Document Detail

Advanced Glycation End Products (AGE) and Diabetes: Cause, Effect, or Both?
MedLine Citation:
PMID:  24292971     Owner:  NLM     Status:  In-Data-Review    
Despite new and effective drug therapies, insulin resistance (IR), type 2 diabetes mellitus (T2D) and its complications remain major medical challenges. It is accepted that IR, often associated with over-nutrition and obesity, results from chronically elevated oxidant stress (OS) and chronic inflammation. Less acknowledged is that a major cause for this inflammation is excessive consumption of advanced glycation end products (AGEs) with the standard western diet. AGEs, which were largely thought as oxidative derivatives resulting from diabetic hyperglycemia, are increasingly seen as a potential risk for islet β-cell injury, peripheral IR and diabetes. Here we discuss the relationships between exogenous AGEs, chronic inflammation, IR, and T2D. We propose that under chronic exogenous oxidant AGE pressure the depletion of innate defense mechanisms is an important factor, which raises susceptibility to inflammation, IR, T2D and its complications. Finally we review evidence on dietary AGE restriction as a nonpharmacologic intervention, which effectively lowers AGEs, restores innate defenses and improves IR, thus, offering new perspectives on diabetes etiology and therapy.
Helen Vlassara; Jaime Uribarri
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Current diabetes reports     Volume:  14     ISSN:  1539-0829     ISO Abbreviation:  Curr. Diab. Rep.     Publication Date:  2014 Jan 
Date Detail:
Created Date:  2013-12-02     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101093791     Medline TA:  Curr Diab Rep     Country:  United States    
Other Details:
Languages:  eng     Pagination:  453     Citation Subset:  IM    
Department of Geriatrics, Mount Sinai School of Medicine, New York, NY, USA.
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