Vitamin E Levels in Ethnic Communities in Malaysia and Its Relation to Glucose Tolerance, Insulin Resistance and Advanced Glycation End Products: A Cross-Sectional Study

Malaysian national morbidity surveys on diabetic prevalence have shown ethnical variation among prediabetic and diabetic populations. In our attempt to understand this variation, we studied the α-tocopherol, insulin resistance, β-cell function and receptor of advanced glycation end-products (RAGE) levels, as risk factors of type 2 diabetes, among the different ethnicities. In total, 299 subjects of Malay, Chinese, Indian and aboriginal Orang Asli (OA) heritage were recruited from urban and rural areas of Malaysia by stratified random sampling. Serum α-tocopherol concentrations were measured using high performance liquid chromatography (HPLC) and insulin concentrations were measured using enzyme-linked immunosorbent assay (ELISA). In subjects with pre-diabetes, OAs had the highest α-tocopherol level, followed by Chinese and Malays (0.8938, 0.8564 and 0.6948 respectively; p < 0.05). In diabetic subjects, Malays had significantly higher RAGE levels compared to Chinese and Indians (5579.31, 3473.40 and 3279.52 pg/mL respectively, p = 0.001). Low α-tocopherol level (OR = 3.021, p < 0.05) and high insulin resistance (OR = 2.423, p < 0.05) were linked strongly to the development of pre-diabetes. Low β-cell function (OR = 5.657, p < 0.001) and high RAGE level (OR = 3.244, p < 0.05) were linked strongly to the development of diabetes from pre-diabetes. These factors might be involved in the development of diabetes, along with genetic and environmental factors.

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Advanced Glycation End Products and Insulin Resistance

Current Pharmaceutical Design ◽

10.2174/138161208784139747 ◽

2008 ◽

Vol 14 (10) ◽

pp. 987-989 ◽

Cited By ~ 89

Author(s):

Hiroyuki Unoki ◽

Sho-ichi Yamagishi

Keyword(s):

Insulin Resistance ◽

Advanced Glycation End Products ◽

Advanced Glycation ◽

Glycation End Products ◽

End Products

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Endogenous Secretory Receptor for Advanced Glycation End Products Protects Endothelial Cells from AGEs Induced Apoptosis

BioMed Research International ◽

10.1155/2018/8216578 ◽

2018 ◽

Vol 2018 ◽

pp. 1-8 ◽

Cited By ~ 3

Author(s):

Guomin Yang ◽

Yinqiong Huang ◽

Xiaohong Wu ◽

Xiahong Lin ◽

Jinting Xu ◽

...

Keyword(s):

Endothelial Cells ◽

Endothelial Cell ◽

Advanced Glycation End Products ◽

Proinflammatory Cytokine ◽

Enzyme Linked Immunosorbent Assay ◽

Advanced Glycation ◽

Expression Levels ◽

Qrt Pcr ◽

Glycation End Products ◽

End Products

Endogenous secretory receptor for advanced glycation end products (esRAGE) binds extracellular RAGE ligands and blocks RAGE activation on the cell surface, protecting endothelial cell function. However, the underlying mechanism remains unclear. Endothelial cells overexpressing the esRAGE gene were generated using a lentiviral vector. Then, quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) were used to assess esRAGE mRNA and protein levels, respectively. Hoechst-PI double staining was used to assess apoptosis. Western blot and qRT-PCR were used to assess the expression levels of apoptosis-related factors and the proinflammatory cytokine NF-кB. Compared with the control group, AGEs significantly induced endothelial cell apoptosis, which was significantly reduced by esRAGE overexpression. Incubation with AGEs upregulated the proapoptotic factor Bax and downregulated the antiapoptotic factor Bcl-2. Overexpression of esRAGE reduced Bax expression induced by AGEs and increased Bcl-2 levels. Furthermore, AGEs increased the expression levels of proinflammatory cytokine NF-кB, which were reduced after esRAGE overexpression. esRAGE protects endothelial cells from AGEs associated apoptosis, by downregulating proapoptotic (Bax) and inflammatory (NF-кB) factors and upregulating the antiapoptotic factor Bcl-2.

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The Modern Western Diet Rich in Advanced Glycation End-Products (AGEs): An Overview of Its Impact on Obesity and Early Progression of Renal Pathology

Nutrients ◽

10.3390/nu11081748 ◽

2019 ◽

Vol 11 (8) ◽

pp. 1748 ◽

Cited By ~ 12

Author(s):

Arianna Bettiga ◽

Francesco Fiorio ◽

Federico Di Marco ◽

Francesco Trevisani ◽

Annalisa Romani ◽

...

Keyword(s):

Chronic Diseases ◽

Advanced Glycation End Products ◽

Cell Function ◽

Advanced Glycation ◽

Covalent Bonds ◽

Physiological Processes ◽

Glycation End Products ◽

End Products ◽

And Function

Advanced glycation end-products (AGEs) are an assorted group of molecules formed through covalent bonds between a reduced sugar and a free amino group of proteins, lipids, and nucleic acids. Glycation alters their structure and function, leading to impaired cell function. They can be originated by physiological processes, when not counterbalanced by detoxification mechanisms, or derive from exogenous sources such as food, cigarette smoke, and air pollution. Their accumulation increases inflammation and oxidative stress through the activation of various mechanisms mainly triggered by binding to their receptors (RAGE). So far, the pathogenic role of AGEs has been evidenced in inflammatory and chronic diseases such as chronic kidney disease, cardiovascular disease, and diabetic nephropathy. This review focuses on the AGE-induced kidney damage, by describing the molecular players involved and investigating its link to the excess of body weight and visceral fat, hallmarks of obesity. Research regarding interventions to reduce AGE accumulation has been of great interest and a nutraceutical approach that would help fighting chronic diseases could be a very useful tool for patients’ everyday lives.

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Relevance of Receptor for Advanced Glycation end Products (RAGE) in Murine Antibody-Mediated Autoimmune Diseases

International Journal of Molecular Sciences ◽

10.3390/ijms20133234 ◽

2019 ◽

Vol 20 (13) ◽

pp. 3234

Author(s):

Alexandra Eichhorst ◽

Christoph Daniel ◽

Rita Rzepka ◽

Bettina Sehnert ◽

Falk Nimmerjahn ◽

...

Keyword(s):

B Cells ◽

Autoimmune Diseases ◽

Advanced Glycation End Products ◽

Plasma Cells ◽

Inflammatory Responses ◽

Joint Inflammation ◽

Enzyme Linked Immunosorbent Assay ◽

Advanced Glycation ◽

Glycation End Products ◽

End Products

It is incompletely understood how self-antigens become targets of humoral immunity in antibody-mediated autoimmune diseases. In this context, alarmins are discussed as an important level of regulation. Alarmins are recognized by various receptors, such as receptor for advanced glycation end products (RAGE). As RAGE is upregulated under inflammatory conditions, strongly binds nucleic acids and mediates pro-inflammatory responses upon alarmin recognition, our aim was to examine its contribution to immune complex-mediated autoimmune diseases. This question was addressed employing RAGE−/− animals in murine models of pristane-induced lupus, collagen-induced, and serum-transfer arthritis. Autoantibodies were assessed by enzyme-linked immunosorbent assay, renal disease by quantification of proteinuria and histology, arthritis by scoring joint inflammation. The associated immune status was determined by flow cytometry. In both disease entities, we detected tendentiously decreased autoantibody levels in RAGE−/− mice, however no differences in clinical outcome. In accordance with autoantibody levels, a subgroup of the RAGE−/− animals showed a decrease in plasma cells, and germinal center B cells and an increase in follicular B cells. Based on our results, we suggest that RAGE deficiency alone does not significantly affect antibody-mediated autoimmunity. RAGE may rather exert its effects along with other receptors linking environmental factors to auto-reactive immune responses.

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Advanced Glycation End Products Inhibition Restores Sphingolipid Rheostat in Mice Liver and Prevents Diet-Induced Insulin Resistance

Free Radical Biology and Medicine ◽

10.1016/j.freeradbiomed.2016.10.465 ◽

2016 ◽

Vol 100 ◽

pp. S176

Author(s):

Alessia Sofia Cento ◽

Debora Nigro ◽

Fausto Chiazza ◽

Federica Dal Bel ◽

Francesco Romaniell ◽

...

Keyword(s):

Insulin Resistance ◽

Advanced Glycation End Products ◽

Advanced Glycation ◽

Glycation End Products ◽

End Products ◽

Mice Liver

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Serum Levels of Advanced Glycation End Products (AGEs) are Independent Correlates of Insulin Resistance in Nondiabetic Subjects

Cardiovascular Therapeutics ◽

10.1111/j.1755-5922.2010.00177.x ◽

2010 ◽

Vol 30 (1) ◽

pp. 42-48 ◽

Cited By ~ 64

Author(s):

Nobuhiro Tahara ◽

Sho-ichi Yamagishi ◽

Takanori Matsui ◽

Masayoshi Takeuchi ◽

Yoshikazu Nitta ◽

...

Keyword(s):

Insulin Resistance ◽

Advanced Glycation End Products ◽

Serum Levels ◽

Advanced Glycation ◽

Glycation End Products ◽

End Products

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Elevated level of the soluble receptor for advanced glycation end-products involved in sarcopenia: an observational study

BMC Geriatrics ◽

10.1186/s12877-021-02487-1 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Shou-En Wu ◽

Yi-Lin Chiu ◽

Tung-Wei Kao ◽

Wei-Liang Chen

Keyword(s):

Muscle Mass ◽

Advanced Glycation End Products ◽

Community Dwelling ◽

Enzyme Linked Immunosorbent Assay ◽

Health Examination ◽

Soluble Receptor ◽

Advanced Glycation ◽

Srage Level ◽

Glycation End Products ◽

End Products

Abstract Background The soluble receptor for advanced glycation end products (sRAGE) has been proposed to serve as a marker for disease severity, but its role in sarcopenia, an age-related progressive loss of muscle mass and function, remains elusive. This study examines the association between sRAGE and sarcopenia. Methods A total of 314 community-dwelling elderly adults who had their health examination at Tri-Service General Hospital from 2017 to 2019 underwent protein analysis with enzyme-linked immunosorbent assay. The relationship with sarcopenia and its detailed information, including components and diagnosis status, were examined using linear and logistic regressions. Results As for sarcopenia components, low muscle mass (β = 162.8, p = 0.012) and strength (β = 181.31, p = 0.011) were significantly correlated with sRAGE, but not low gait speed (p = 0.066). With regard to disease status, confirmed sarcopenia (β = 436.93, p < 0.001), but not probable (p = 0.448) or severe sarcopenia (p = 0.488), was significantly correlated with sRAGE. In addition, females revealed a stronger association with sRAGE level by showing significant correlations with low muscle mass (β = 221.72, p = 0.014) and low muscle strength (β = 208.68, p = 0.043). Conclusions sRAGE level showed a positive association with sarcopenia, illustrating its involvement in the evolution of sarcopenia. This association is more evident in female groups, which may be attributed to the loss of protection from estrogen in postmenopausal women. Utilizing sRAGE level as a prospective marker for sarcopenia deserves further investigation in future studies.

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