Endogenous sodium pump inhibitors: common pathogenetic mechanisms of impaired glucose tolerance and preeclampsia
- Authors: Reznik VA1, Fedorova OV2, Tapil’skaya NI1, Bagrov AY.2,3
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Affiliations:
- Saint Petersburg State Pediatric Medical Academy
- National Institute of Aging, National Institute of Health
- I.M. Sechenov Institute of Evolutionary Physiology and Biochemistry
- Issue: Vol 98, No 6 (2017)
- Pages: 998-1004
- Section: Experimental medicine
- URL: https://kazanmedjournal.ru/kazanmedj/article/view/7257
- DOI: https://doi.org/10.17750/KMJ2017-998
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Abstract
Aim. Study of the influence of sodium chloride overconsumption by pregnant rats with induced diabetes mellitus on the synthesis of marinobufagenin and Na/K-ATPase activity. Methods. The study was performed on 72 female Sprague Dawley rats. Type 2 diabetes mellitus was induced by administration of 65 mg/kg streptozotocin on day 4 after birth. Increased intake of salt was achieved by replacement of drinking water with 1.8% sodium chloride solution on days 12 to 19 of pregnancy. Results. In intact rats, pregnancy was associated with a two-fold increase of marinobufagenin level in the blood and mild impairment of glucose tolerance. Pregnant rats with induced diabetes mellitus apart from fetal macrosomia exhibited greater impairment of glucose tolerance and higher levels of marinobufagenin compared to those in intact pregnant animals. Compared to healthy pregnant rats, salt supplementation for laboratory animals with diabetes was associated with an increase in systolic blood pressure, decreased fetal and placental weight, five-fold elevation of marinobufagenin excretion, and in 42% - with inhibition of Na/K-ATPase activity in erythrocytes. In nonpregnant rats, pre-treatment with anti-marinobufagenin antibodies produced an exaggerated increase of blood levels of glucose and insulin in oral glucose tolerance test. Conclusion. Marinobufagenin is an important factor of pathogenesis of both preeclampsia and diabetes mellitus, and regulation of glucose tolerance may be one of the physiological functions of endogenous cardiotonic steroids.
Keywords
About the authors
V A Reznik
Saint Petersburg State Pediatric Medical Academy
Email: tapnatalia@yandex.ru
Saint Petersburg, Russia
O V Fedorova
National Institute of Aging, National Institute of Health
Email: tapnatalia@yandex.ru
Baltimore, USA
N I Tapil’skaya
Saint Petersburg State Pediatric Medical Academy
Email: tapnatalia@yandex.ru
Saint Petersburg, Russia
A Ya Bagrov
National Institute of Aging, National Institute of Health; I.M. Sechenov Institute of Evolutionary Physiology and Biochemistry
Email: tapnatalia@yandex.ru
Baltimore, USA; Saint Petersburg, Russia
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