Abstract
Type 2 diabetes mellitus (T2DM) is developed due to the development of insulin resistance (IR) and pancreatic β cell dysfunction with subsequent hyperglycaemia. Hyperglycaemia-induced oxidative stress and endoplasmic reticulum (ER) stress enhances inflammatory disorders, leading to further pancreatic β cell dysfunction. These changes trigger autophagy activation, which recycles cytoplasmic components and injured organelles. Autophagy regulates pancreatic β cell functions by different mechanisms. Though the exact role of autophagy in T2DM is not completely elucidated, that could be beneficial or detrimental. Therefore, this review aims to discuss the exact role of autophagy in the pathogenesis of T2DM.