Neurog3, a basic helix-loop-helix (bHLH) transcription factor, is of great significance in the development of pancreatic islet cells and enteroendocrine cells. In the pancreas, it is crucial for the generation of four major islet cell types (α, β, δ, and γ), and in the intestine, it drives the differentiation of enteroendocrine cells. Its activity is involved in cell fate determination pathways during organogenesis [1,2,3,6].

In mouse models, loss of Neurog3 led to depletion of intestinal enteroendocrine cells and an increase in goblet cells. Reduced Neurog3 gene dosage shifted enteroendocrine progenitors towards the goblet cell lineage, indicating that Neurog3 gene dosage controls the fate choice of enteroendocrine progenitors [2]. In humans, homozygous mutations of NEUROG3 manifest with neonatal or childhood diabetes. Mice lacking Neurog3 do not form pancreatic islet cells, including insulin-secreting beta cells, highlighting its essential role in pancreatic endocrine cell development [3,4,5].

In conclusion, Neurog3 is a master regulator in the development of pancreatic and intestinal endocrine cells. Studies using gene knockout (KO) mouse models have revealed its critical functions in cell fate determination and differentiation. Understanding the role of Neurog3 provides insights into the pathogenesis of diabetes and other related endocrine disorders, offering potential targets for therapeutic interventions in these disease areas [2,3,4,5].