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• W2164438863 abstract "Aging is accompanied by increased oxidative stress (OS) and accumulation of advanced glycation end products (AGEs). AGE formation in food is temperature-regulated, and ingestion of nutrients prepared with excess heat promotes AGE formation, OS, and cardiovascular disease in mice. We hypothesized that sustained exposure to the high levels of pro-oxidant AGEs in normal diets (RegAGE) contributes to aging via an increased AGE load, which causes AGER1 dysregulation and depletion of anti-oxidant capacity, and that an isocaloric, but AGE-restricted (by 50%) diet (LowAGE), would decrease these abnormalities. C57BL6 male mice with a life-long exposure to a LowAGE diet had higher than baseline levels of tissue AGER1 and glutathione/oxidized glutathione and reduced plasma 8-isoprostanes and tissue RAGE and p66shc levels compared with mice pair-fed the regular (RegAGE) diet. This was associated with a reduction in systemic AGE accumulation and amelioration of insulin resistance, albuminuria, and glomerulosclerosis. Moreover, lifespan was extended in LowAGE mice, compared with RegAGE mice. Thus, OS-dependent metabolic and end organ dysfunction of aging may result from life-long exposure to high levels of glycoxidants that exceed AGER1 and anti-oxidant reserve capacity. A reduced AGE diet preserved these innate defenses, resulting in decreased tissue damage and a longer lifespan in mice. Aging is accompanied by increased oxidative stress (OS) and accumulation of advanced glycation end products (AGEs). AGE formation in food is temperature-regulated, and ingestion of nutrients prepared with excess heat promotes AGE formation, OS, and cardiovascular disease in mice. We hypothesized that sustained exposure to the high levels of pro-oxidant AGEs in normal diets (RegAGE) contributes to aging via an increased AGE load, which causes AGER1 dysregulation and depletion of anti-oxidant capacity, and that an isocaloric, but AGE-restricted (by 50%) diet (LowAGE), would decrease these abnormalities. C57BL6 male mice with a life-long exposure to a LowAGE diet had higher than baseline levels of tissue AGER1 and glutathione/oxidized glutathione and reduced plasma 8-isoprostanes and tissue RAGE and p66shc levels compared with mice pair-fed the regular (RegAGE) diet. This was associated with a reduction in systemic AGE accumulation and amelioration of insulin resistance, albuminuria, and glomerulosclerosis. Moreover, lifespan was extended in LowAGE mice, compared with RegAGE mice. Thus, OS-dependent metabolic and end organ dysfunction of aging may result from life-long exposure to high levels of glycoxidants that exceed AGER1 and anti-oxidant reserve capacity. A reduced AGE diet preserved these innate defenses, resulting in decreased tissue damage and a longer lifespan in mice. Environmental and genetic factors including elevated oxidant stress (OS), cumulative DNA damage, altered gene expression, telomere shortening, and energy utilization are among the postulated mechanisms of senescence and aging in organisms from yeast to mammals.1Masoro EJ Overview of caloric restriction and ageing.Mech Ageing Dev. 2005; 126: 913-922Crossref PubMed Scopus (845) Google Scholar, 2Quarrie JK Riabowol KT Murine models of lifespan extension.Sci Aging Knowledge Environ. 2004; 31: re5Google Scholar, 3Madsen MA Hsieh CC Boylston WH Flurkey K Harrison D Papaconstantinou J Altered oxidative stress response of the long-lived Snell dwarf mouse.Biochem Biophys Res Commun. 2004; 318: 998-1005Crossref PubMed Scopus (36) Google Scholar, 4Zimmerman JA Malloy V Krajcik R Orentreich N Nutrition control of aging.Exp Gerontol. 2003; 38: 47-52Crossref PubMed Scopus (230) Google Scholar, 5Kaeberlein M Hu D Kerr EO Tsuchiya M Westman EA Dang N Fields S Kennedy BK Increased life span due to caloric restriction in respiratory-deficient yeast.PLoS Genet. 2005; 1: 614-621Crossref Scopus (149) Google Scholar The effects of increased OS are thought to be partly mediated by oxidative changes in proteins, lipids, and nucleic acids, which alter their function.6Bokov A Chaudhuri A Richardson A The role of oxidative damage and stress in aging.Mech Ageing Dev. 2004; 125: 811-826Crossref PubMed Scopus (482) Google Scholar Excess OS can be diminished by manipulating genetic or environmental factors. Genetic models of increased longevity include loss-of-function mutations of the GH/IGF-1 axis and downstream signaling,7Longo VD Finch CE Evolutionary medicine: from dwarf model systems to healthy centenarians.Science. 2003; 299: 1342-1346Crossref PubMed Scopus (489) Google Scholar, 8Anderson RM Latorre-Esteves M Neves AR Lavu S Medvedik O Taylor C Howitz KT Santos H Sinclair DA Yeast life-span extension by caloric restriction is independent of NAD fluctuation.Science. 2003; 302 (2124): 2124Crossref PubMed Scopus (134) Google Scholar, 9Shimokawa I Higami Y Tsuchiya T Otani H Komatsu T Chiba T Yamaza H Life span extension by reduction of the growth hormone-insulin-like growth factor-1 axis: relation to caloric restriction.FASEB J. 2003; 17: 1108-1109PubMed Google Scholar, 10Holzenberger M Dupont J Ducos B Leneuve P Geloen A Even PC Cervera L Le Bouc Y IGF-1 receptor regulates lifespan and resistance to oxidative stress in mice.Nature. 2003; 421: 182-187Crossref PubMed Scopus (1593) Google Scholar as well as p66Shc,11Migliaccio E Giorgio M Mele S Pelicci G Reboldi P Pandolfi PP Lanfrancone L The p66shc adaptor protein controls oxidative stress response and life span in mammals.Nature. 1999; 402: 309-313Crossref PubMed Scopus (1458) Google Scholar the FOXO transcription factors,12Nemoto S Finkel T Redox regulation of forkhead proteins through a p66shc-dependent signaling pathway.Science. 2002; 295: 2450-2452Crossref PubMed Scopus (731) Google Scholar catalase,13Schriner SE Linford NJ Martin GM Treuting P Ogburn CE Emond M Coskun PE Ladiges W Wolf N Van Remmen H Wallace DC Rabinovitch PS Extension of murine life span by overexpression of catalase targeted to mitochondria.Science. 2005; 308: 1909-1911Crossref PubMed Scopus (1342) Google Scholar and anti-oxidant mimetics.14Melov S Ravenscroft J Malik S Gill MS Walker DW Clayton PE Wallace DC Malfroy B Doctrow SR Lithgow GJ Extension of life-span with superoxide dismutase/catalase mimetics.Science. 2000; 289: 1567-1569Crossref PubMed Scopus (764) Google Scholar The most widely studied environmental intervention that prevents excess OS and extends lifespan is caloric restriction, which mimics many of the changes observed in the genetic models.1Masoro EJ Overview of caloric restriction and ageing.Mech Ageing Dev. 2005; 126: 913-922Crossref PubMed Scopus (845) Google Scholar, 5Kaeberlein M Hu D Kerr EO Tsuchiya M Westman EA Dang N Fields S Kennedy BK Increased life span due to caloric restriction in respiratory-deficient yeast.PLoS Genet. 2005; 1: 614-621Crossref Scopus (149) Google ScholarOxidants in vivo are multiple, heterogeneous, and include nonenzymatic reaction derivatives of free amine-containing nucleic acids, peptides, or lipids with ambient reducing sugars, termed advanced glycation/lipoxidation products (AGE/ALE or glycotoxins).15Requena JR Ahmed MU Fountain CW Degenhardt TP Reddy S Perez C Lyons TJ Jenkins AJ Baynes JW Thorpe SR Carboxymethylethanolamine, a biomarker of phospholipid modifications during the Maillard reaction in vivo.J Biol Chem. 1997; 272: 17473-17479Crossref PubMed Scopus (94) Google Scholar, 16Brownlee M Biochemistry and molecular cell biology of diabetic complications.Nature. 2001; 414: 813-820Crossref PubMed Scopus (6925) Google Scholar Protein and lipid-derived AGE include Nε-carboxy-methyl-lysine (CML), Nε-carboxyethyl-lysine, methyl-glyoxal-hydroimidazolone, their precursors, and/or derivatives. These are products of normal metabolism in organisms ranging from single cells to mammals and are turned over or neutralized by receptors that promote AGE uptake and degradation, such as AGER1,17Lu C He JC Cai W Liu H Zhu L Vlassara H Advanced glycation endproduct (AGE) receptor 1 is a negative regulator of the inflammatory response to AGE in mesangial cells.Proc Natl Acad Sci USA. 2004; 101: 11767-11772Crossref PubMed Scopus (195) Google Scholar and are excreted by the kidney.18Makita Z Radoff S Rayfield EJ Yang Z Skolnik E Delaney V Friedman EA Cerami A Vlassara H Advanced glycosylation endproducts in patients with diabetic nephropathy.N Engl J Med. 1991; 325: 836-842Crossref PubMed Scopus (821) Google Scholar Thus, AGER1 functions to decrease OS. On the other hand, other AGE receptors promote OS after binding, the prime example being RAGE.19Vlassara H Moldawer L Chan B Macrophage/monocyte receptor for non-enzymatically glycosylated proteins is up-regulated by cachectin/tumor necrosis factor.J Clin Invest. 1989; 84: 1813-1820Crossref PubMed Scopus (61) Google Scholar, 20He C Koschinsky T Buenting C Vlassara H Presence of diabetic complications in type I diabetic patients correlates with low expression of mononuclear cell AGE-receptor-1 and elevated serum AGE.Mol Med. 2001; 7: 159-168PubMed Google Scholar, 21Singh R Barden A Mori T Beilin L Advanced glycation end-products: a review.Diabetologia. 2001; 44: 129-146Crossref PubMed Scopus (1912) Google Scholar AGE receptors can be up-regulated in vitro22Vlassara H Uribarri J Glycoxidation and diabetic complications: modern lesson and a warning?.Rev Endocr Metab Disord. 2004; 5: 181-188Crossref PubMed Scopus (83) Google Scholar; however, when AGEs are chronically elevated, ie, in diabetes, AGER1 can be down-regulated,23Schmidt AM Yan SD Yan SF Stern DM The multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses.J Clin Invest. 2001; 108: 949-955Crossref PubMed Scopus (1045) Google Scholar but OS-promoting receptors, such as RAGE, are enhanced. RAGE promotes the formation of reactive oxygen species, inflammation, stress-responses, and apoptotic events.19Vlassara H Moldawer L Chan B Macrophage/monocyte receptor for non-enzymatically glycosylated proteins is up-regulated by cachectin/tumor necrosis factor.J Clin Invest. 1989; 84: 1813-1820Crossref PubMed Scopus (61) Google Scholar, 20He C Koschinsky T Buenting C Vlassara H Presence of diabetic complications in type I diabetic patients correlates with low expression of mononuclear cell AGE-receptor-1 and elevated serum AGE.Mol Med. 2001; 7: 159-168PubMed Google Scholar, 21Singh R Barden A Mori T Beilin L Advanced glycation end-products: a review.Diabetologia. 2001; 44: 129-146Crossref PubMed Scopus (1912) Google Scholar Excess AGEs are present in several diseases common in aging, including diabetes, cardiovascular disease, and chronic kidney disease (CKD).15Requena JR Ahmed MU Fountain CW Degenhardt TP Reddy S Perez C Lyons TJ Jenkins AJ Baynes JW Thorpe SR Carboxymethylethanolamine, a biomarker of phospholipid modifications during the Maillard reaction in vivo.J Biol Chem. 1997; 272: 17473-17479Crossref PubMed Scopus (94) Google Scholar, 16Brownlee M Biochemistry and molecular cell biology of diabetic complications.Nature. 2001; 414: 813-820Crossref PubMed Scopus (6925) Google Scholar, 18Makita Z Radoff S Rayfield EJ Yang Z Skolnik E Delaney V Friedman EA Cerami A Vlassara H Advanced glycosylation endproducts in patients with diabetic nephropathy.N Engl J Med. 1991; 325: 836-842Crossref PubMed Scopus (821) Google Scholar, 19Vlassara H Moldawer L Chan B Macrophage/monocyte receptor for non-enzymatically glycosylated proteins is up-regulated by cachectin/tumor necrosis factor.J Clin Invest. 1989; 84: 1813-1820Crossref PubMed Scopus (61) Google Scholar, 20He C Koschinsky T Buenting C Vlassara H Presence of diabetic complications in type I diabetic patients correlates with low expression of mononuclear cell AGE-receptor-1 and elevated serum AGE.Mol Med. 2001; 7: 159-168PubMed Google Scholar, 21Singh R Barden A Mori T Beilin L Advanced glycation end-products: a review.Diabetologia. 2001; 44: 129-146Crossref PubMed Scopus (1912) Google Scholar, 24Liu HX Zheng F Cao Q Ren B Zhu L Striker G Vlassara H Amelioration of oxidant stress by the defensin lysozyme.Am J Physiol. 2006; 290: E824-E832Google Scholar, 25Yao D Taguchi T Matsumura T Pestell R Edelstein D Giardino I Suske G Ahmed N Thornalley PJ Sarthy VP Hammes HP Brownlee M Methylglyoxal modification of mSin3A links glycolysis to angiopoietin-2 transcription.Cell. 2006; 124: 275-286Abstract Full Text PDF PubMed Scopus (70) Google Scholar, 26Monnier VM, Sell DR, Genuth S: Glycation products as markers and predictors of the progression of diabetic complications. The Maillard Reaction, Chemistry at the Interface of Nutrition, Aging, and Disease. Edited by JW Baynes, VM Monnier, JM Ames, SR Thorpe. Annals of the New York Academy of Science, 2005, vol. 1043Google ScholarNutrients that are thermally prepared for consumption are a rich source of protein- or fat-derived oxidation derivatives, including AGEs, and a host of toxic compounds in foods, some of which have been implicated in oncogenesis.27O'Brien J Nutritional and toxicological aspects of the Maillard browning reaction in foods.Crit Rev Food Sci Nutr. 1989; 28: 211-248Crossref PubMed Scopus (393) Google Scholar, 28Birlouez-Aragon I Pischetsrieder M Leclere J Morales FJ Hasenkopf K Kientsch-Engel R Ducauze CJ Rutledge D Assessment of protein glycation markers in infant formulas.Food Chem. 2004; 87: 253-259Crossref Scopus (114) Google Scholar, 29Glomb MA Schirnich RT Detection of alpha-dicarbonyl compounds in Maillard reaction systems and in vivo.J Agric Food Chem. 2001; 49: 5543-5550Crossref PubMed Scopus (85) Google Scholar, 30van Boekel MA Kinetic aspects of the Maillard reaction: a critical review.Nahrung. 2001; 45: 150-159Crossref PubMed Scopus (261) Google Scholar, 31Cai W Gao QD Zhu L Peppa M He C Vlassara H Oxidative stress-inducing carbonyl compounds from common foods: novel mediators of cellular dysfunction.Mol Med. 2002; 8: 337-346PubMed Google Scholar, 32Cheng K Chen F Wang M Heterocyclic amines: chemistry and health.Mol Nutr Food Res. 2006; 50: 1150-1170Crossref PubMed Scopus (91) Google Scholar Laboratory rodent food is high in protein, low in fat, supplemented with micronutrients, and routinely heated to ensure safety. The temperatures currently used are sufficiently high to inadvertently cause standard mouse chow to be rich in oxidant AGEs, not unlike levels present in the usual Western diet.27O'Brien J Nutritional and toxicological aspects of the Maillard browning reaction in foods.Crit Rev Food Sci Nutr. 1989; 28: 211-248Crossref PubMed Scopus (393) Google Scholar, 30van Boekel MA Kinetic aspects of the Maillard reaction: a critical review.Nahrung. 2001; 45: 150-159Crossref PubMed Scopus (261) Google ScholarLowering the intake of dietary AGEs or glycotoxins, by restricting the temperature used in nutrient preparation, reduces circulating and tissue levels of AGEs.33He C Sabol J Mitsuhashi T Vlassara H Dietary glycotoxins: inhibition of reactive products by aminoguanidine facilitates renal clearance and reduces tissue sequestration.Diabetes. 1999; 48: 1308-1315Crossref PubMed Scopus (170) Google Scholar, 34Yang CW Vlassara H Striker GE Striker LJ Administration of AGEs in vivo induces genes implicated in diabetic glomerulosclerosis.Kidney Int. 1995; 49: S55-S58Google Scholar, 35Yang CW Hattori M Vlassara H He CJ Carome MA Yamato E Elliot S Striker GE Striker LJ Overexpression of TGF-β1 mRNA is associated with upregulation of glomerular tenascin and laminin gene expression in diabetic NOD mice.J Am Soc Nephrol. 1995; 5: 1610-1617PubMed Google Scholar, 36Li YM Steffes M Donnelly T Liu C Fuh H Basgen J Bucala R Vlassara H Prevention of cardiovascular and renal pathology of aging by the advance glycation inhibitor aminoguanidine.Proc Natl Acad Sci USA. 1996; 93: 3902-3907Crossref PubMed Scopus (164) Google Scholar, 37Vlassara H Cai W Crandall J Goldberg T Oberstein R Dardaine V Peppa M Rayfield EJ Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy.Proc Natl Acad Sci USA. 2002; 99: 15596-15601Crossref PubMed Scopus (585) Google Scholar, 38Lin RY Choudhury RP Cai W Lu M Fallon JT Fisher EA Vlassara H Dietary glycotoxins promote diabetic atherosclerosis in apolipoprotein E-deficient mice.Atherosclerosis. 2003; 168: 213-220Abstract Full Text Full Text PDF PubMed Scopus (162) Google Scholar, 39Koschinsky T He CJ Mitsuhashi T Bucala R Liu C Buenting C Heitmann K Vlassara H Orally absorbed reactive glycation products (glycotoxins): an environmental risk factor in diabetic nephropathy.Proc Natl Acad Sci USA. 1997; 94: 6474-6479Crossref PubMed Scopus (671) Google Scholar, 40Uribarri J Peppa M Cai W Goldberg T Lu M He C Vlassara H Restriction of dietary glycotoxins reduces excessive advanced glycation end products in renal failure patients.J Am Soc Nephrol. 2003; 14: 728-731Crossref PubMed Scopus (288) Google Scholar This was associated with a decrease in OS and inflammatory responses in patients with diabetes37Vlassara H Cai W Crandall J Goldberg T Oberstein R Dardaine V Peppa M Rayfield EJ Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy.Proc Natl Acad Sci USA. 2002; 99: 15596-15601Crossref PubMed Scopus (585) Google Scholar and CKD,40Uribarri J Peppa M Cai W Goldberg T Lu M He C Vlassara H Restriction of dietary glycotoxins reduces excessive advanced glycation end products in renal failure patients.J Am Soc Nephrol. 2003; 14: 728-731Crossref PubMed Scopus (288) Google Scholar and in animals a LowAGE diet prevents the development of insulin resistance and diabetes,41Sandu O Song K Cai W Zheng F Uribarri J Vlassara H Insulin resistance and type 2 diabetes in high-fat-fed mice are linked to high glycotoxin intake.Diabetes. 2005; 54: 2314-2319Crossref PubMed Scopus (164) Google Scholar, 42Hofmann SM Dong HJ Li Z Cai W Altomonte J Thung SN Zeng F Fisher EA Vlassara H Improved insulin sensitivity is associated with restricted intake of dietary glycoxidation products in the db/db mouse.Diabetes. 2002; 51: 2082-2089Crossref PubMed Scopus (260) Google Scholar cardiovascular disease,38Lin RY Choudhury RP Cai W Lu M Fallon JT Fisher EA Vlassara H Dietary glycotoxins promote diabetic atherosclerosis in apolipoprotein E-deficient mice.Atherosclerosis. 2003; 168: 213-220Abstract Full Text Full Text PDF PubMed Scopus (162) Google Scholar and CKD.43Zheng F He C Cai W Hattori M Steffes M Vlassara H Prevention of diabetic nephropathy in mice by a diet low in glycoxidation products.Diabetes Metab Res Rev. 2002; 18: 224-237Crossref PubMed Scopus (197) Google ScholarBecause it was not known whether a decreased intake of AGEs affects normal aging or lifespan in normal animals, we compared the effects of dietary AGE intake on age-related changes such as OS, glucose/insulin metabolism, kidney disease, and lifespan in mice pair-fed a regular diet or an isocaloric diet exposed to lower temperature (LowAGE diet). We found that the LowAGE diet contained lower oxidant AGEs and preserved anti-oxidant reserves, prevented kidney disease, and extended lifespan. These events could be attributable to suppressed OS-regulatory mechanisms and may be related to preservation of the capacity of AGER1 to respond to the increased AGE load that characterizes normal aging.Materials and MethodsAnimals and DietsC57BL/6 mice (n = 84, male, 4 months of age) from the NIA caloric restriction colonies were individually caged and provided free access to water. Mice were assigned to two dietary groups (Table 1): a regular NIH-31 open formula (Harlan Teklad, Madison, WI) ad lib (RegAGE), and a rodent chow diet (LabDiet 5053; LabDiet, Purina Mills, Richmond, IN), equal in calories, nutrient, and micronutrient content to RegAGE, but, by limiting exposure to the standard temperature during manufacture, contained less measurable CML-like AGEs (LowAGE diet, ∼50% of RegAGE diet).38Lin RY Choudhury RP Cai W Lu M Fallon JT Fisher EA Vlassara H Dietary glycotoxins promote diabetic atherosclerosis in apolipoprotein E-deficient mice.Atherosclerosis. 2003; 168: 213-220Abstract Full Text Full Text PDF PubMed Scopus (162) Google Scholar, 42Hofmann SM Dong HJ Li Z Cai W Altomonte J Thung SN Zeng F Fisher EA Vlassara H Improved insulin sensitivity is associated with restricted intake of dietary glycoxidation products in the db/db mouse.Diabetes. 2002; 51: 2082-2089Crossref PubMed Scopus (260) Google Scholar, 43Zheng F He C Cai W Hattori M Steffes M Vlassara H Prevention of diabetic nephropathy in mice by a diet low in glycoxidation products.Diabetes Metab Res Rev. 2002; 18: 224-237Crossref PubMed Scopus (197) Google Scholar Thus, compared with RegAGE, which is first steam-conditioned and pelleted at 70 to 75°C, for 1 to 2 minutes, and then dried at 55°C for 30 minutes, LowAGE was only exposed to 80°C for 1 minute, during pelleting. Micronutrient content was in excess of established requirements.38Lin RY Choudhury RP Cai W Lu M Fallon JT Fisher EA Vlassara H Dietary glycotoxins promote diabetic atherosclerosis in apolipoprotein E-deficient mice.Atherosclerosis. 2003; 168: 213-220Abstract Full Text Full Text PDF PubMed Scopus (162) Google Scholar, 42Hofmann SM Dong HJ Li Z Cai W Altomonte J Thung SN Zeng F Fisher EA Vlassara H Improved insulin sensitivity is associated with restricted intake of dietary glycoxidation products in the db/db mouse.Diabetes. 2002; 51: 2082-2089Crossref PubMed Scopus (260) Google Scholar, 43Zheng F He C Cai W Hattori M Steffes M Vlassara H Prevention of diabetic nephropathy in mice by a diet low in glycoxidation products.Diabetes Metab Res Rev. 2002; 18: 224-237Crossref PubMed Scopus (197) Google Scholar Diets were purchased in small amounts (<5 kg) and kept at 4°C. Food consumption was monitored daily, for the first 4 weeks, by weighing the food of each individual mouse to assess exact intake, and weekly thereafter. After establishing the daily intake of RegAGE mice, the identical amount was given to both LowAGE and RegAGE mice. Throughout the study, food was completely consumed between feedings. Half of these mice (n = 20/dietary group) were used for procedures, ie, blood collection and glucose tolerance testing or sacrifice and tissue retrieval, and the remaining (n = 22/diet group) were used for analysis of survival curves.Table 1Characteristics of MouseRegularLowProtein (g)20.020.0Fat4.54.5Carbohydrate (g)54.854.8Total calories (kcal/g)4.04.0AGE6.0 × 1043.0 × 104Food/day/mouse (g)5.05.0AGE intake/day (U)30.0 × 1015.5 × 104Total calories/day (kcal)20.020.1 Open table in a new tab Body weight was monitored two times per week during the first 3 months and then monthly because none of the groups showed sudden weight loss. At intervals, blood was collected from the tail vein of nonanesthetized mice (n = 5/group) and serum was separated and frozen for subsequent analyses. At sacrifice, tissue segments were placed in 2% freshly prepared paraformaldehyde in phosphate-buffered saline or were snap-frozen at −80°C.All mice were maintained in a specific pathogen-free environment, with the room temperature maintained at 72°F, 50% humidity, and 12:12 light/dark cycles, at the Center for Laboratory Animal Science, Mount Sinai School of Medicine. Sentinel mice in the same room were examined every 3 months and tested sero-negative for pneumonia virus of mice, mouse hepatitis virus, mouse minute virus, lymphocytic choriomeningitis virus, mouse adenovirus, and Sendai virus and tested negative for parasites (eg, pinworm) and other routine pathogens. All experimental procedures complied with the Guide for the Care and Use of Laboratory Animals (Department of Health, Education, and Welfare, publication no. NIH 78-23, 1996).AGE MeasurementsBecause CML-like AGEs, present in both the normal mouse chow as well as the tissues of animals and humans, and correlate with other AGEs and oxidants, ie, methyl glyoxal or lipid oxidation derivatives such as 8-isoprostanes, it is used as a surrogate marker of other AGEs.31Cai W Gao QD Zhu L Peppa M He C Vlassara H Oxidative stress-inducing carbonyl compounds from common foods: novel mediators of cellular dysfunction.Mol Med. 2002; 8: 337-346PubMed Google Scholar AGE concentrations in mouse sera, tissues, urine, and diets were determined by enzyme-linked immunosorbent assay, using monoclonal antibodies reacting with CML-like (4G9; Alteon, Northvale, NJ) or methyl-glyoxal-like epitopes.31Cai W Gao QD Zhu L Peppa M He C Vlassara H Oxidative stress-inducing carbonyl compounds from common foods: novel mediators of cellular dysfunction.Mol Med. 2002; 8: 337-346PubMed Google Scholar, 37Vlassara H Cai W Crandall J Goldberg T Oberstein R Dardaine V Peppa M Rayfield EJ Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy.Proc Natl Acad Sci USA. 2002; 99: 15596-15601Crossref PubMed Scopus (585) Google Scholar, 40Uribarri J Peppa M Cai W Goldberg T Lu M He C Vlassara H Restriction of dietary glycotoxins reduces excessive advanced glycation end products in renal failure patients.J Am Soc Nephrol. 2003; 14: 728-731Crossref PubMed Scopus (288) Google Scholar, 41Sandu O Song K Cai W Zheng F Uribarri J Vlassara H Insulin resistance and type 2 diabetes in high-fat-fed mice are linked to high glycotoxin intake.Diabetes. 2005; 54: 2314-2319Crossref PubMed Scopus (164) Google Scholar, 42Hofmann SM Dong HJ Li Z Cai W Altomonte J Thung SN Zeng F Fisher EA Vlassara H Improved insulin sensitivity is associated with restricted intake of dietary glycoxidation products in the db/db mouse.Diabetes. 2002; 51: 2082-2089Crossref PubMed Scopus (260) Google Scholar Based on HPLC/GC-MS, the CML-bovine serum albumin standard contained 23 modified lys/mol, whereas the methyl-glyoxal-bovine serum albumin standard contained 23 modified arginine/mol.31Cai W Gao QD Zhu L Peppa M He C Vlassara H Oxidative stress-inducing carbonyl compounds from common foods: novel mediators of cellular dysfunction.Mol Med. 2002; 8: 337-346PubMed Google Scholar CML immunoreactivity (based on 4G9 monoclonal antibody) correlates with that of methyl-glyoxal-derivatives (based on 3D11 monoclonal antibody).31Cai W Gao QD Zhu L Peppa M He C Vlassara H Oxidative stress-inducing carbonyl compounds from common foods: novel mediators of cellular dysfunction.Mol Med. 2002; 8: 337-346PubMed Google ScholarMetabolic StudiesAt 4 and 24 months, an intraperitoneal glucose tolerance test (5% dextrose solution; 2 mg/g body weight) was performed in subgroups from each dietary group (n = 5), after an overnight fast.41Sandu O Song K Cai W Zheng F Uribarri J Vlassara H Insulin resistance and type 2 diabetes in high-fat-fed mice are linked to high glycotoxin intake.Diabetes. 2005; 54: 2314-2319Crossref PubMed Scopus (164) Google Scholar, 42Hofmann SM Dong HJ Li Z Cai W Altomonte J Thung SN Zeng F Fisher EA Vlassara H Improved insulin sensitivity is associated with restricted intake of dietary glycoxidation products in the db/db mouse.Diabetes. 2002; 51: 2082-2089Crossref PubMed Scopus (260) Google Scholar Blood samples were taken before and at intervals between 5 and 120 minutes after glucose infusion. Blood glucose was determined with an Elite glucometer (Bayer, Mishawaka, IN). Serum insulin levels were measured by enzyme-linked immunosorbent assay (Ultra-Sensitive mouse insulin kit; Alpco Diagnostics, Windham, NH).Urinary Albumin Excretion RateRenal function was evaluated at 4 and 24 months by determining the urinary albumin/creatinine ratio in 24-hour urine samples collected from each group (n = 5). Urinary creatinine and albumin were measured using a DCA 2000 microalbumin/creatinine reagent cartridge with a DCA 2000 analyzer (Bayer Corp., Elkhart, IN).Renal HistopathologyKidney specimens obtained at 4 and 28 months (n = 5), were fixed in 10% buffered formalin and embedded in paraffin. Sections, stained by periodic acid-Schiff (PAS) were used to assess glomerulosclerosis.43Zheng F He C Cai W Hattori M Steffes M Vlassara H Prevention of diabetic nephropathy in mice by a diet low in glycoxidation products.Diabetes Metab Res Rev. 2002; 18: 224-237Crossref PubMed Scopus (197) Google Scholar At least 20 glomeruli per slide were chosen for quantification using IP Lab (BD Biosciences, San Jose, CA) for Macintosh OSX, version 3.9.Determination of Glutathione (GSH), Oxidized Glutathione (GSSG), and F2-Isoprostanes (8-Isoprostane)At 4 and 24 months, five animals from each of the diet groups were anesthetized. Whole blood was collected via cardiac puncture and plasma was separated by centrifugation. Levels of GSH and GSSG in whole blood were analyzed colorimetrically (Oxis Research, Portland, OR) using the manufacturer's recommendations and quantified by an enzyme-linked immunosorbent assay reader (412 nm).31Cai W Gao QD Zhu L Peppa M He C Vlassara H Oxidative stress-inducing carbonyl compounds from common foods: novel mediators of cellular dysfunction.Mol Med. 2002; 8: 337-346PubMed Google Scholar, 41Sandu O Song K Cai W Zheng F Uribarri J Vlassara H Insulin resistance and type 2 diabetes in high-fat-fed mice are linked to high glycotoxin intake.Diabetes. 2005; 54: 2314-2319Crossref PubMed Scopus (164) Google Scholar 8-Isoprostane (8-epi-PGF2α) levels were determined in fresh plasma samples, using an enzyme immunoassay kit (Cayman Chemical, Ann Arbor, MI).41Sandu O Song K Cai W Zheng F Uribarri J Vlassara H Insulin resistance and type 2 diabetes in high-fat-fed mice are linked to high glycotoxin intake.Diabetes. 2005; 54: 2314-2319Crossref PubMed Scopus (164) Google ScholarWestern Blot Analysis: AGER1, RAGE, p66shcEqual amounts of tissue (kidney cortex, spleen) protein extracts (50 μg) were separated on 10% or 8% sodium dodecyl sulfate-polyacrylamide gels and transferred to nitrocellulose membranes. The membranes were blocked in TTBS (Tris-buffered saline with 0.1% Tween" @default.
• W2164438863 created "2016-06-24" @default.
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• W2164438863 date "2007-06-01" @default.
• W2164438863 modified "2023-10-05" @default.
• W2164438863 title "Reduced Oxidant Stress and Extended Lifespan in Mice Exposed to a Low Glycotoxin Diet" @default.
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