The DOI matches its Crossref record; 25 of the 26 references it cites were found in a registry or an index.
Restriction of Advanced Glycation End Products Improves Insulin Resistance in Human Type 2 Diabetes
Open accessAbstract
OBJECTIVE: Increased oxidative stress (OS) and impaired anti-OS defenses are important in the development and persistence of insulin resistance (IR). Several anti-inflammatory and cell-protective mechanisms, including advanced glycation end product (AGE) receptor-1 (AGER1) and sirtuin (silent mating-type information regulation 2 homolog) 1 (SIRT1) are suppressed in diabetes. 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. RESEARCH DESIGN AND METHODS: The study randomly assigned 36 subjects, 18 type 2 diabetic patients (age 61 ± 4 years) and 18 healthy subjects (age 67 ± 1.4 years), to a standard diet (>20 AGE equivalents [Eq]/day) or an isocaloric AGE-restricted diet (<10 AGE Eq/day) for 4 months. Circulating metabolic and inflammatory markers were assessed. Expression and activities of AGER1 and SIRT1 were examined in patients’ peripheral blood mononuclear cells (PMNC) and in AGE-stimulated, AGER1-transduced (AGER1+), or AGER1-silenced human monocyte-like THP-1 cells. RESULTS: Insulin and homeostasis model assessment, leptin, tumor necrosis factor-α and nuclear factor-κB p65 acetylation, serum AGEs, and 8-isoprostanes decreased in AGE-restricted type 2 diabetic patients, whereas PMNC AGER1 and SIRT1 mRNA, and protein levels normalized and adiponectin markedly increased. AGEs suppressed AGER1, SIRT-1, and NAD+ levels in THP-1 cells. These effects were inhibited in AGER1+ but were enhanced in AGER1-silenced cells. CONCLUSIONS: Food-derived pro-oxidant AGEs may contribute to IR in clinical type 2 diabetes and suppress protective mechanisms, AGER1 and SIRT1. AGE restriction may preserve native defenses and insulin sensitivity by maintaining lower basal OS.
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“In blood vessels, accumulated AGEs also interact with mononuclear, endothelial, and smooth muscle cells, resulting in cellular dysfunction, tissue damage, and atherosclerosis development55–57,59.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [55]
In the citing paper
“Restriction of dietary AGEs can reduce and/or reverse these effects by enhancing insulin sensitivity and upregulating AGE-R1 and SIRT1 expression while suppressing NF-κB, tumor necrosis factor-alpha (TNF-α), leptin, and serum AGEs in type 2 DM55.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [55]
In the citing paper
“The accumulation and exposure to AGEs exacerbate oxidative stress and inflammation and initiate the oxidation of low-density lipoproteins (LDLs), which are harmful to cardiovascular function.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [55]
In the citing paper
“Endogenous and exogenous AGEs provoke the initiation and progression of NAFLD.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [55]
In the citing paper
“The aggregation of AGEs decreases the levels of the most important cellular antioxidant peptides, glutathione (GSH), SIRT1, and tissue inhibitor of metalloproteinase 3 (TIMP3), accompanied by increased oxidative stress and inflammation, promoting inflammatory liver injury and fibrosis in experimental animal models and NAFLD patients55–57,124–126.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [55]
In the citing paper
“AGER1 can counteract AGE-induced oxidative stress [61,62] as well as inhibit the activation of NF-𝜅B by promoting a sirtuin1-dependent deacetylation and suppression of NF-𝜅B.[63,64]”
From The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction (2021) · cites this paper as [63]
In the citing paper
“with an AGE-restricted diet improving insulin sensitivity in T2DM with a normalization of the expression of AGER1 and sir-tuin1 as well as a decrease in NF-𝜅B acetylation circulating TNF𝛼, serum AGEs, and leptin.[63]”
From The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction (2021) · cites this paper as [63]
In the citing paper
“In light of the central role of insulin in regulating energy balance, insulin resistance may be a mechanism underpinning the ability of AGEs to disrupt hypothalamic control of energy balance.[63,131,133]”
From The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction (2021) · cites this paper as [63]
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Citations
Cites
Inflammation and insulin resistance
Shoelson, S. E. (2006) · Journal of Clinical Investigation · doi:10.1172/jci29069 · Cited by 4,769
Macrophages, inflammation, and insulin resistance
Olefsky, J. M., & Glass, C. K. (2010) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021909-135846 · Cited by 2,733
Mammalian Sirtuins: Biological Insights and Disease Relevance
Haigis, M. C., & Sinclair, D. A. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev.pathol.4.110807.092250 · Cited by 2,085
Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk
Malik, V. S., Popkin, B. M., Bray, G. A., Després, J.-P., & Hu, F. B. (2010) · Circulation · doi:10.1161/circulationaha.109.876185 · Cited by 1,641
Increasing Prevalence of the Metabolic Syndrome Among U.S. Adults
Ford, E. S., Giles, W. H., & Mokdad, A. H. (2004) · Diabetes Care · doi:10.2337/diacare.27.10.2444 · Cited by 1,488
Advanced glycation end products in foods and a practical guide to their reduction in the diet
Uribarri, J., Woodruff, S., Goodman, S., Cai, W., Chen, X., Pyzik, R., Yong, A., Striker, G. E., & Vlassara, H. (2010) · Journal of the American Dietetic Association · doi:10.1016/j.jada.2010.03.018 · Cited by 1,289
Self-citationKoschinsky, T., He, C.-J., Mitsuhashi, T., Bucala, R., Liu, C., Buenting, C., Heitmann, K., & Vlassara, H. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.12.6474 · Cited by 792
Self-citationVlassara, H., Cai, W., Crandall, J., Goldberg, T., Oberstein, R., Dardaine, V., Peppa, M., & Rayfield, E. J. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.242407999 · Cited by 668
Self-citationDietary fat, insulin sensitivity and the metabolic syndrome
Riccardi, G., Giacco, R., & Rivellese, A. A. (2004) · Clinical Nutrition · doi:10.1016/j.clnu.2004.02.006 · Cited by 634
SIRT1 Exerts Anti-Inflammatory Effects and Improves Insulin Sensitivity in Adipocytes
Yoshizaki, T., Milne, J. C., Imamura, T., Schenk, S., Sonoda, N., Babendure, J. L., Lu, J.-C., Smith, J. J., Jirousek, M. R., & Olefsky, J. M. (2008) · Molecular and Cellular Biology · doi:10.1128/mcb.00705-08 · Cited by 420
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Gupta, A., & Uribarri, J. (2016) · Hormone Research in Paediatrics · doi:10.1159/000444053 · Cited by 4,023
Self-citationAdvanced Glycation End Products and Oxidative Stress in Type 2 Diabetes Mellitus
Nowotny, K., Jung, T., Höhn, A., Weber, D., & Grune, T. (2015) · Biomolecules · doi:10.3390/biom5010194 · Cited by 1,095
Advanced Glycation End Products and Diabetes Mellitus: Mechanisms and Perspectives
Khalid, M., Petroianu, G. A., & Adem, A. (2022) · Biomolecules · doi:10.3390/biom12040542 · Cited by 972
Advanced glycation endproducts in food and their effects on health
Poulsen, M. W., Hedegaard, R. V., Andersen, J. M., de Courten, B., Bügel, S., Nielsen, J., Skibsted, L. H., & Dragsted, L. O. (2013) · Food and Chemical Toxicology · doi:10.1016/j.fct.2013.06.052 · Cited by 751
Advanced Glycation End Products (AGE) and Diabetes: Cause, Effect, or Both?
Vlassara, H., & Uribarri, J. (2014) · Current Diabetes Reports · doi:10.1007/s11892-013-0453-1 · Cited by 594
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Metadata
- Authors
- Uribarri, J., Cai, W., Ramdas, M., Goodman, S., Pyzik, R., Chen, X., Zhu, L., Striker, G. E., & Vlassara, H.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Vlassara, Helen
- Venue
- Diabetes Care
- Publisher
- American Diabetes Association
- Published
- 2011-06-17
- Volume
- 34
- Issue
- 7
- Pages
- 1610-1616
- ISSN
- 0149-5992 (ISSN-L)
- 1935-5548
- PMC
- PMC3120204
- OpenAlex
- W2061906058
- Cited by
- 320
- References
- 26
- Citations by year
- 2026: 2 · 2025: 14 · 2024: 19 · 2023: 20 · 2022: 24 · 2021: 25 · 2020: 25 · 2019: 16 · 2018: 26 · 2017: 30 · 2016: 26 · 2015: 32 · 2014: 10 · 2013: 31 · 2012: 13
- FWCI
- 11.59
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Diabetes Care (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R37AG023188, R01AG009453)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK091231)
- National Center for Research Resources (M01RR000071)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- advanced glycation end products, insulin resistance, type 2 diabetes, SIRT1, oxidative stress, inflammation, NAD+, adiponectin, TNF-α, NF-κB p65 acetylation, 8-isoprostane, peripheral blood mononuclear cells, THP-1 cells
- MeSH terms
- Receptor for Advanced Glycation End Products, Aged, Cells, Cultured, Diabetes Mellitus, Type 2, Female, Humans, Hypoglycemic Agents, Inflammation, Insulin Resistance, Leukocytes, Mononuclear, Male, Middle Aged, Receptors, Immunologic, Glycation End Products, Advanced, Oxidative Stress, Sirtuin 1
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