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 Yamada, Y.
Right arrow Articles by Tarui, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yamada, Y.
Right arrow Articles by Tarui, S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

J. Biochem, 1988, Vol. 104, No. 4 576-579
© 1988 Japanese Biochemical Society

research-article

Increases in Hepatic Fructose-2,6-Bisphosphate Level and Fructose-6-Phosphate,2-Kinase Activity in Rats with Ventromedial Lesions of the Hypothalamus1

Yuya Yamada2, Takao Shimizu, Naoko Hara, Ikuo Mineo, Masanori Kawachi, Hiroaki Kiyokawa, Kentaro Yamada3, Shigenori Fujioka, Yuji Matsuzawa, Norio Kono and Seiichiro Tarui

The Second Department of Internal Medicine, Osaka University Medical School Fukushima-ku, Osaka, Osaka 553

2To whom correspondence should be addressed

To investigate altered fructose-2,6-bisphosphate (fructose-2,6-P2)metabolism, we measured fructose-2,6-P2 levels and fructose-6-phosphate,2-kinase (fructose-6-P,2-kinase) activities in various tissues, including liver, kidney, heart, and skeletal muscle, of ventromedial hypothalamus (VMH)-lesioned rats during feeding and starvation. The plasma insulin level was 6 times or more higher in these rats than in the controls. The fructose-2,6-P2 level in liver was much greater in VMH-lesioned rats than in the controls: 15.1±2.2 nmol/g tissue versus 7.7±0.7 in the fed state, 5.3±1.1 versus 1.6±0.4 in the starved state. In kidney, heart, and skeletal muscle, fructose-2,6-P2 levels were not different between the two animal groups. The activity of hepatic fructose-6-P,2-kinase remained high after 20 h of starvation in VMH-lesioned rats, whereas it was decreased markedly in the controls. The hepatic concentration of fructose-6-phosphate was also high in VMH-lesioned rats. Both fructose-6-P,2-kinase activity and fructose-6-phosphate concentration in the liver of starved VMH-lesioned rats were comparable to those of control rats in fed conditions. These results indicate that the alteration of fructose-2,6-P2 metabolism is characteristic of liver in VMH-lesioned rats, and that the increase in hepatic fructose-2,6-P2 may activate hepatic glycolysis not only during feeding but also during starvation, leading to the enhanced lipogenesis in these obese rats.

1This study was supported in part by Grants-in-Aid for Scientific Research and for Scientific Research on Priority Areas from the Ministry of Education, Science and Culture of Japan, and by a Basic Research Grant from the Muscular Dystrophy Association, of the United States.

3Present address: Internal Medicine of Endocrinology and Metabolism, Kurume University Medical School, Kurume, Fukuoka 830.


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




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.