Pathogenetical linkage of the Nitric oxide synthase isoforms disbalance in pancreatic islets with chronical prenatal hyperglycemia
DOI:
https://doi.org/10.14739/2310-1210.2016.1.64088Keywords:
NOS isoforms, Pancreatic Islets, Gestational Diabetes Mellitus, ExpressionAbstract
The aim was to study patterns of the nNOS, iNOS and eNOS expression in pancreatic islets in prepubescent male offsprings of female rats with experimental gestational diabetes mellitus.
Materials and methods. The study was carried out in 10 prepubescent male offsprings of female rats with normal pregnancy and in 10 prepubescent male offsprings of female rats with experimental gestational diabetes mellitus. The expression of nNOS, iNOS and eNOS was evaluated in histological slices of pancreatic islets.
Results. It was found that the largest area of enzyme expression of eNOS was detected in control animals. On the other hand the immunoreactive material enzyme was maximal for iNOS. Chronic fetal hyperglycaemia affects the allocation of NOS isoforms in pancreatic islets. Higher immunoreactive material enzyme and nNOS contain, increase of iNOS area and the most significant increase of contain and area of fluorescence of eNOS compared with other expression indexes were detected. We believe the affection of glucose homeostasis in fetus during the last trimester of the pregnancy changes the relation of patterns of the expression of NOS isoforms, and it can lead to the formation of metabolic violation in adults.
References
Kolesnik, Yu. M., Gancheva, O. V., & Kamyshnyj, A. M. (2005). Rol′ gestacionnogo diabeta u krys linii Vistar v metabolicheskikh narusheniyakh u potomstva [The role of gestational diabetes in Wistar rats in metabolic desorders of offsprings]. Zaporozhskij medicinskij zhurnal, 30(3), 107. [in Ukrainian].
Grekova, T. A., Kolesnik, Yu. M., & Gancheva, O. V. (2010). Vliyanie prenatalnoj giperglikemii na sostoyanie alfa-, beta-, del′ta- i amilinsinteziruyuschikh kletok ostrovkov Langergansa samcov krys v vozrastnoj dinamike [The Influence of hyperglycaemia on prenatal condition of alpha-, beta-, delta- and amylinsynthetizing islet cells in male rats in the age dynamics]. Fundamentalna ta klinichna endokrynolohiia: problemy, zdobutky, perspektyvy (Deviati Danylevski chytannia) Proceedings of the Scientific and Practical Conference with international participationб (pp. 31–32). Kharkiv. [in Ukrainian].
(2008) Consensus Statement Updated on Management of Hyperglycemia in Type 2 Diabetes. Diabetes Care., 31, 1–11.
Abramov, A. V., Tikhonovskaya, M. A., & Kolesnik, Yu. M. (2004). Osobennosti vliyaniya khronicheskogo prenatal′nogo stressa na strukturno-funkcional′nuyu organizaciyu beta-e′ndokrinocitov [Features of the chronic influence of prenatal stress on the structural and functional organization of the beta endocrinocytes]. Klinichna ta eksperymentalna patolokhiia, 3(2), 176–179. [in Ukrainian].
Evers, I. M., Valk, H. W., & Mol, B.W.L. (2002). Macrosornia despite good glycemic control in type I diabetic pregnancy; results of a nationwide study in The Netherlands. Diabetologia, 45(3), 1484–1489.
Ozanne, S. E. (2001). Metabolic programming in animals. British Medical Bulletin, 60(1), 143–152. doi: 10.1093/bmb/60.1.143.
Dabelea, D., Pettitt, D., Hanson, R., Imperatore, G., Bennett, P., & Knowler, W. (1999). Birth weight, type 2 diabetes, and insulin resistance in Pima Indian children and young adults. Diabetes Care, 22(6), 944–950.
Bertin, E., Gangnerau, M., Bellon, G., Bailbé, D., Arbelot De Vacqueur, A., & Portha, B. (2002). Development of β-cell mass in fetuses of rats deprived of protein and/or energy in last trimester of pregnancy. American Journal Of Physiology - Regulatory, Integrative And Comparative Physiology, 283(3), R623-R630. doi: 10.1152/ajpregu.00037.2002.
Basralı, F., Nasırcılar Ülker S., Koçer, G., Ülker Karadamar, P., Özyurt, D., Cengiz, M., & Kemal Şentürk, Ü. (2015). Effect of magnesium on vascular reactivity in NOS inhibition-induced hypertension. Magnes Res, 28(2), 64–74. doi: 10.1684/mrh.2015.0383.
Sönmez, M., Kılıç, E., Karabulut, D., Çilenk, K., Deligönül, E., & Dündar, M. (2016). Nitric oxide synthase in diabetic rat testicular tissue and the effects of pentoxifylline therapy. Systems Biology In Reproductive Medicine, 62(1), 22–30. doi: 10.3109/19396368.2015.1085605.
Ali, M., Chen, X., & Didion, S. (2015). Heterozygous eNOS deficiency is associated with oxidative stress and endothelial dysfunction in diet-induced obesity. Physiol Rep., 3(12), el2630. doi: 10.14814/phy2.12630.
Kolesnyk, Yu. M., Bielienichev, I. F., Abramov, A. V., Gancheva, O. V., Kamyshnyi, A. M., & Grekova, T. A. (patentee) (2006) Patent 17281 Ukraina МПК G09 №23/28. Sposib modeliuvannia hestatsiinoho diabetu u shchuriv linii Vistar dlia vyvchennia yoho naslidkiv dlia nashchadkiv [Patent 17281 of Ukraine МПК G09 №23/28. Method of Modeling of Gestational Diabetes in Wistar Rats to Study Its Effects on Offsprings]. Biull., 9. [in Ukrainian].
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