Gut as a source of new β‐cells and Segi's cap

A deficit of β‐cells is a salient feature in both type 1 and type 2 diabetes mellitus. Due to the absolute lack of supplying β‐cells for organ or cell transplantation, there is an urgent need to explore the efficient method to generate insulin‐producing cells. Cell conversion of intestinal cryptic epithelial cells to insulin‐producing β‐like cells is a novel and promising therapeutic target. Activation of β‐cell differentiation factors or modulation of terminally differentiated factors with forkhead homeobox O1 effectively induced such conversion, and suppressed hyperglycemia in streptozotocin‐induced and non‐obese diabetic (NOD) mice. Segi's cap, which was discovered >80 years ago, is composed of an aggregation of primitive granulated enteroendocrine cells, enterochromaffin cells, Paneth cells and goblet cells in the intestinal villi, and is only detected at the fetal stage. Its role has long been unknown, but the present study disclosed that it likely provides an underpin of newly generated β‐like cells.