Research Highlights

doi:10.1038/nindia.2013.126 Published online 23 September 2013

What triggers inflammation in diabetics?

Over activation of certain proteins that modulate the immuno-metabolism could be the reason behind sub-clinical inflammation and insulin resistance among patients with type 2 diabetes, new research has shown .

The correlation between the immune system and metabolic disorders is well established. However, the specific mechanism through which inflammation causes insulin resistance and diabetes is still not clear.

Recent studies have found that specific pattern recognition receptors (PRRs), including nucleotide-binding oligomerization domain proteins (NODs), mediate chronic inflammation. Interestingly, these NODs detect gut bacterial flora and their cell-wall components, respond to dietary factors and phytochemicals, modulate the innate immune response and thereby influence both insulin secretion and insulin action.

Researchers have now shown that increased expression and activation of NODs in monocytes is an underlying trigger of inflammation and insulin resistance in diabetes patients. "While Asian Indians are considered highly insulin-resistant and more prone to diabetes, this research throws light on the inflammatory underpinnings of insulin resistance and diabetes", says Muthuswamy Balasubramanyam, a co-author of the study.

Integrating traditional markers of blood glucose regulation with inflammatory and metabolic biomarkers could make for a better strategy for prevention and treatment of type 2 diabetes, he adds. 

The authors of this work are from: Madras Diabetes Research Foundation, Dr. Mohan's Diabetes Specialities Centre & National Institutes of Health-International Center for Excellence in Research, Chennai, India.


References

  1. Shiny, A. et al. Convergence of innate immunity and insulin resistance as evidenced by increased nucleotide oligomerization domain (NOD) expression and signaling in monocytes from patients with type 2 diabetes. Cytokine (2013) doi: 10.1016/j.cyto.2013.08.003