作者: Brendan Leighton , Garth J.S. Cooper
DOI: 10.1016/0968-0004(90)90015-4
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摘要: Decreased responsiveness of glucose metabolism to insulin in skeletal muscle and the liver (insulin resistance or insensitivity) is characteristic many conditions, including non-insulin-dependent (type II) diabetes mellitus. Most current work this area centres on hypothesis that primary defect an impairment binding and/or transduction signal affected tissues. However, studies imply defects post-insulin receptor signaling pathways are importance causation resistance. Amylin, a novel pancreatic hormone, secreted along with from beta-cells, can modulate effects, produce liver.