, New York, NY 10029, USA
Diabetes Metab Res Rev 17:436-43. 2001..Various AGE-binding peptides or soluble receptors have emerged as potential sequestering agents for toxic AGEs as potential therapies for diabetic complications... - Advanced glycation in health and disease: role of the modern environmentHelen Vlassara
Mount Sinai School of Medicine, Box 1640, One Gustave Levy Place, New York, NY 10029, USA
Ann N Y Acad Sci 1043:452-60. 2005.... - Insulin resistance and type 2 diabetes in high-fat-fed mice are linked to high glycotoxin intakeOana Sandu
The Brookdale Department of Geriatrics, Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, One Gustave Levy Place, Box 1640, New York, NY 10029, USA
Diabetes 54:2314-9. 2005..05). These results demonstrate that the development of insulin resistance and type 2 diabetes during prolonged high-fat feeding are linked to the excess AGEs/advanced lipoxidation end products inherent in fatty diets... - Advanced glycoxidation end products in commonly consumed foodsTeresia Goldberg
Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
J Am Diet Assoc 104:1287-91. 2004..CONCLUSIONS: The results indicate that diet can be a significant environmental source of AGEs, which may constitute a chronic risk factor for cardiovascular and kidney damage... - Reduced oxidant stress and extended lifespan in mice exposed to a low glycotoxin diet: association with increased AGER1 expressionWeijing Cai
Mount Sinai School of Medicine, Box 1640, One Gustave Levy Place, New York, NY 10029, USA
Am J Pathol 170:1893-902. 2007..A reduced AGE diet preserved these innate defenses, resulting in decreased tissue damage and a longer lifespan in mice... - Circulating glycotoxins and dietary advanced glycation endproducts: two links to inflammatory response, oxidative stress, and agingJaime Uribarri
Division of Nephrology, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
J Gerontol A Biol Sci Med Sci 62:427-33. 2007..AGEs are readily derived from heat-treated foods. We propose that the excess consumption of certain AGEs via the diet enhances OS and inflammatory responses in healthy adults, especially in elderly persons... - Glycoxidation and inflammation in renal failure patientsMelpomeni Peppa
Department of Geriatrics, Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, NY 10029, USA
Am J Kidney Dis 43:690-5. 2004..This finding opens the possibility for using anti-AGE strategies in the prevention and treatment of CVD in patients with chronic renal failure... - Advanced glycation end product receptor-1 transgenic mice are resistant to inflammation, oxidative stress, and post-injury intimal hyperplasiaMassimo Torreggiani
Division of Experimental Diabetes and Aging, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
Am J Pathol 175:1722-32. 2009.... - High levels of dietary advanced glycation end products transform low-density lipoprotein into a potent redox-sensitive mitogen-activated protein kinase stimulant in diabetic patientsWeijing Cai
Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA
Circulation 110:285-91. 2004..CONCLUSIONS: Exposure to daily dietary glycoxidants enhances LDL-induced vascular toxicity via redox-sensitive mitogen-activated protein kinase activation. This can be prevented by dietary AGE restriction... - Endothelial dysfunction in patients with chronic kidney disease results from advanced glycation end products (AGE)-mediated inhibition of endothelial nitric oxide synthase through RAGE activationEllena Linden
Division of Nephrology, Department of Medicine, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA
Clin J Am Soc Nephrol 3:691-8. 2008.... - Fetal or neonatal low-glycotoxin environment prevents autoimmune diabetes in NOD miceMelpomeni Peppa
Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, Box 1640, New York, NY 10029, USA
Diabetes 52:1441-8. 2003..005). Therefore, high AGE intake may provide excess antigenic stimulus for T-cell-mediated diabetes or direct beta-cell injury in NOD mice; both processes are ameliorated by maternal or neonatal exposure to L-AGE nutrition... - Dietary glycotoxins promote diabetic atherosclerosis in apolipoprotein E-deficient miceReigh-Yi Lin
Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, Box 1640, One Gustave L. Levy Place, New York, NY 10029, USA
Atherosclerosis 168:213-20. 2003..The marked anti-atherogenic effects of an AGE-restricted diet in this model may provide the basis for relevant clinical studies... - Presence of diabetic complications in type 1 diabetic patients correlates with low expression of mononuclear cell AGE-receptor-1 and elevated serum AGEC J He
Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, New York 10029, USA
Mol Med 7:159-68. 2001.... - AGER1 regulates endothelial cell NADPH oxidase-dependent oxidant stress via PKC-delta: implications for vascular diseaseWeijing Cai
Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, Box 1640, One Gustave Levy Place, New York, NY 10029, USA
Am J Physiol Cell Physiol 298:C624-34. 2010..In conclusion, circulating AGEs induce NADPH-dependent ROS generation in vascular aging in both in vitro and in vivo models. Furthermore, AGER1 provides protection against AGE-induced ROS generation via NADPH... - AGE-receptor-1 counteracts cellular oxidant stress induced by AGEs via negative regulation of p66shc-dependent FKHRL1 phosphorylationWeijing Cai
Division of Diabetes and Aging Research, The Brookdale Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10019, USA
Am J Physiol Cell Physiol 294:C145-52. 2008..This represents a key mechanism by which AGER1 maintains cellular resistance against OS. Thus the decrease of AGER1 noted in aging and diabetes may further enhance OS and reduce innate antioxidant defenses... - Restriction of dietary glycotoxins reduces excessive advanced glycation end products in renal failure patientsJaime Uribarri
Division of Experimental Diabetes and Aging, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA
J Am Soc Nephrol 14:728-31. 2003..Moreover, dietary restriction of AGE is an effective and feasible method to reduce excess toxic AGE and possibly cardiovascular associated mortality... - Single oral challenge by advanced glycation end products acutely impairs endothelial function in diabetic and nondiabetic subjectsJaime Uribarri
Division of Nephrology, Department of Medicine, Mount Sinai School of Medicine, One Gustave Levy Pl, New York, NY 10029, USA
Diabetes Care 30:2579-82. 2007..The current study was designed to test the acute effects of dietary advanced glycation end products (AGEs) on endothelial function of diabetic and nondiabetic subjects... - Oxidative stress-inducing carbonyl compounds from common foods: novel mediators of cellular dysfunctionWeijing Cai
Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
Mol Med 8:337-46. 2002..01) and aminoguanidine-HCl (AG, 100 uM, p < 0.01). CONCLUSION: Thus, food-derived AGE, prior to absorption, contain potent carbonyl species, that can induce oxidative stress and promote inflammatory signals... - Improved insulin sensitivity is associated with restricted intake of dietary glycoxidation products in the db/db mouseSusanna M Hofmann
Brookdale Department of Genetics, Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029 6574, USA
Diabetes 51:2082-9. 2002..02). These results demonstrate that reduced AGE intake leads to lower levels of circulating AGE and to improved insulin sensitivity in db/db mice... - Lowering of dietary advanced glycation endproducts (AGE) reduces neointimal formation after arterial injury in genetically hypercholesterolemic miceReigh Yi Lin
Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, Box 1640, One Gustave L Levy Place, New York, NY 10029 6574, USA
Atherosclerosis 163:303-11. 2002.... - Advanced glycation end products inhibit glucose-stimulated insulin secretion through nitric oxide-dependent inhibition of cytochrome c oxidase and adenosine triphosphate synthesisZhengshan Zhao
Department of Geriatrics and Adult Development, Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, New York 10029, USA
Endocrinology 150:2569-76. 2009..We conclude that AGEs inhibit cytochrome c oxidase and ATP production, leading to the impairment of glucose-stimulated insulin secretion through iNOS-dependent nitric oxide production... - Induction of diabetes in aged C57B6 mice results in severe nephropathy: an association with oxidative stress, endoplasmic reticulum stress, and inflammationJin Wu
Division of Experimental Diabetes and Aging, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Am J Pathol 176:2163-76. 2010..The expression of tumor-necrosis factor-alpha in 22-month-old diabetic kidneys may play a role in inflammation, ER stress, and apoptosis. Thus, diabetes may accelerate the underlying kidney aging process present in old mice... - Advanced glycation end product (AGE) receptor 1 suppresses cell oxidant stress and activation signaling via EGF receptorWeijing Cai
Division of Experimental Diabetes and Aging, Brookdale Department of Geriatrics, and Division of Nephrology, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA
Proc Natl Acad Sci U S A 103:13801-6. 2006..AGER1 could serve as a model for developing therapeutic targets against vascular and kidney disorders related to diabetes and aging... - Adverse effects of dietary glycotoxins on wound healing in genetically diabetic miceMelpomeni Peppa
Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, New York 10029, USA
Diabetes 52:2805-13. 2003..Thus, increased diet-derived AGE intake may be a significant retardant of wound closure in diabetic mice; dietary AGE restriction may improve impaired diabetic wound healing... - Advanced glycoxidation. A new risk factor for cardiovascular disease?Melpomeni Peppa
Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
Cardiovasc Toxicol 2:275-87. 2002..Prospective outcome and controlled studies are needed to further support this relationship... - Dietary glycotoxins correlate with circulating advanced glycation end product levels in renal failure patientsJaime Uribarri
Department of Medicine, Division of Nephrology, Mount Sinai School of Medicine, New York, NY 10029, USA
Am J Kidney Dis 42:532-8. 2003..Although elevated AGE levels in patients with renal failure have been attributed to impaired renal clearance and increased endogenous AGE formation, recent data suggest an important role for diet as a source of AGEs... - Amelioration of oxidant stress by the defensin lysozymeHuixian Liu
Department of Geriatrics, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA
Am J Physiol Endocrinol Metab 290:E824-32. 2006..Thus LZ provides protection against acute and chronic oxidant injury by mechanisms involving suppression of ROS generation and of OS response genes... - Advanced glycation endproduct (AGE) receptor 1 is a negative regulator of the inflammatory response to AGE in mesangial cellsChangyong Lu
Department of Geriatrics and Adult Development, Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, NY 10029, USA
Proc Natl Acad Sci U S A 101:11767-72. 2004.... - Oxidative stress-induced JNK activation contributes to proinflammatory phenotype of aging diabetic mesangial cellsJin Wu
Divison of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
Am J Physiol Renal Physiol 297:F1622-31. 2009..Proinflammatory phenotype of mesangial cells may contribute to chronic inflammatory lesions and disease progression of aging diabetic mice... - Prevention of diabetic nephropathy in mice by a diet low in glycoxidation productsFeng Zheng
Mount Sinai School of Medicine, New York, NY 10029-6574, USA
Diabetes Metab Res Rev 18:224-37. 2002..Avoidance of dietary AGEs provides sustained protection against DN in mice; providing the rationale for similar studies in human diabetic patients... - Advanced glycation end products and diabetic complications: a general overviewMelpomeni Peppa
Division of Experimental Diabetes and Aging, Department of Geriatrics, Mount Sinai School of Medicine, NY, NY 10029, USA
Hormones (Athens) 4:28-37. 2005.... - Advanced glycation end products in foods and a practical guide to their reduction in the dietJaime Uribarri
Division of Nephrology, Mount Sinai School of Medicine, New York, NY, USA
J Am Diet Assoc 110:911-16.e12. 2010..The new dAGE database provides a valuable instrument for estimating dAGE intake and for guiding food choices to reduce dAGE intake... - Targeted disruption of Slc19a2, the gene encoding the high-affinity thiamin transporter Thtr-1, causes diabetes mellitus, sensorineural deafness and megaloblastosis in miceKimihiko Oishi
Department of Pediatrics, Mount Sinai School of Medicine, New York, NY 10029, USA
Hum Mol Genet 11:2951-60. 2002..Thus, Slc19a2(-/-) mice have provided new insights into the TRMA disease pathogenesis and will provide a tool for studying the role of thiamin homeostasis in diabetes mellitus more broadly... - Lysozyme enhances renal excretion of advanced glycation endproducts in vivo and suppresses adverse age-mediated cellular effects in vitro: a potential AGE sequestration therapy for diabetic nephropathy?F Zheng
Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, NY 10029 6574, USA
Mol Med 7:737-47. 2001.... - Reduced acute vascular injury and atherosclerosis in hyperlipidemic mice transgenic for lysozymeHuixian Liu
The Brookdale Department of Geriatrics, Division of Experimental Diabetes and Aging, Mount Sinai School of Medicine, New York, New York 10029, USA
Am J Pathol 169:303-13. 2006..This effect may be due to the antioxidant properties of LZ, which is possibly linked to the AGE-binding domain region of the molecule... - Prevention and reversal of diabetic nephropathy in db/db mice treated with alagebrium (ALT-711)Melpomeni Peppa
Department of Geriatrics, Mount Sinai School of Medicine, New York, NY, USA
Am J Nephrol 26:430-6. 2006..Alagebrium (ALT-711) has been shown to improve renal dysfunction in animal models of diabetes... - Restriction of advanced glycation end products improves insulin resistance in human type 2 diabetes: potential role of AGER1 and SIRT1Jaime Uribarri
Department of Medicine, The Mount Sinai School of Medicine, New York, New York, USA
Diabetes Care 34:1610-6. 2011..Because basal OS in type 2 diabetic patients is influenced by the consumption of AGEs, we examined whether AGE consumption also affects IR and whether AGER1 and SIRT1 are involved... - Diabetes-induced oxidative stress and low-grade inflammation in porcine coronary arteriesLifeng Zhang
Department of Surgery, Thomas Jefferson University, Philadelphia, PA 19107, USA
Circulation 108:472-8. 2003..These results suggest the involvement of AGEs in the development of accelerated coronary atherosclerosis in diabetes... - Prevention Conference VI: Diabetes and Cardiovascular Disease: Writing Group II: pathogenesis of atherosclerosis in diabetesRobert H Eckel
Circulation 105:e138-43. 2002 - Aging and glycoxidant stressMelpomeni Peppa
Endocrine Unit, 2nd Dept of Internal Medicine Propaedeutic, Research Institute and Diabetes Center, Athens University, Medical School, Athens, Greece
Hormones (Athens) 7:123-32. 2008..Long-term studies are in progress and will help establish definitive causality between age-related disease states and modern dietary practices in Western societies... - Dietary advanced glycation endproducts and oxidative stress: in vivo effects on endothelial function and adipokinesAlin Stirban
Diabetes Center North Rhine Westphalia, Bad Oeynhausen, Germany
Ann N Y Acad Sci 1126:276-9. 2008..The postprandial excursions in glucose, insulin, and triglycerides were similar between both meals. A meal rich in AGEs induces acute endothelial and adipocyte dysfunction. These effects were prevented by changing the cooking method... - Diabetes and advanced glycoxidation end productsAmy G Huebschmann
Division of General Internal Medicine, Department of Medicine, University of Colorado Denver and Health Sciences Center, Mailstop F-729, Aurora, CO 80045, USA
Diabetes Care 29:1420-32. 2006 - Effects of low- and high-advanced glycation endproduct meals on macro- and microvascular endothelial function and oxidative stress in patients with type 2 diabetes mellitusMonica Negrean
Diabetes Clinic, Heart and Diabetes Centre NRW Bad Oeynhausen, Ruhr University Bochum, Germany
Am J Clin Nutr 85:1236-43. 2007..An advanced glycation endproducts (AGEs)-rich diet induces significant increases in inflammatory and endothelial dysfunction markers in type 2 diabetes mellitus (T2DM)... - Benfotiamine prevents macro- and microvascular endothelial dysfunction and oxidative stress following a meal rich in advanced glycation end products in individuals with type 2 diabetesAlin Stirban
Heart and Diabetes Center NRW, Georgstrasse 11, 32545 Bad Oeynhausen, Germany
Diabetes Care 29:2064-71. 2006.... - Glycotoxins: a missing link in the "relationship of dietary fat and meat intake in relation to risk of type 2 diabetes in men"Melpomeni Peppa
Diabetes Care 25:1898-9. 2002
Research Grants
- AGING AND VASCULAR DISEASE: ROLE OF GLYCATIONHelen Vlassara; Fiscal Year: 2007..diabetes, diet. The proposed studies will expand our understanding of this basic process and may allow us to identify ways to prevent AGE-induced vascular injury due to diabetes and aging. ..
- Effects of Glycoxidative Stress on Human AgingHelen Vlassara; Fiscal Year: 2010....
- Vascular Response and Glycoxidant HomeostasisHelen Vlassara; Fiscal Year: 2007..The elucidation of AGER1 mechanisms, which influence the regulation of AGE clearance (positively) and/or the pro-OS, inflammatory pathways (negatively) may generate new therapeutic targets against human vascular disease. ..
- Effects of Glycoxidative Stress on Human AgingHelen Vlassara; Fiscal Year: 2007..It is hoped that the data will lay the groundwork for future studies evaluating optimal methods of nutrient preparation as ways to ameliorate a major environmental promoter of pro-oxidant events, and thus aging. ..
- Vascular Response and Glycoxidant HomeostasisHelen Vlassara; Fiscal Year: 2009..The elucidation of AGER1 mechanisms, which influence the regulation of AGE clearance (positively) and/or the pro-OS, inflammatory pathways (negatively) may generate new therapeutic targets against human vascular disease. ..
- AGING AND VASCULAR DISEASE--ROLE OF GLYCATIONHelen Vlassara; Fiscal Year: 2001..Based on the multifaceted properties of the AGE receptor system, these studies should provide a molecular basis for the future epidemiology and treatment of age-related vascular disease. ..
- AGE-RECEPTORS AND KIDNEY DISEASEHelen Vlassara; Fiscal Year: 2003....