The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Disruption of insulin receptor substrate 2 causes type 2 diabetes because of liver insulin resistance and lack of compensatory beta-cell hyperplasia.
Open accessAbstract
To investigate the role of insulin receptor substrate (IRS)-2 in vivo, we generated IRS-2-deficient mice by gene targeting. Although homozygous IRS-2-deficient mice (IRS-2-/- mice) had a body weight similar to wild-type mice, they progressively developed type 2 diabetes at 10 weeks. IRS-2-/- mice showed insulin resistance and a defect in the insulin-stimulated signaling pathway in liver but not in skeletal muscle. Despite insulin resistance, the amount of beta-cells was reduced to 83% of that in wild-type mice, which was in marked contrast to the 85% increase in the amount of beta-cells in IRS-1-deficient mice (IRS-1-/- mice) to compensate for insulin resistance. Thus, IRS-2 plays a crucial role in the regulation of beta-cell mass. On the other hand, insulin secretion by the same number of cells in response to glucose measured ex vivo was significantly increased in IRS-2-/- mice compared with wild-type mice but was decreased in IRS-1-/- mice. These results suggest that IRS-1 and IRS-2 may play different roles in the regulation of beta-cell mass and the function of individual beta-cells.
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Citations
Cites
Insulin Resistance or Insulin Deficiency: Which Is the Primary Cause of NIDDM?
Taylor, S. I., Accili, D., & Imai, Y. (1994) · Diabetes · doi:10.2337/diab.43.6.735 · Cited by 289
Self-citation
Cited by
The PI3K/AKT Pathway in Obesity and Type 2 Diabetes
Huang, X., Liu, G., Guo, J., & Su, Z. (2018) · International Journal of Biological Sciences · doi:10.7150/ijbs.27173 · Cited by 1,673
“However, insulin has consistently been shown to play an important role in pancreatic cells [139], mainly through PI3K/AKT”
BackgroundDisruption of Adiponectin Causes Insulin Resistance and Neointimal Formation
Kubota, N., Terauchi, Y., Yamauchi, T., Kubota, T., Moroi, M., Matsui, J., Eto, K., Yamashita, T., Kamon, J., Satoh, H., et al. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.c200251200 · Cited by 1,208
Self-citationCopps, K. D., & White, M. F. (2012) · Diabetologia · doi:10.1007/s00125-012-2644-8 · Cited by 1,017
Globular adiponectin protected ob/ob mice from diabetes and ApoE-deficient mice from atherosclerosis
Yamauchi, T., Kamon, J., Waki, H., Imai, Y., Shimozawa, N., Hioki, K., Uchida, S., Ito, Y., Takakuwa, K., Matsui, J., et al. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m209033200 · Cited by 911
Self-citationGarofalo, R. S., Orena, S. J., Rafidi, K., Torchia, A. J., Stock, J. L., Hildebrandt, A. L., Coskran, T., Black, S. C., Brees, D. J., Wicks, J. R., et al. (2003) · Journal of Clinical Investigation · doi:10.1172/jci16885 · Cited by 726
Metadata
- Authors
- Kubota, N., Tobe, K., Terauchi, Y., Eto, K., Yamauchi, T., Suzuki, R., Tsubamoto, Y., Komeda, K., Nakano, R., Miki, H., Satoh, S., Sekihara, H., Sciacchitano, S., Lesniak, M., Aizawa, S., Nagai, R., Kimura, S., Akanuma, Y., Taylor, S. I., & Kadowaki, T.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2000-11-01
- Volume
- 49
- Issue
- 11
- Pages
- 1880-1889
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2153977812
- Cited by
- 521
- References
- 1
- FWCI
- 22.53
- Type
- journal article
- Language
- en
- Open access
- bronze
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- The paper
- Kubota, N., Tobe, K., Terauchi, Y., Eto, K., Yamauchi, T., Suzuki, R., Tsubamoto, Y., Komeda, K., Nakano, R., Miki, H., Satoh, S., Sekihara, H., Sciacchitano, S., Lesniak, M., Aizawa, S., Nagai, R., Kimura, S., Akanuma, Y., Taylor, S. I., & Kadowaki, T. (2000). Disruption of insulin receptor substrate 2 causes type 2 diabetes because of liver insulin resistance and lack of compensatory beta-cell hyperplasia. Diabetes. https://doi.org/10.2337/diabetes.49.11.1880
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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