Ruiying Hu

Key words Insulin Diabetes stress response insulin secretion glucose uORF translation Introduction Type 2 diabetes (T2D) arises when endocrine islet β cells cannot secrete enough insulin to regulate blood glucose homeostasis (1, 2). This disease usually starts with obesity-related insulin resistance. In response, β cells increase their mass and secretory function to boost insulin output. This adaptation (or compensation) can maintain lifetime glucose homeostasis in most obese subjects (3).

Abstract In response to obesity-related metabolic stress, islet β-cells adapt (or compensate) by increasing their secretory function and mass. Yet, for unknown reasons, this compensation is reversed in some individuals at some point to induce β-cell failure and overt type 2 diabetes (T2D). We have previously shown that transcription factor Myt3 (St18) and its paralogs, Myt1 and Myt2, prevent β-cell failure.

Abstract Genetic and environmental factors together cause islet β-cell failure, leading to Type 2 diabetes (T2D). Yet how they integrate to regulate β-cells remains largely unclear. Here, we examined how two members of the Myelin transcription factor family (MYT1, 2, and 3) prevent human β-cell failure under obesity-related stress. We have reported that obesity-related nutrient levels induce these factors. They prevent β-cell failure in mouse islets and human β-cell lines.