title: Increases in hepatic fructose-2,6-bisphosphate level and fructose-6-phosphate,2-kinase activity in rats with ventromedial lesions of the hypothalamus.
abstract: 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.
authors.affiliation: Second Department of Internal Medicine, Osaka University Medical School.
authors.forename: Y
authors.initials: Y
authors.lastname: Yamada
authors.forename: T
authors.initials: T
authors.lastname: Shimizu
authors.forename: N
authors.initials: N
authors.lastname: Hara
authors.forename: I
authors.initials: I
authors.lastname: Mineo
authors.forename: M
authors.initials: M
authors.lastname: Kawachi
authors.forename: H
authors.initials: H
authors.lastname: Kiyokawa
authors.forename: K
authors.initials: K
authors.lastname: Yamada
authors.forename: S
authors.initials: S
authors.lastname: Fujioka
authors.forename: Y
authors.initials: Y
authors.lastname: Matsuzawa
authors.forename: N
authors.initials: N
authors.lastname: Kono
mesh_terms: D000818:Animals; D005635:Fructosediphosphates / Q000378:metabolism*; D005636:Fructosephosphates / Q000378:metabolism; D006598:Hexosediphosphates / Q000378:metabolism*; D007033:Hypothalamus, Middle / Q000502:physiology*; D008055:Lipids / Q000096:biosynthesis; D008099:Liver / Q000378:metabolism; D008297:Male; D009132:Muscles / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D009765:Obesity / Q000378:metabolism; D025481:Phosphofructokinase-2; D010770:Phosphotransferases / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D005635:Fructosediphosphates; D005636:Fructosephosphates; D006598:Hexosediphosphates; D008055:Lipids; C027618:fructose-6-phosphate; C027652:fructose 2,6-diphosphate; D010770:Phosphotransferases; D025481:Phosphofructokinase-2