An α-glucosidase inhibitor, acarbose treatment decreases serum levels of glyceraldehyde-derived advanced glycation end products (AGEs) in patients with type 2 diabetes

Tsunosue, Miwako; Mashiko, Naomi; Ohta, Y.; Matsuo, Y.; Ueda, Kenichi; Ninomiya, Masayuki; Tanaka, Shoichi; Hoshiko, Masaru; Yoshiyama, Yasutsugu; Takeuchi, Masayoshi; Ueda, Shinichiro; Yamagishi, Sho‐ichi

doi:10.1007/s10238-009-0074-9

Cited by 30 publications

(34 citation statements)

References 9 publications

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“…Moreover, atrovastatin, pioglitazone and α-glucosidase inhibitor have been shown to significantly decrease serum levels of glyceraldehyde-derived AGEs, which are associated with reduced biomarker levels for organ damage in diabetic, chronic kidney disease or NASH subjects (120,(124)(125)(126)(127)(128).…”

Section: Measuring Serum Levels Of Ages and Its Clinical Utilitymentioning

confidence: 99%

Advanced Glycation End Products: A Molecular Target for Vascular Complications in Diabetes

Yamagishi

Nakamura

Suematsu

et al. 2015

Mol Med

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141

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Section: Measuring Serum Levels Of Ages and Its Clinical Utilitymentioning

confidence: 99%

Advanced Glycation End Products: A Molecular Target for Vascular Complications in Diabetes

Yamagishi

Nakamura

Suematsu

et al. 2015

Mol Med

Self Cite

141

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“…An increasing body of evidence suggests that TAGE are involved in the pathogeneses of various disorders including hypertension, Alzheimer's disease, diabetic vascular complications, CVD, NAFLD/NASH, and cancer growth and metastasis [7,8,[18][19][20][21][22][23]79,[87][88][89][90][91]114,[121][122][123][124][125][126] . We found evidence that TAGE are involved in the pathogenesis of NASH in humans [7,23,114] .…”

Section: Resultsmentioning

confidence: 99%

“…In recent studies, we found that: (1) the serum concentration of TAGE, but not CML, was independently associated with HOMA-IR in non-diabetic subjects [87] ; (2) in T2DM patients, the serum TAGE concentration, but not those of Glu-AGEs or hemoglobin A1c (HbA1c), can be used as a biomarker of cumulative postprandial hyperglycemia [88] ; (3) the serum concentration of TAGE, but not those of HbA1c or CML, was demonstrated to be an independent predictor of vascular inflammation (as evaluated by [ 18 F] fluorodeoxyglucose-positron emission tomography in outpatients who visited Kurume University Hospital) [89] ; (4) in healthy subjects, the serum TAGE concentration was found to be independently associated with a reduction in the number of circulating EPC and the impairment of the migratory activity of EPC [90] ; and (5) a Japanese trial assessing the utility of pitavastatin and atorvastatin as treatments for acute coronary syndrome reported that high baseline TAGE concentrations were associated with plaque progression [91] . These results suggested that the serum TAGE concentration, but not those of HbA1c, CML, or Glu-AGEs, might be a useful biomarker for predicting atherosclerosis progression and future cardiovascular events.…”

Section: Putative Molecular Mechanisms Responsible For the Associatiomentioning

confidence: 99%

“…In a previous study, 50 mg acarbose (dosing schedule: thrice a day for a 12-wk period) were administered to 13 Japanese T2DM patients who were free from inflammatory conditions, atherosclerotic heart disease, and microangiopathy and had never taken oral hypoglycemic agents. The patients' serum TAGE concentrations as well as their serum levels of other biological molecules were assessed before and after the administration of acarbose [88] . The DM patients' serum free fatty acid and TAGE concentrations had fallen significantly after 12 wk' acarbose treatment.…”

Section: The Inhibition Of Tage Synthesis: Acarbosementioning

confidence: 99%

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Involvement of the TAGE-RAGE system in non-alcoholic steatohepatitis: Novel treatment strategies

Takeuchi

Takino

Sakasai-Sakai

et al. 2014

WJH

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Non-alcoholic fatty liver disease (NAFLD) is a major cause of liver disease around the world. It includes a spectrum of conditions from simple steatosis to non-alcoholic steatohepatitis (NASH) and can lead to fibrosis, cirrhosis, liver failure, and/or hepatocellular carcinoma. NAFLD is also associated with other medical conditions such as obesity, diabetes mellitus (DM), metabolic syndrome, hypertension, insulin resistance, hyperlipidemia, and cardiovascular disease (CVD). In diabetes, chronic hyperglycemia contributes to the development of both macro-and microvascular conditions through a variety of metabolic pathways. Thus, it can cause a variety of metabolic and hemodynamic conditions, including upregulated advanced glycation end-products (AGEs) synthesis. In our previous study, the most abundant type of toxic AGEs (TAGE); i.e. , glyceraldehyde-derived AGEs, were found to make a significant contribution to the pathogenesis of DM-induced angiopathy. Furthermore, accumulating evidence suggests that the binding of TAGE with their receptor (RAGE) induces oxidative damage, promotes inflammation, and causes changes in intracellular signaling and the expression levels of certain genes in various cell populations including hepatocytes and hepatic stellate cells. All of these effects could facilitate the pathogenesis of hypertension, cancer, diabetic vascular complications, CVD, dementia, and NASH. Thus, inhibiting TAGE synthesis, preventing TAGE from binding to RAGE, and downregulating RAGE expression and/or the expression of associated effector molecules all have potential as therapeutic strategies against NASH. Here, we examine the contributions of RAGE and TAGE to various conditions and novel treatments that target them in order to prevent the development and/or progression of NASH. Key words: Non-alcoholic fatty liver disease; Non-alcoholic steatohepatitis; Advanced glycation end-products; Toxic advanced glycation end-products; Receptor for advanced glycation end-products; Toxic advanced glycation end-products-receptor for advanced glycation end-products system; Diabetes mellitus; Cardiovascular disease; Dietary fructose; Dietary advanced glycation end-products TOPIC HIGHLIGHT

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“…[84,85] Patients with type 2 diabetes treated with acarbose have reduced serum levels of glyceraldehyde-derived AGEs. [86] Acarbose treatment can significantly reduce the level of some inflammatory factors that are present in higher levels in diabetes patients than healthy individuals including AGEs. [87] In addition, acarbose has been shown to inhibit the formation of aortic collagen glycosylation in diabetic rats.…”

Section: ɑ-Glucosidase Inhibitorsmentioning

confidence: 99%

Hypoglycemic Drugs and Advanced Glycation End products

2019

ARC Journal of Diabetes and Endocrinology

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Recent data showed that 9.1% of adults worldwide have diabetes, and 318 million adults have a high risk of developing diabetes in the future. Diabetes and its complications have serious impact on human health. In the early stages of diabetes, excessive advanced glycation endproducts (AGEs) accumulate in the body and bind to its receptor RAGE, which impairs glucose regulation. In the later stages of diabetes, increased blood glucose can accelerate the production of more AGEs. AGEs play a pivotal role in the development of diabetes and its complications. In recent years, AGEs have become one of the research hotspots. The search for potential drug targets that can block or reduce the accumulation of AGEs has attracted increasing attention. This review summarizes the role of AGEs and the effects of various hypoglycemic agents on AGEs from the perspective of mechanisms, in order to provide reference for the further search for targeted drugs against AGEs.

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An α-glucosidase inhibitor, acarbose treatment decreases serum levels of glyceraldehyde-derived advanced glycation end products (AGEs) in patients with type 2 diabetes

Cited by 30 publications

References 9 publications

Advanced Glycation End Products: A Molecular Target for Vascular Complications in Diabetes

Advanced Glycation End Products: A Molecular Target for Vascular Complications in Diabetes

Involvement of the TAGE-RAGE system in non-alcoholic steatohepatitis: Novel treatment strategies

Hypoglycemic Drugs and Advanced Glycation End products

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