An update on the role of inflammation in insulin resistance and islet β cell failure- A crosstalk between immune cells, adipose tissue, cytokines, and oxidative stress
Krishnaraju Venkatesan, Premalatha Paulsamy, Saud Alqahtani, Yahya I. Asiri, Taha Alqahtani, Ali Alqahtani, Durgaramani Sivadasan, Rehab Ahmed, Hassabelrasoul Elfadil, Khalid A. Asseri, Absar Ahmed Qureshi, Malarkodi Velraj, Kalpana Krishnaraju
Abstract
One of the characteristics of type 2 diabetes mellitus (T2DM) is the growing malfunctioning of β-cells and the presence of insulin resistance. The recent literature on this aspect is reviewed in this paper, with a particular emphasis placed on the inflammatory pathways that are responsible for the pathophysiology of type 2 diabetes. As a result of these recent discoveries, our understanding of how inflammation contributes to an increased risk of developing type 2 diabetes is being improved. This review focuses on the intricate relationship between immune cells, adipose tissue, cytokines, chemokines, hypoxia, oxidative stress, increased fatty acids, and hyperglycemia. These factors play a significant role in impacting β-cell dysfunction and insulin resistance. Our primary focus has been on the latest developments in the evolution of type 2 diabetes, which encompass a variety of inflammatory processes that have the potential to generate insulin resistance, as well as dysfunctional β-cells. In conclusion, it has been indicated that inflammation plays a significant role in the etiology of type 2 diabetes, and that this role cannot be ignored. The ever-evolving notion of insulin resistance and Islet β cell failure, both of which possess inflammatory components, presents unprecedented prospects for the implementation of anti-inflammatory treatments in order to rectify the metabolic repercussions of type 2 diabetes.