The distribution of the islets of Langerhans in pancreas of euglycemic spontaneously hypertensive rats

Authors

  • T. V. Abramova Zaporizhzhia State Medical University,

DOI:

https://doi.org/10.14739/2310-1237.2016.1.72359

Keywords:

Hypertension, Islets of Langerhans, Insulin

Abstract

Considering the fact, that pancreatic beta cells are responsible for production of all insulin needed to maintain the glucose homeostasis, the problem of beta cells pull control in patients with hypertension is rather topical. It cannot be ruled, that genetical defects of congenital hypertension formation can affect the mechanisms of maintaining of the cell mass of pancreatic endocrinocytes and lead to violation of glucose metabolism and diabetes mellitus development. Moreover, the violation of cytoarchitectonics of pancreatic islets of Langerhans may lead to impairment of the insulin secretion, which can be due to local impairment of the blood circulation in patients with hypertension.

The aim was to study the features of SHR islets’ distribution in pancreas.

Materials and methods. The glucose blood level and the insulin concentration were measured from tail vein. The immunofluorescence analysis was made and data were processed with statistical application kit with evaluation of reliability of differences in experimental groups with Student’s t-criterion.

Results. The object of current study was the animals with fasting normoglycemia and Wistar rats with 3.94 mmol/l fasting glucose level. The morphometrical assay showed 78.8% of pancreatic islets in SHR are small islets, while in Wistar rats their share is 44.3%. Noteworthy is the great amount of solely beta-cells in SHR and total absence of large islets.

Conclusions. The violation of pancreas’ cytoarchitectonic and changes of islets’ distribution with prevailing of small islets with area less than 1500 µm2 were observed.

Beta-cells in normoglycemic SHR were characterized with 2-fold increased concentration of immunoreactive insulin compared with normotensive Wistar rats.

 

References

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 influence of the chronic prenatal stress to structural and functional organization of beta endocrinocites]. Klіnіchna ta eksperymentalna, patolohiia, 2(1), 176-179. [in Ukrainian].

Grekova, T. A. (2010). Vliyanie prenatal'noj giperglikemii na morfofunkcional'noe sostoyanie e′ndokrinnogo apparata podzheludochnoj zhelezy samcov krys v vozrastnoj dinamike [The influence of prenatal hyperglycemia to morphofunctional state of endocrine apparatus of pancreas in male rats within the age dynamics]. Zaporozhskij medicinskij zhurnal, 12(4), 12–15. [in Ukrainian].

Kolesnik, Yu. M., Gancheva, O. V., Abramov, A. V., & Kamyshnyj, A. M. (2007). Krysy linii SHR so spontannoj gipertenziej kak model' dlya izucheniya metabolicheskikh narushenij [Spontaneously hypertensive rats as the model for metabolic violations study] Zaporozhskij medicinskij zhurnal, 1, 5–10. [in Ukrainian].

Kolesnik, Yu. M., Grekova, T. A., Abramov, A. V., & Tikhonovskaya, M. A. (2009). Osobennosti postnatal'nogo morfogeneza insulyarnogo apparata podzheludochnoj zhelezy samcov krys [Features of the postnatal morphogenesis of the insular apparatus of the pancreas in male rats]. Patologiya, 6(3), 67–68. [in Ukrainian].

Ackermann, A. & Gannon, M. (2007). Molecular regulation of pancreatic beta-cell mass development, maintenance, and expansion. Journal Of Molecular Endocrinology, 38(2), 193–206.

Gancheva, O., Kolesnik, Y., Abramova, T., Samoylenko, N., & Abramov, A. (2013). Metabolic disturbances in hypertensive rats. Clinichna Pahrmacia, 17(4), 56–58.

Jennings, R., Berry, A., Strutt, J., Gerrard, D., & Hanley, N. (2015). Human pancreas development. Development, 142(18), 3126–3137. doi: 10.1242/dev.120063.

Jia, G., DeMarco, V., & Sowers, J. (2015). Insulin resistance and hyperinsulinaemia in diabetic cardiomyopathy. Nat Rev Endocrinol, 12(3), 144–153. doi:10.1038/nrendo.2015.216.

Jonker, S. & Louey, S. (2016). Endocrine and other physiologic modulators of perinatal cardiomyocyte endowment. J Endocrinol, 228(1), R1–R18. doi: 10.1530/JOE-15-0309.

Kelly, C., McClenaghan, N., & Flatt, P. (2011). Role of islet structure and cellular interactions in the control of insulin secretion. Islets, 3(2), 41–47. doi: 10.4161/isl.3.2.14805.

Mandavia, C., Aroor, A., DeMarco, V., & Sowers, J. (2013). Molecular and metabolic mechanisms of cardiac dysfunction in diabetes. Life Sciences, 92(11), 601–608. doi: 10.1016/j.lfs.2012.10.028.

Roglic, G. & Unwin, N. (2010). Mortality attributable to diabetes: Estimates for the year 2010. Diabetes Research And Clinical Practice, 87(1), 15–19. doi: 10.1016/j.diabres.2009.10.006.

Downloads

How to Cite

1.
Abramova TV. The distribution of the islets of Langerhans in pancreas of euglycemic spontaneously hypertensive rats. Pathologia [Internet]. 2016Jun.23 [cited 2024Oct.8];(1). Available from: http://pat.zsmu.edu.ua/article/view/72359

Issue

Section

Original research