Type 2 Diabetes: Cellular and Molecular Pathophysiology

Dear Colleagues,

Type 2 diabetes (T2D) is one of the most common metabolic disorders worldwide, and its development is primarily caused by a combination of two main factors: defective insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues, such as muscle, adipose, and liver, to respond to insulin. Glucose homeostasis requires a tight regulation between glycemia and insulin synthesis, release, and activity. Defects in any of these processes can lead to a metabolic imbalance responsible for the development of impaired glucose regulation. This Special Issue offers an open access forum that aims to bring together a collection of original research and review articles addressing our expanding knowledge of the cellular and molecular mechanisms that underlie the progression from normal glucose tolerance to T2D. We hope to provide a useful resource for understanding the various factors that affect glucose homeostasis, some of which could ultimately be used in the development of better prediction models for the disease, or could potentially serve as therapeutic targets. Suggested potential topics include new metabolic pathways for the development of T2D, the impact of obesity on T2D, the beta cell, lessons learned from monogenic diabetes, and the pathophysiology of T2D complications.

Dr. Leslie Joan Baier
Guest Editor

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