Methylglyoxal: possible link between hyperglycaemia and immune suppression?

Trends in Endocrinology and Metabolism : TEM
Claire L Price, Stella C Knight


No matter the cause of diabetes, the result is always hyperglycaemia. This excess glucose metabolism drives several damage pathways and raises concentrations of the reactive dicarbonyl, methylglyoxal (MG). MG can modify the structure and function of target molecules by forming advanced glycation end-products (AGEs) that act through their receptor (RAGE) to perpetuate vascular and neuronal injury responsible for long-term complications of diabetes. Diabetes patients also suffer lower resistance to many common infections, although the cause(s) for this lower resistance remains elusive. Here, we review recent evidence concerning immune suppression in diabetes and discuss the effects of MG on components of the immune system. We suggest that MG could be a missing link between hyperglycaemia and immune suppression in diabetes.


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Related Concepts

Diabetes Mellitus
Hyperglycemia, Postprandial
Therapeutic Immunosuppression
Glycosylation End Products, Advanced
Oxidative Stress
Blood Vessel
C-reactive protein

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