To investigate altered fructose-2,6-bisphosphate (fructose-2,6-P 2 )metabolism, we measured fructose-2,6-P 2 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-P 2 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-P 2 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-P 2 metabolism is characteristic of liver in VMH-lesioned rats, and that the increase in hepatic fructose-2,6-P 2 may activate hepatic glycolysis not only during feeding but also during starvation, leading to the enhanced lipogenesis in these obese rats.
|Original language||English (US)|
|Number of pages||4|
|Journal||Journal of Biochemistry|
|State||Published - Jan 1 1988|
ASJC Scopus subject areas
- Molecular Biology