Pancreatic beta cells are the only cell type in our body capable of producing and secreting insulin to instruct the insulin-sensitive cells and tissues of our bodies to absorb nutrients after a meal. Accurate control of insulin release is of critical importance; too little insulin leads to diabetes, while an excess of insulin can cause potentially fatal hypoglycaemia. Yet, the pancreas of most people will control insulin secretion safely and effectively over decades and in response to glucose excursions driven by tens of thousands of meals. Because we only become aware of the important contributions of the pancreas when it fails to maintain glucose homeostasis, it is easy to forget just how well insulin release from a healthy pancreas is matched to insulin need to ensure stable blood glucose levels. Beta cells achieve this feat by extensive crosstalk with the rest of the endocrine cell types in the islet, notably the glucagon-producing alpha cells and somatostatin-producing delta cells. Here I will review the important paracrine contributions that each of these cells makes to the stimulation and subsequent inhibition of insulin release in response to a transient nutrient stimulation, and make the case that a breakdown of this local crosstalk contributes to the pathophysiology of diabetes.

胰腺 β 细胞是我们体内唯一能够产生和分泌胰岛素以指导我们身体的胰岛素敏感细胞和组织在餐后吸收营养的细胞类型。准确控制胰岛素释放至关重要；过少的胰岛素会导致糖尿病，而过多的胰岛素会导致潜在的致命性低血糖症。然而，大多数人的胰腺将在几十年内安全有效地控制胰岛素分泌，并应对数万顿饭引起的葡萄糖偏移。因为我们只有在胰腺无法维持葡萄糖稳态时才会意识到胰腺的重要贡献，所以很容易忘记健康胰腺的胰岛素释放与确保稳定血糖水平的胰岛素需求的匹配程度。Beta 细胞通过与胰岛中其他内分泌细胞类型（特别是产生胰高血糖素的 alpha 细胞和产生生长抑素的 delta 细胞）进行广泛的串扰来实现这一壮举。在这里，我将回顾这些细胞中的每一个对刺激和随后抑制胰岛素释放的重要旁分泌贡献，以响应短暂的营养刺激，并说明这种局部串扰的破坏有助于糖尿病的病理生理学。