RÉSUMÉ
The dysregulation of the ß-cell functional mass, which is a reduction in the number of ß-cells and their ability to secure adequate insulin secretion, represents a key mechanistic factor leading to the onset of type 2 diabetes (T2D). Obesity is recognised as a leading cause of ß-cell loss and dysfunction and a risk factor for T2D. The natural history of ß-cell failure in obesity-induced T2D can be divided into three steps: (1) ß-cell compensatory hyperplasia and insulin hypersecretion, (2) insulin secretory dysfunction, and (3) loss of ß-cell mass. Adipose tissue (AT) secretes many hormones/cytokines (adipokines) and fatty acids that can directly influence ß-cell function and viability. As this secretory pattern is altered in obese and diabetic patients, it is expected that the cross-talk between AT and pancreatic ß-cells could drive the maintenance of the ß-cell integrity under physiological conditions and contribute to the reduction in the ß-cell functional mass in a dysmetabolic state. In the current review, we summarise the evidence of the ability of the AT secretome to influence each step of ß-cell failure, and attempt to draw a timeline of the alterations in the adipokine secretion pattern in the transition from obesity to T2D that reflects the progressive deterioration of the ß-cell functional mass.
