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

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.