Myo-inositol normalizes decreased sodium permeability of the blood-brain barrier in streptozotocin diabetes
1989; Elsevier BV; Volume: 29; Issue: 3 Linguagem: Inglês
10.1016/0306-4522(89)90148-6
ISSN1873-7544
AutoresGitte M. Knudsen, Johannes Jakobsen, David I. Barry, A.M. Compton, David R. Tomlinson,
Tópico(s)Regulation of Appetite and Obesity
ResumoThe effect of a dietary supplement of an aldose reductase inhibitor (ponalrestat) or of myo-inositol on sodium transport into the rat brain and on concentrations of saccharide and polyols in cortical brain tissue and sciatic nerve was investigated in control rats and in streptozotocin-diabetic rats after a diabetes duration of 2 weeks. In untreated diabetes, the neocortical blood-brain barrier permeability for sodium decreased by 28% (3.4 ± 0.4 vs 4.7 ±1.6 × 10−5ml/s g,mean±SD) as compared to controls. Levels of glucose, sorbitol and fructose increased in brain as well as in nerve tissues, whereas myo-inositol depletion was not demonstrable. Ponalrestat treatment of diabetic animals had no effect upon the decreased neocortical blood-brain barrier permeability to sodium (3.5 ±0.9 vs 4.7 ± 1.1 × 10−5ml/s g) despite normalization of brain and nerve content of sorbitol and fructose. Myo-inositol supplementation of diabetic rats normalized sodium passage into the brain (4.2 ± 1.1 vs 4.4 ±0.5 × 10−5ml/s g). Brain concentrations of monosaccharides and polyols were normalized as compared to the myo-inositol treated control group and nerve concentrations of glucose, sorbitol, and fructose were significantly increased. Myo-inositol treatment leads to a normalization of blood-brain barrier permeability; it is suggested that myo-inositol exerts a restituting effect upon Na+/K+-ATPase activity of the cerebral endothelial cells.
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