Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by KATO, S.
Right arrow Articles by ICHIHARA, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by KATO, S.
Right arrow Articles by ICHIHARA, A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

J. Biochem, 1982, Vol. 92, No. 3 699-708
© 1982 Japanese Biochemical Society

research-article

Regulatory Relation between Insulin Receptor and Its Functional Responses in Primary Cultured Hepatocytes of Adult Rats1

Satoshi KATO, Toshikazu NAKAMURA and Akira ICHIHARA

Institute for Enzyme Research, School of Medicine, The University of Tokushima Tokushima, Tokushima 770

The relation between changes of insulin receptor and various metabolic responses were studied in adult rat hepatocytes in primary culture. In cells cultured for 3 h without insulin, the number of high affinity sites and the dissociation constant (Kd) of insulin receptor, determined from a Scatchard plot, were 1.05 × 105 sites/cell and 1.5 × 10–9 M, respectively. The receptor number increased 2-fold, but the Kd value remained constant during 2-days culture in insulin-free medium (up-regulation). Addition of dexamethasone (Dex), growth hormone, glucagon or triiodothyronine did not change the number of insulin receptors or the Kd value. In contrast, 1-day culture in insulin (1 × 10–7 M) medium decreased the receptor number by half (down-regulation) without change of the Kd value. Short-term responses of glycogenesis, amino acid transport and lipogenesis by insulin increased as the receptor number increased. In these cases, the sensitivity to insulin (Ka: half dose for the maximum response) did not change in cells with different receptor numbers, but the maximum response changed. These results show that hepatocytes, unlike adipocytes, do not have spare receptors of insulin. During down-regulation, the receptor number decreased by only half, but the insulin responses were lost almost completely. The receptor number returned to the normal level after culture in insulin-free medium for 12 h, but recovery of the responses took longer, suggesting that for the insulin response not only change of receptor number, but also other regulatory mechanisms for post-receptor processes, such as desensitization, are involved.

1 This work was supported by Grants-in-Aid (Nos. 544029 and 587046) for Scientific Research from the Ministry of Education, Science and Culture of Japan.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 EndocrinologyHome page
Y. Cho, M. Ariga, Y. Uchijima, K. Kimura, J.-Y. Rho, Y. Furuhata, F. Hakuno, K. Yamanouchi, M. Nishihara, and S.-I. Takahashi
The Novel Roles of Liver for Compensation of Insulin Resistance in Human Growth Hormone Transgenic Rats
Endocrinology, November 1, 2006; 147(11): 5374 - 5384.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.