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Role of obesity related inflammation in pathogenesis of peripheral artery disease in patients of type 2 diabetes mellitus

  • Review Article
  • Published:
Journal of Diabetes & Metabolic Disorders Aims and scope Submit manuscript

Abstract

Objective

Type 2 diabetes mellitus (T2DM) has emerged as one of the greatest global health challenges of twenty-first century. Visceral obesity is one of the most important determinant of insulin resistance (IR) as well as T2DM complications. Therefore this review focuses on the molecular mechanism of obesity induced inflammation, signaling pathways contributing to diabetes, as well as role of lifestyle interventions and medical therapies in the prevention and management of T2DM.

Method

Articles were searched on digital data base PubMed, Cochrane Library, and Web of Science. The key words used for search included Type 2 diabetes mellitus, obesity, insulin resistance, vascular inflammation and peripheral arterial disease.

Result

Visceral obesity is associated with chronic low grade inflammation and activation of immune systems which are involved in pathogenesis of obesity related IR and T2DM.

Conclusion

Metabolic dysregulation of adipose tissue leads to local hypoxia, misfolded/unfolded protein response and increased circulating free fatty acids, which in turn initiate inflammatory signaling cascades in the population of infiltrating cells. Mechanism that relates the role of adipocytokines with insulin sensitivity and glucose homeostasis might throw a light on the development of therapeutic interventions and subsequently might result in the reduction of vascular complications.

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Data Availability

Data supporting the findings of the study were derived from resources which are in public domain (https://www.ncbi.nlm.nih.gov/pmc/, https://scholar.google.com/) and included with doi along with references.

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Yadav, U., Kumar, N. & Sarvottam, K. Role of obesity related inflammation in pathogenesis of peripheral artery disease in patients of type 2 diabetes mellitus. J Diabetes Metab Disord 22, 175–188 (2023). https://doi.org/10.1007/s40200-023-01221-5

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