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Cited by 220

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Tissue-specific Ablation of the GLUT4 Glucose Transporter or the Insulin Receptor Challenges Assumptions about Insulin Action and Glucose Homeostasis

Open access
Minokoshi, Yasuhiko, Kahn, C.Ronald, Kahn, Barbara B.·2003·Journal of Biological Chemistry

Abstract

The prevalence of type 2 diabetes mellitus is growing worldwide. Most forms of type 2 diabetes are polygenic with complex inheritance patterns strongly influenced by environmental factors. The specific gene defects are unknown, but they affect both insulin action and insulin secretion. Glucose homeostasis is maintained by the fine orchestration of insulin secretion and insulin action to promote glucose transport into muscle and adipocytes and to inhibit hepatic glucose output. Resistance to these effects of insulin is a classic pathogenic feature of obesity and type 2 diabetes.

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Crossref · 10.1074/jbc.r300019200

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Metadata

Authors
Minokoshi, Y., Kahn, C. R., & Kahn, B. B.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2003-09
Volume
278
Issue
36
Pages
33609-33612
ISSN
0021-9258 (ISSN-L)
OpenAlex
W2062244719
Cited by
220
References
9
FWCI
4.93
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Tissue-specific Ablation of the GLUT4 Glucose Transporter or the Insulin Receptor Challenges Assumptions about Insulin Action and Glucose Homeostasis. https://app.cochat.ai/papers/10.1074/jbc.r300019200
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Minokoshi, Y., Kahn, C. R., & Kahn, B. B. (2003). Tissue-specific Ablation of the GLUT4 Glucose Transporter or the Insulin Receptor Challenges Assumptions about Insulin Action and Glucose Homeostasis. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.r300019200

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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.