Journal
NATURE REVIEWS MOLECULAR CELL BIOLOGY
Volume 19, Issue 1, Pages 31-44Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrm.2017.89
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Categories
Funding
- NIH [DK57539, DK64819, DK58282, HL81723, DK52852, HL125649]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL125649, P01HL087123] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK057539, R01DK058282, P30DK020541, P30DK026687, R56DK052852, P30DK063608, T32DK007328, R37DK058282, R01DK064819, R01DK052852] Funding Source: NIH RePORTER
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The mechanism of insulin action is a central theme in biology and medicine. In addition to the rather rare condition of insulin deficiency caused by autoimmune destruction of pancreatic beta-cells, genetic and acquired abnormalities of insulin action underlie the far more common conditions of type 2 diabetes, obesity and insulin resistance. The latter predisposes to diseases ranging from hypertension to Alzheimer disease and cancer. Hence, understanding the biochemical and cellular properties of insulin receptor signalling is arguably a priority in biomedical research. In the past decade, major progress has led to the delineation of mechanisms of glucose transport, lipid synthesis, storage and mobilization. In addition to direct effects of insulin on signalling kinases and metabolic enzymes, the discovery of mechanisms of insulin-regulated gene transcription has led to a reassessment of the general principles of insulin action. These advances will accelerate the discovery of new treatment modalities for diabetes.
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