Cited by 742Metabolism, Diabetes, and CancerPancreatic function and diabetesDiabetes, Cardiovascular Risks, and Lipoproteins

Biochemical and cellular properties of insulin receptor signalling

Open access
Haeusler, Rebecca A., McGraw, Timothy E., Accili, Domenico·2018·Nature Reviews Molecular Cell Biology

Abstract

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 β-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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Crossref · 10.1038/nrm.2017.89

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  • Insulin primarily induces glucose uptake in fat and muscle, but not liver.

    “consistent with insulin primarily inducing glucose uptake in the fat and muscle, but not liver 59”

    From Amphiregulin from regulatory T cells promotes liver fibrosis and insulin resistance in non-alcoholic steatohepatitis (2024) · cites this paper as [59]

    The Glucose uptake section says insulin’s effect on glucose uptake is most pronounced in adipocytes and muscle cells. The copy does not establish the categorical ‘but not liver’ distinction: it says insulin stimulates uptake in many cell types and, in the Abstract, promotes glucose utilization in the liver. (LLM, conf=0.83)

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2 of the 254 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. [140]Gonzalez E McGraw TE Insulin-modulated Akt subcellular localization determines Akt isoformspecific signaling Proc Natl Acad Sci USA 106 7004 7009 2009 19372382 PMC2678468

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Authors
Haeusler, R. A., McGraw, T. E., & Accili, D.
Affiliations
  • Columbia University (US)
  • Weill Cornell Medicine (US)
  • Columbia University Irving Medical Center (US)
Corresponding author
Accili, Domenico
Venue
Nature Reviews Molecular Cell Biology
Published
2017-10-04
Volume
19
Issue
1
Pages
31-44
ISSN
  • 1471-0072 (ISSN-L)
  • 1471-0080
OpenAlex
W2763635492
Cited by
739
References
254
Citations by year
2026: 61 · 2025: 87 · 2024: 99 · 2023: 97 · 2022: 121 · 2021: 108 · 2020: 67 · 2019: 60 · 2018: 34 · 2017: 3 · 2016: 1
FWCI
4.20
Type
journal article
Language
en
Open access
Locations
  • Nature Reviews Molecular Cell Biology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (R01HL125649, P01HL087123)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK057539, R01DK058282, R37DK058282, R01DK052852, T32DK007328, P30DK026687, P30DK063608, P30DK020541, R01DK064819)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
insulin receptor signaling, insulin action, insulin resistance, type 2 diabetes, obesity, glucose transport, lipid metabolism, insulin deficiency, pancreatic beta cells
MeSH terms
Animals, Humans, Insulin, Receptor, Insulin, Transcription, Genetic, Signal Transduction

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