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

被引:19
作者
Franzon, R [1 ]
Chiarani, F [1 ]
Mendes, RH [1 ]
Belló-Klein, A [1 ]
Wyse, ATS [1 ]
机构
[1] Univ Fed Rio Grande Sul, Dept Bioquim, Inst Ciencias Basicas Saude, BR-90035003 Porto Alegre, RS, Brazil
关键词
Na+; K+-ATPase; brain; diabetes; soy; streptozotocin;
D O I
10.1016/j.diabres.2004.11.010
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 (similar to 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. (c) 2004 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:107 / 112
页数:6
相关论文
共 50 条
  • [41] Na+, K+-ATPase Signaling and Bipolar Disorder
    Lichtstein, David
    Ilani, Asher
    Rosen, Haim
    Horesh, Noa
    Singh, Shiv Vardan
    Buzaglo, Nahum
    Hodes, Anastasia
    INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2018, 19 (08)
  • [42] Role of Na+,K+-ATPase in Bone Remodeling
    Pasatetskaya, N. A.
    Klimshin, S. I.
    Lopatina, E. V.
    BULLETIN OF EXPERIMENTAL BIOLOGY AND MEDICINE, 2023, 174 (05) : 678 - 680
  • [43] Binding domain of oligomycin on Na+,K+-ATPase
    Homareda, H
    Ishii, T
    Takeyasu, K
    EUROPEAN JOURNAL OF PHARMACOLOGY, 2000, 400 (2-3) : 177 - 183
  • [44] TRANSMEMBRANE ORGANIZATION OF THE NA+, K+-ATPASE MOLECULE
    MODYANOV, N
    LUTSENKO, S
    CHERTOVA, E
    EFREMOV, R
    GULYAEV, D
    ACTA PHYSIOLOGICA SCANDINAVICA, 1992, 146 : 49 - 58
  • [45] Ion permeation through the Na+,K+-ATPase
    Reyes, Nicolas
    Gadsby, David C.
    NATURE, 2006, 443 (7110) : 470 - 474
  • [46] DECREASE OF NERVE NA+,K+-ATPASE ACTIVITY IN THE PATHOGENESIS OF HUMAN DIABETIC NEUROPATHY
    SCARPINI, E
    BIANCHI, R
    MOGGIO, M
    SCIACCO, M
    FIORI, MG
    SCARLATO, G
    JOURNAL OF THE NEUROLOGICAL SCIENCES, 1993, 120 (02) : 159 - 167
  • [47] Angiotensin-converting enzyme activity in retinas of Streptozotocin-induced and Zucker diabetic rats - The effect of angiotensin II on Na+,K+-ATPase activity
    Ottlecz, A
    Bensaoula, T
    Eichberg, J
    Peterson, RG
    INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 1996, 37 (11) : 2157 - 2164
  • [48] Effect of the pyridoindole antioxidant stobadine on the cardiac Na+,K+-ATPase in rats with streptozotocin-induced diabetes
    Vlkovicova, J.
    Javorkova, V.
    Stefek, M.
    Kysel'ova, Z.
    Gajdosikova, A.
    Vrbjar, N.
    GENERAL PHYSIOLOGY AND BIOPHYSICS, 2006, 25 (02) : 111 - 124
  • [49] Reduction of Na+,K+-ATPase Activity in Hippocampus of Rats Subjected to Chemically Induced Hyperhomocysteinemia
    Emílio L. Streck
    Cristiane Matte
    Paula S. Vieira
    Fernanda Rombaldi
    Clóvis M. D. Wannmacher
    Moacir Wajner
    Angela T. S. Wyse
    Neurochemical Research, 2002, 27 : 1593 - 1598
  • [50] Alanine Prevents the Decrease of Na+,K+-ATPase Activity in Experimental Phenylketonuria
    Angela T.S. Wyse
    Maria E. Noriler
    Luiz F. Borges
    Petterson J. Floriano
    Cleide G. Silva
    Moacir Wajner
    Clovis M.D. Wannmacher
    Metabolic Brain Disease, 1999, 14 : 95 - 101