The DOI matches its Crossref record; 32 of the 33 references it cites were found in a registry or an index.
Functional inactivation of the IGF-I and insulin receptors in skeletal muscle causes type 2 diabetes
Open accessAbstract
Peripheral insulin resistance and impaired insulin action are the primary characteristics of type 2 diabetes. The first observable defect in this major disorder occurs in muscle, where glucose disposal in response to insulin is impaired. We have developed a transgenic mouse with a dominant-negative insulin-like growth factor-I receptor (KR-IGF-IR) specifically targeted to the skeletal muscle. Expression of KR-IGF-IR resulted in the formation of hybrid receptors between the mutant and the endogenous IGF-I and insulin receptors, thereby abrogating the normal function of these receptors and leading to insulin resistance. Pancreatic beta-cell dysfunction developed at a relative early age, resulting in diabetes. These mice provide an excellent model to study the molecular mechanisms underlying the development of human type 2 diabetes.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“IGF1 acts primarily on skeletal muscle, where it elicits its insulin-sensitizing effects [228] (Figure 2).”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [228]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Lillioja, S., Mott, D. M., Spraul, M., Ferraro, R., Foley, J. E., Ravussin, E., Knowler, W. C., Bennett, P. H., & Bogardus, C. (1993) · New England Journal of Medicine · doi:10.1056/nejm199312303292703 · Cited by 1,508
Molecular and Cellular Aspects of the Insulin-Like Growth Factor I Receptor
LeRoith, D., Werner, H., Beitner‐Johnson, D., & Roberts, C. T. (1995) · Endocrine Reviews · doi:10.1210/edrv-16-2-143 · Cited by 1,424
Self-citationNormal growth and development in the absence of hepatic insulin-like growth factor I
Yakar, S., Liu, J., STANNARD, B. S., Butler, A. A., Accili, D., Sauer, B., & LeRoith, D. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.13.7324 · Cited by 1,418
Self-citationMichael, M. D., Kulkarni, R. N., Postic, C., Previs, S. F., Shulman, G. I., Magnuson, M. A., & Kahn, C. R. (2000) · Molecular Cell · doi:10.1016/s1097-2765(05)00015-8 · Cited by 1,296
Self-citationShulman, G. I., Rothman, D. L., Jue, T., Stein, P., DeFronzo, R. A., & Shulman, R. G. (1990) · New England Journal of Medicine · doi:10.1056/nejm199001253220403 · Cited by 1,248
Self-citationBrüning, J. C., Michael, M. D., Winnay, J. N., Hayashi, T., Hörsch, D., Accili, D., Goodyear, L. J., & Kahn, C. R. (1998) · Molecular Cell · doi:10.1016/s1097-2765(00)80155-0 · Cited by 1,173
Kulkarni, R., Brüning, J. C., Winnay, J. N., Postic, C., Magnuson, M. A., & Kahn, C. R. (1999) · Cell · doi:10.1016/s0092-8674(00)80546-2 · Cited by 1,148
Zisman, A., Peroni, O. D., Abel, E. D., Michael, M. D., Mauvais-Jarvis, F., Lowell, B. B., Wojtaszewski, J. F. P., Hirshman, M. F., Virkamaki, A., Goodyear, L. J., et al. (2000) · Nature Medicine · doi:10.1038/78693 · Cited by 743
(1997) · Diabetes reviews · Cited by 671
Early neonatal death in mice homozygous for a null allele of the insulin receptor gene
Accili, D., Drago, J., Lee, E. J., Johnson, M. D., Cool, M. H., Salvatore, P., Asico, L. D., José, P. A., Taylor, S. I., & Westphal, H. (1996) · Nature Genetics · doi:10.1038/ng0196-106 · Cited by 594
Cardiac and adipose tissue abnormalities but not diabetes in mice deficient in GLUT4
Katz, E. B., Stenbit, A. E., Hatton, K. S., DePinho, R. A., & Charron, M. J. (1995) · Nature · doi:10.1038/377151a0 · Cited by 467
A Generic Intron Increases Gene Expression in Transgenic Mice
Choi, T., Huang, M. T. F., Gorman, C., & Jaenisch, R. (1991) · Molecular and Cellular Biology · doi:10.1128/mcb.11.6.3070 · Cited by 356
Troglitazone action is independent of adipose tissue.
Burant, C., Sreenan, S., Hirano, K., Tai, T. A., Lohmiller, J. J., Lukens, J. N., Davidson, N. O., Ross, S. R., & Graves, R. A. (1997) · Journal of Clinical Investigation · doi:10.1172/jci119839 · Cited by 331
Kim, J. K., Michael, M. D., Previs, S. F., Peroni, O. D., Mauvais-Jarvis, F., Neschen, S., Kahn, B. B., Kahn, C. R., & Shulman, G. I. (2000) · Journal of Clinical Investigation · doi:10.1172/jci8305 · Cited by 331
Self-citationTargeted disruption of the insulin receptor gene in the mouse results in neonatal lethality.
Joshi, R. L., Lamothe, B., Cordonnier, N., Mesbah, K., Monthioux, E., Jami, J., & Bucchini, D. (1996) · The EMBO Journal · doi:10.1002/j.1460-2075.1996.tb00498.x · Cited by 281
Kato, H., Faria, T. N., STANNARD, B. S., Roberts, C. T., & LeRoith, D. (1993) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)53824-2 · Cited by 244
Self-citationWojtaszewski, J. F. P., Higaki, Y., Hirshman, M. F., Michael, M. D., Dufresne, S. D., Kahn, C. R., & Goodyear, L. J. (1999) · Journal of Clinical Investigation · doi:10.1172/jci7961 · Cited by 237
GENETICS OF NON-INSULIN-DEPENDENT (TYPE-II) DIABETES MELLITUS
Kahn, C. R., Vicent, D., & Doria, A. (1996) · Annual Review of Medicine · doi:10.1146/annurev.med.47.1.509 · Cited by 213
Lauro, D., Kido, Y., Castle, A. L., Zarnowski, M. J., Hayashi, H., Ebina, Y., & Accili, D. (1998) · Nature Genetics · doi:10.1038/3112 · Cited by 140
Self-citationA Generic Intron Increases Gene Expression in Transgenic Mice
Choi, T., Huang, M. T. F., Gorman, C. M., et al. (1991) · Molecular and Cellular Biology · doi:10.1128/mcb.11.6.3070-3074.1991 · Cited by 116
Higaki, Y., Wojtaszewski, J. F. P., Hirshman, M. F., Withers, D. J., Towery, H. H., White, M. F., & Goodyear, L. J. (1999) · Journal of Biological Chemistry · doi:10.1074/jbc.274.30.20791 · Cited by 104
Federici, M., Zucaro, L., Porzio, O., Massoud, R. G., Borboni, P., Lauro, D., & Sesti, G. (1996) · Journal of Clinical Investigation · doi:10.1172/jci119117 · Cited by 79
Insulin-Like Growth Factor-1 Therapy in Diabetes: Physiologic Basis, Clinical Benefits, and Risks
Kolaczynski, J. W., & Caro, J. F. (1994) · Annals of Internal Medicine · doi:10.7326/0003-4819-120-1-199401010-00009 · Cited by 61
Federici, M., Lauro, D., D’Adamo, M., Giovannone, B., Porzio, O., Mellozzi, M., Tamburrano, G., Sbraccia, P., & Sesti, G. (1998) · Diabetes · doi:10.2337/diab.47.1.87 · Cited by 61
Nutritional state regulates insulin receptor and IRS-1 phosphorylation and expression in chicken
Dupont, J., Derouet, M., Simon, J., & Taouis, M. (1998) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1998.274.2.e309 · Cited by 59
Self-citationExpression of a dominant-negative mutant human insulin receptor in the muscle of transgenic mice.
Chang, P.-Y., Benecke, H., MARCHAND‐BRUSTEL, Y. L., Lawitts, J. A., & Moller, D. E. (1994) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)33969-8 · Cited by 56
Frattali, A. L., Treadway, J. L., & Pessin, J. E. (1992) · Journal of Cellular Biochemistry · doi:10.1002/jcb.240480108 · Cited by 55
Frick, F., Oscarsson, J., Vikman, K., Ottosson, M., Yoshida, N., & Edén, S. (2000) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.2000.278.4.e729 · Cited by 42
Insulin/IGF‐I receptor hybrids: A mechanism for increasing receptor diversity
Moxham, C. P., & Jacobs, S. (1992) · Journal of Cellular Biochemistry · doi:10.1002/jcb.240480205 · Cited by 39
Ota, A., Shen‐Orr, Z., Roberts, C. T., & LeRoith, D. (1989) · Molecular Brain Research · doi:10.1016/0169-328x(89)90030-2 · Cited by 34
Self-citationJullien, D., Heydrick, S. J., Gautier, N., OBBERGHEN, E. V., & MARCHAND‐BRUSTEL, Y. L. (1996) · Diabetes · doi:10.2337/diab.45.7.869 · Cited by 16
Available, N. A. N. (1999) · Diabetologia · doi:10.1007/s001250051318 · Cited by 8
Research works printed but not linked: 1
- 10.1016/S1097-2765(00)00010-1 · DOI · Paper page
Cited by
Sorted by citations
PPARs and the complex journey to obesity
Evans, R. M., Barish, G. D., & Wang, Y.-X. (2004) · Nature Medicine · doi:10.1038/nm1025 · Cited by 1,650
Huang, S., & Czech, M. (2007) · Cell Metabolism · doi:10.1016/j.cmet.2007.03.006 · Cited by 1,450
Copps, K. D., & White, M. F. (2012) · Diabetologia · doi:10.1007/s00125-012-2644-8 · Cited by 1,017
“The binding of insulin to the insulin receptor (IR), and in muscle tissues to hybrid insulin/ IGF1 receptors (IR/IGF1R) [7], promotes the autophosphorylation of a trio of regulatory loop tyrosine residues, disinhibiting IR tyrosine kinase activity toward IRS [8].”
BackgroundVigneri, P., Frasca, F., Sciacca, L., Pandini, G., & Vigneri, R. (2009) · Endocrine Related Cancer · doi:10.1677/erc-09-0087 · Cited by 1,009
The many faces of insulin-like peptide signalling in the brain
Fernandez, A. M., & Torres-Alemán, I. (2012) · Nature reviews. Neuroscience · doi:10.1038/nrn3209 · Cited by 872
Metadata
- Authors
- Fernández, A. M., Kim, J. K., Yakar, S., Dupont, J., Hernandez-Sanchez, C., Castle, A. L., Filmore, J., Shulman, G. I., & Le Roith, D.
- Affiliations
- National Institutes of Health (US)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2001-08-01
- Volume
- 15
- Issue
- 15
- Pages
- 1926-1934
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC312754
- OpenAlex
- W2125231550
- Cited by
- 369
- References
- 33
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 8 · 2023: 14 · 2022: 11 · 2021: 18 · 2020: 15 · 2019: 7 · 2018: 7 · 2017: 12 · 2016: 16 · 2015: 25 · 2014: 15 · 2013: 13 · 2012: 19
- Type
- posted content
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- other-oa
- Locations
- Genes & Development (publishedVersion, other-oa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Ministerio de Educación y Cultura
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK080756, R01DK040936)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Keywords
- type 2 diabetes, insulin resistance, IGF-1 receptor, insulin receptor, skeletal muscle, dominant negative receptor, hybrid receptors, transgenic mouse model, beta-cell dysfunction, glucose disposal
- MeSH terms
- Insulin Secretion, Aging, Animals, Blood Glucose, Diabetes Mellitus, Type 2, Fatty Acids, Nonesterified, Glucose, Humans, Hyperinsulinism, Insulin, Insulin Resistance, Islets of Langerhans, Liver, Mice, Transgenic, Prediabetic State, Receptor, Insulin, Triglycerides, Glucose Clamp Technique, Mutagenesis, Site-Directed, Receptor, IGF Type 1, Muscle, Skeletal, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
