Regulation of fructose 2,6-bisphosphate concentration in white adipose tissue

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Abstract
Injection of insulin to fed rats diminished the concentration of fructose-2,6-bisphosphate in white adipose tissue. Incubation of epididymal fat-pads or adipocytes with insulin stimulated lactate release and sugar detritiation and also decreased fructose-2,6-bisphosphate concentration. Such a decrease was, however, not observed in fat-pads from starved or alloxan-diabetic rats. Incubation of adipocytes from fed rats with various concentrations of glucose or fructose led to a dose-dependent rise in fructose-2,6-bisphosphate which correlated with lactate output and detritiation of 3-3H-labeled sugar. In adipocytes from fed rats, palmitate stimulated the detritiation of [3-3H]glucose without affecting lactate production and fructose-2,6-bisphosphate concentration. Incubation of epididymal fat-pads from fed rats in the presence of antimycin stimulated lactate output, but decreased fructose-2,6-bisphosphate concentration. Changes in lipolytic rates brought about by noradrenaline [norepinephrine] insulin, adenosine and corticotropin in adipocytes from fed rats were not related to changes in fructose-2,6-bisphosphate or to rates or lactate output. In fed rats, the activity of 6-phosphofructo-2-kinase was not changed after treatment of adipocytes with insulin, noradrenaline or adenosine. The decrease in fructose-2,6-bisphosphate concentration observed after insulin treatment may be explained by the increase in sn-glycerol-3-phosphate, an inhibitor of 6-phosphofructo-2-kinase.