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Fructose 2, 6‐Bisphosphate in Hypoglycemic Rat Brain
Author(s) -
Ambrosio Santiago,
Ventura Francesc,
Rosa Jose Luis,
Bartrons Ramon
Publication year - 1991
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1991.tb02116.x
Subject(s) - fructose , fructose 2,6 bisphosphate , metabolite , hypoglycemia , medicine , endocrinology , glycolysis , coma (optics) , hexokinase , cerebral cortex , chemistry , insulin , biology , biochemistry , phosphofructokinase , metabolism , physics , optics
Fructose 2,6‐bisphosphate has been studied during hypoglycemia induced by insulin administration (40 IU/kg). No changes in content of cerebral fructose 2,6‐bisphosphate were found in mild hypoglycemia, but the level of this compound was markedly decreased in hypoglycemic coma and recovered after 30 min of glucose administration. To correlate a possible modification of the concentration of the metabolite with selective regional damage occurring during hypoglycemic coma, we have analyzed four cerebral areas (cortex, striatum, cerebellum, and hippocampus). Fructose 2,6‐bisphosphate concentrations were similar in the four areas analyzed; severe hypoglycemia decreased levels of the metabolite to the same extent in all the brain areas studied. The decrease in content of fructose 2,6‐bisphosphate was not always accompanied by a parallel decrease in ATP levels, a result suggesting that the low levels of the bisphosphorylated metabolite during hypoglycemic coma could be due to the decreased 6‐phosphofructo‐2‐kinase activity, mainly as a consequence of the fall in concentration of its substrate (fructose 6‐phosphate). These results suggest that fructose 2,6‐bisphosphate could play a permissive role in cerebral tissue, maintaining activation of 6‐phosphofructo‐l‐kinase and glycolysis.