Abstract：
Insulin, a key hormone produced by pancreatic beta cells precisely regulates glucose metabolism in vertebrates. In type 1 diabetes, the beta cell mass is destroyed, a process triggered by a combination of environmental and genetic factors. This ultimately results in absolute insulin deficiency and dysregulated glucose metabolism resulting in a number of detrimental pathophysiological effects. The traditional focus of treating type 1 diabetes has been to control blood sugar levels through the administration of exogenous insulin. Newer approaches aim to replace the beta cell mass through pancreatic or islet transplantation. Type 2 diabetes results from a relative insulin deficiency for the prevailing insulin resistance. Treatments are generally aimed at reducing insulin resistance and/or augmenting insulin secretion and the use of insulin itself is often required. It is increasingly being recognized that the beta cell mass is dynamic and increases insulin secretion in response to beta cell mitogens and stress signals to maintain glycemia within a very narrow physiological range. This review critically discusses the role of adrenergic, adenosine and opioid pathways and their interrelationship in insulin secretion, beta cell proliferation and regeneration.
摘要：
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