The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Adipose-specific overexpression of GLUT4 reverses insulin resistance and diabetes in mice lacking GLUT4 selectively in muscle
Abstract
Adipose tissue plays an important role in glucose homeostasis and affects insulin sensitivity in other tissues. In obesity and type 2 diabetes, glucose transporter 4 (GLUT4) is downregulated in adipose tissue, and glucose transport is also impaired in muscle. To determine whether overexpression of GLUT4 selectively in adipose tissue could prevent insulin resistance when glucose transport is impaired in muscle, we bred muscle GLUT4 knockout (MG4KO) mice to mice overexpressing GLUT4 in adipose tissue (AG4Tg). Overexpression of GLUT4 in fat not only normalized the fasting hyperglycemia and glucose intolerance in MG4KO mice, but it reduced these parameters to below normal levels. Glucose infusion rate during a euglycemic clamp study was reduced 46% in MG4KO compared with controls and was restored to control levels in AG4Tg-MG4KO. Similarly, insulin action to suppress hepatic glucose production was impaired in MG4KO mice and was restored to control levels in AG4Tg-MG4KO. 2-Deoxyglucose uptake during the clamp was increased approximately twofold in white adipose tissue but remained reduced in skeletal muscle of AG4Tg-MG4KO mice. AG4Tg and AG4Tg-MG4KO mice have a slight increase in fat mass, a twofold elevation in serum free fatty acids, an ∼50% increase in serum leptin, and a 50% decrease in serum adiponectin. In MG4KO mice, serum resistin is increased 34% and GLUT4 overexpression in fat reverses this. Overexpression of GLUT4 in fat also reverses the enhanced clearance of an oral lipid load in MG4KO mice. Thus overexpression of GLUT4 in fat reverses whole body insulin resistance in MG4KO mice without restoring glucose transport in muscle. This effect occurs even though AG4Tg-MG4KO mice have increased fat mass and low adiponectin and is associated with normalization of elevated resistin levels.
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.
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
Weyer, C., Funahashi, T., Tanaka, S., Hotta, K., Matsuzawa, Y., Pratley, R. E., & Tataranni, P. A. (2001) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.86.5.7463 · Cited by 3,541
Leptin stimulates fatty-acid oxidation by activating AMP-activated protein kinase
Minokoshi, Y., Kim, Y.-B., Peroni, O. D., Fryer, L. G. D., Müller, C., Carling, D., & Kahn, B. B. (2002) · Nature · doi:10.1038/415339a · Cited by 2,053
Self-citationGlucose Transporters and Insulin Action — Implications for Insulin Resistance and Diabetes Mellitus
Shepherd, P. R., & Kahn, B. B. (1999) · New England Journal of Medicine · doi:10.1056/nejm199907223410406 · Cited by 1,295
Self-citationWarram, J. H., Martin, B. C., Krolewski, A. S., Soeldner, J. S., & Kahn, C. R. (1990) · Annals of Internal Medicine · doi:10.7326/0003-4819-113-12-909 · Cited by 1,038
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
Self-citationCline, G. W., Petersen, K. F., Krssak, M., Shen, J., Hundal, R. S., Trajanoski, Z., Inzucchi, S., Dresner, A., Rothman, D. L., & Shulman, G. I. (1999) · New England Journal of Medicine · doi:10.1056/nejm199907223410404 · Cited by 675
Zierath, J. R., He, L., Gumà, A., Wahlström, E. O., Klip, A., & Wallberg-Henriksson, H. (1996) · Diabetologia · doi:10.1007/bf02658504 · Cited by 402
Functional inactivation of the IGF-I and insulin receptors in skeletal muscle causes type 2 diabetes
Fernández, A. M., Kim, J. K., Yakar, S., Dupont, J., Hernandez-Sanchez, C., Castle, A. L., Filmore, J., Shulman, G. I., & Le Roith, D. (2001) · Genes & Development · doi:10.1101/gad.908001 · Cited by 369
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-citationGlucose toxicity and the development of diabetes in mice with muscle-specific inactivation of GLUT4
Kim, J. K., Zisman, A., Fillmore, J. J., Peroni, O. D., Kotani, K., Perret, P., Zong, H., Dong, J., Kahn, C. R., Kahn, B. B., et al. (2001) · Journal of Clinical Investigation · doi:10.1172/jci10294 · Cited by 202 · cited 8×
“Nevertheless, the increase in glucose transport in WAT may contribute to the restoration of glucose homeostasis.”
BackgroundMethodInfluentialSelf-citation
Cited by
Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes
Yang, Q., Graham, T. E., Mody, N., Preitner, F., Peroni, O. D., Zabolotny, J. M., Kotani, K., Quadro, L., & Kahn, B. B. (2005) · Nature · doi:10.1038/nature03711 · Cited by 2,086
Self-citationBhatti, J. S., Bhatti, G. K., & Reddy, P. H. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.11.010 · Cited by 1,655
The Human Obesity Gene Map: The 2005 Update
Rankinen, T., Zuberi, A., Chagnon, Y. C., Weisnagel, S. J., Argyropoulos, G., Walts, B., Pérusse, L., & Bouchard, C. (2006) · Obesity · doi:10.1038/oby.2006.71 · Cited by 1,119
Functional Properties and Genomics of Glucose Transporters
Zhao, F.-Q., & Keating, A. (2007) · Current Genomics · doi:10.2174/138920207780368187 · Cited by 549
Glucose transporters in adipose tissue, liver, and skeletal muscle in metabolic health and disease
Chadt, A., & Al-Hasani, H. (2020) · Pflügers Archiv - European Journal of Physiology · doi:10.1007/s00424-020-02417-x · Cited by 510
Metadata
- Authors
- Carvalho, E., Kotani, K., Peroni, O. D., & Kahn, B. B.
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2005-10
- Volume
- 289
- Issue
- 4
- Pages
- E551-E561
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2107503521
- Cited by
- 238
- References
- 10
- FWCI
- 6.76
- Type
- journal article
- Language
- en
- Open access
- closed
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
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Adipose-specific overexpression of GLUT4 reverses insulin resistance and diabetes in mice lacking GLUT4 selectively in muscle. https://app.cochat.ai/papers/10.1152/ajpendo.00116.2005
- The paper
- Carvalho, E., Kotani, K., Peroni, O. D., & Kahn, B. B. (2005). Adipose-specific overexpression of GLUT4 reverses insulin resistance and diabetes in mice lacking GLUT4 selectively in muscle. American Journal of Physiology-Endocrinology and Metabolism. https://doi.org/10.1152/ajpendo.00116.2005
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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.
