Dietary soy prevents brain Na +, K +-ATPase reduction in streptozotocin diabetic rats

• Published in: Diabetes research and clinical practice 2005-08, Vol.69 (2), p.107-112
• Main Authors: Franzon, Renata, Chiarani, Fábria, Mendes, Roberta H., Belló-Klein, Adriane, Wyse, Angela T.S.
• Format: Article
• Language: English
• Subjects: Animals; Brain; Caseins; Cell Membrane - enzymology; Cerebral Cortex - drug effects; Cerebral Cortex - enzymology; Diabetes; Diabetes Mellitus, Experimental - enzymology; Dietary Proteins - therapeutic use; Hippocampus - enzymology; Hypothalamus - enzymology; Na +, K +-ATPase; Rats; Rats, Wistar; Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors; Sodium-Potassium-Exchanging ATPase - metabolism; Soy; Soybean Proteins - administration & dosage; Soybean Proteins - therapeutic use; Streptozotocin; Synaptic Membranes - enzymology
• ISSN: 0168-8227; 1872-8227
• DOI: 10.1016/j.diabres.2004.11.010

The aim of this study was to investigate Na +, K +-ATPase activity in cerebral cortex, hippocampus and hypothalamus of diabetic rats. The action of dietary soy protein on the effect produced by diabetes on this activity was also tested. Forty-nine-day-old Wistar were divided into two groups: diabetes streptozotocin (50 mg/kg body weight) and control (citrate solution). Rats were sacrificed 56 days later. In other set of experiments, rats received a dietary with casein (control) from day 21 to the 49 of postnatal-age and were subjected to diabetes or received citrate (control). One week later, rats received a special dietary with soy protein with isoflavones or casein (control) from day 56 to the 105 of postnatal-age. Results showed that diabetic rats presented a reduction (∼40%) of Na +, K +-ATPase activity in all structures studied. Pretreatment with soy protein prevented the inhibitory effects of diabetes on the enzyme activity. Assuming the possibility that these effects might also occur in the human condition, our findings may be relevant to explain, at least in part, the neurologic dysfunction associated with diabetes and might support a novel therapeutic strategy (soy protein) to slow the progression of neurodegeneration in this disorder.