Pancreatic beta-cell loss and preservation in type 2 diabetes.

摘要: Abstract Background : In most individuals, the need to respond progressive states of insulin resistance is met by increasing production. For insulin-resistant patients, however, balance between supply and demand may fail from loss pancreatic beta-cell function, eventually leading type 2 diabetes mellitus. Objective The aim this review was discuss current concepts underlying potential failure in progression toward therapies that alter process. Methods Data included were identified through a MEDLINE search for articles published 1966 April 2003. Search terms used beta cell, diabetes, resistance, obesity, cardiovascular disease, thiazolidinediones , metformin . Results Evidence function include altered conversion proinsulin insulin, changes pulsed oscillatory secretion, quantitative reductions release. Potential mechanisms are glucose toxicity, lipotoxicity, poor tolerance increased secretory demand, reduction mass. Conclusion Current clinical management focused on treatment signs symptoms late-stage disease rather than addressing causes, which be amenable currently available therapies, based broad understanding existing data, practice experience, rational speculation.