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AGE restriction in diabetes mellitus: a paradigm shift
Helen Vlassara1, Gary E Striker
1Division of Experimental Diabetes and Aging, Brookdale Department of Geriatrics, Mount Sinai School of Medicine, New York, NY 10029, USA. helen.vlassara@ mssm.edu
Nature Reviews. Endocrinology
|May 26, 2011
Summary
Advanced glycation endproducts (AGEs) in processed foods promote oxidative stress and inflammation, initiating type 1 and type 2 diabetes. Restricting dietary AGEs can prevent diabetes and its complications.
Area of Science:
- Metabolic disorders
- Nutritional science
- Environmental health
Background:
- Elevated oxidative stress and inflammation are precursors to type 1 and type 2 diabetes mellitus.
- Increasing incidence of diabetes and obesity suggests environmental, not genetic, causes.
- Thermally processed foods contain pro-oxidant advanced glycation endproducts (AGEs), contributing to overnutrition and inflammation.
Purpose of the Study:
- To investigate the role of food-derived AGEs as environmental initiators of oxidative stress and diabetes.
- To explore AGE restriction as a therapeutic strategy for preventing diabetes and its complications.
Main Methods:
- Studies in genetic and nongenetic animal models of diabetes.
- Analysis of data from healthy humans and individuals with diabetes mellitus.
- Focus on AGE restriction without altering energy or nutrient intake.
Main Results:
- Dietary AGEs promote oxidative stress, inflammation, and injury to insulin-producing and insulin-responsive cells, driving diabetes development.
- AGE restriction in mice reduced oxidative stress, alleviated inflammation, prevented diabetes and complications, and extended lifespan.
- In humans, high dietary AGEs correlate with insulin resistance and inflammation; AGE restriction improves these markers.
Conclusions:
- Food-derived AGEs are novel initiators of oxidative stress that precedes diabetes mellitus.
- AGE restriction represents a paradigm shift in therapeutic strategies for diabetes and its associated complications.
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