Effects of Long-Term Streptozotocin Diabetes on Cytoskeletal and Cytosolic Phosphofructokinase and the Levels of Glucose 1,6-Bisphosphate and Fructose 2,6-Bisphosphate in Different Rat Muscles

1994 ◽  
Vol 53 (2) ◽  
pp. 137-144 ◽  
Author(s):  
M. Chenzion ◽  
T. Livnat ◽  
R. Beitner
1996 ◽  
Vol 116 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Süleyman Aydin ◽  
Yusuf Öztürk ◽  
V.Melih Altan ◽  
Nuray Yildizoğlu-Ari ◽  
A.Tanju Özçelikay

2014 ◽  
Vol 60 ◽  
pp. 140-146 ◽  
Author(s):  
Tomislav Mašek ◽  
Natalija Filipović ◽  
Lejla Ferhatović Hamzić ◽  
Livia Puljak ◽  
Kristina Starčević

2012 ◽  
Vol 302 (1) ◽  
pp. R75-R83 ◽  
Author(s):  
Scott C. Thomson ◽  
Timo Rieg ◽  
Cynthia Miracle ◽  
Hadi Mansoury ◽  
Jean Whaley ◽  
...  

Tubuloglomerular feedback (TGF) stabilizes nephron function from minute to minute and adapts to different steady-state inputs to maintain this capability. Such adaptation inherently renders TGF less efficient at buffering long-term disturbances, but the magnitude of loss is unknown. We undertook the present study to measure the compromise between TGF and TGF adaptation in transition from acute to chronic decline in proximal reabsorption (Jprox). As a tool, we blocked proximal tubule sodium-glucose cotransport with the SGLT2 blocker dapagliflozin in hyperglycemic rats with early streptozotocin diabetes, a condition in which a large fraction of proximal fluid reabsorption owes to SGLT2. Dapagliflozin acutely reduced proximal reabsorption leading to a 70% increase in early distal chloride, a saturated TGF response, and a major reduction in single nephron glomerular filtration rate (SNGFR). Acute and chronic effects on Jprox were indistinguishable. Adaptations to 10–12 days of dapagiflozin included increased reabsorption by Henle's loop, which caused a partial relaxation in the increased tone exerted by TGF that could be explained without desensitization of TGF. In summary, TGF contributes to long-term fluid and salt balance by mediating a persistent decline in SNGFR as the kidney adapts to a sustained decrease in Jprox.


Cell Calcium ◽  
1994 ◽  
Vol 16 (2) ◽  
pp. 81-86 ◽  
Author(s):  
Y. Öztürk ◽  
S. Aydin ◽  
V.M. Altan ◽  
N. Yildizoǧlu-Ari ◽  
A.T. Özçelikay

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Alexander O. Shpakov ◽  
Kira V. Derkach ◽  
Irina V. Moyseyuk ◽  
Oksana V. Chistyakova

One of the causes of complications in type 1 diabetes mellitus (T1DM) is the changes in adenylyl cyclase (AC) signaling system, identified on the early stages of the disease. However, the most significant disturbances in this system occur on the later stages of T1DM, which ultimately leads to severe complications, but functional state of the AC system in late T1DM is poorly understood. The aim of this work was to study alterations in AC system sensitive to biogenic amines and polypeptide hormones in the heart, brain, and testes of male rats with long-term, 7-month, streptozotocin T1DM and to assess the influence on them of 135-day therapy with intranasal insulin. It was shown that AC effects of β-adrenergic agonists in the heart, serotonin receptor agonists and PACAP-38 in the brain, chorionic gonadotropin and PACAP-38 in the testes, and somatostatin in all investigated tissues in long-term T1DM were drastically decreased. The treatment with intranasal insulin (0.48 IU/day) significantly restored these effects. The results were obtained suggesting that long-term T1DM induces significant alterations in hormone-sensitive AC system in the heart, brain, and testes that are much more pronounced, compared with short-term T1DM, and include a large number of hormonal regulations.


Life Sciences ◽  
1980 ◽  
Vol 27 (22) ◽  
pp. 2121-2124 ◽  
Author(s):  
J.W. Bauman

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