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Cited by 252

The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.

Mouse models of insulin resistance

Hribal, Marta Letizia, Oriente, Francesco, Accili, Domenico·2002·American Journal of Physiology-Endocrinology and Metabolism

Abstract

The hallmarks of type 2 diabetes are impaired insulin action in peripheral tissues and decreased pancreatic β-cell function. Classically, the two defects have been viewed as separate entities, with insulin resistance arising primarily from impaired insulin-dependent glucose uptake in skeletal muscle, and β-cell dysfunction arising from impaired coupling of glucose sensing to insulin secretion. Targeted mutagenesis and transgenesis involving components of the insulin action pathway have changed our understanding of these phenomena. It appears that the role of insulin signaling in the pathogenesis of type 2 diabetes has been overestimated in classic insulin target tissues, such as skeletal muscle, whereas it has been overlooked in liver, pancreatic β-cells, and brain, which had been thought not to be primary insulin targets. We review recent progress and try to reconcile areas of apparent controversy surrounding insulin signaling in skeletal muscle and pancreatic β-cells.

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Crossref · 10.1152/ajpendo.00561.2001

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Metadata

Authors
Hribal, M. L., Oriente, F., & Accili, D.
Venue
American Journal of Physiology-Endocrinology and Metabolism
Published
2002-05-01
Volume
282
Issue
5
Pages
E977-E981
ISSN
  • 0193-1849 (ISSN-L)
  • 1522-1555
OpenAlex
W2171814772
Cited by
252
References
31
FWCI
16.64
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Mouse models of insulin resistance. https://app.cochat.ai/papers/10.1152/ajpendo.00561.2001
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Hribal, M. L., Oriente, F., & Accili, D. (2002). Mouse models of insulin resistance. American Journal of Physiology-Endocrinology and Metabolism. https://doi.org/10.1152/ajpendo.00561.2001

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.