Features of the planimetric organization of the endocrine part of the pancreas in hypertensive rats of the SHR line
Keywords:rats inbred SHR, Wistar rat, pancreas, pancreatic islets, endocrinocyte, immunofluorescence, insulin, glucagon
Analysis of the endocrine structure of the pancreas and assessment of its degree of heterogeneity is key to assessing such important physiological parameters as islet endocrinocyte mass in healthy people or functional reserve of β-cells in patients with type 1 and type 2 diabetes.
The aim of the study is to perform a comparative planimetric analysis of pancreatic islets of normotensive Wistar rats and hypertensive SHR rats, using the method of double immunofluorescent staining of endocrinocytes.
Materials and methods. The study was performed on the pancreas of SHR and Wistar rats. Insulin and glucagon in the islets of the pancreas were determined by immunofluorescence. The immunofluorescence reaction was studied with an AxioImager-M2 fluorescent microscope.
Results. Planimetric analysis showed the presence of pancreatic islets of all types in the pancreatic tissue of SHR and Wistar rats. The number of single endocrinocytes in SHR hypertensive animals was 2.3 times higher (P < 0.001), and the number of giant islets was 34.2 % higher (P < 0.001), than in normotensive Wistar rats. The presence of regions in some endocrinocytes, that show immunoreactivity to both hormones at once – insulin and glucagon. Such areas were present in islets of all types of both rat lines, however, the total rates in hypertensive rats of the SHR line were 21.8 % lower (P < 0.001), than in normotensive rats of the Wistar line.
Conclusions. Planimetric analysis showed, that the pancreatic islets in normotensive Wistar rats and hypertensive SHR rats occupy 1.4 % of the cross-sectional area of the pancreas. In hypertensive rats the SHR line in the gland by 16.9 % larger total area of the material immunoreactive to insulin. In contrast to Wistar rats, the number of single α-endocrinocytes in the pancreas of hypertensive SHR rats was significantly increased.
Parween, S., Kostromina, E., Nord, C., Eriksson, M., Lindstrom, P., & Ahlgren, U. (2016). Intra-islet lesions and lobular variations in beta-cell mass expansion in ob/ob mice revealed by 3D imaging of intact pancreas. Scientific Reports, 6(34885), 1-11. https://doi.org/10.1038/srep34885
Wang, L. J., & Kaufman, D. B. (2016). Digital Image Analysis to Assess Quantity and Morphological Quality of Isolated Pancreatic Islets. Cell transplantation, 25(7), 1219-1225. https://doi.org/10.3727/096368915X689947
Rickels, M. R., & Robertson, R. P. (2019). Pancreatic Islet Transplantation in Humans: Recent Progress and Future Directions. Endocrine reviews, 40(2), 631-668. https://doi.org/10.1210/er.2018-00154
Campbell-Thompson, M., & Tang, S. C. (2021). Pancreas Optical Clearing and 3-D Microscopy in Health and Diabetes. Frontiers in endocrinology, 12, 644826. https://doi.org/10.3389/fendo.2021.644826
Dybala, M. P., Olehnik, S. K., Fowler, J. L., Golab, K., Millis, J. M., Golebiewska, J., Bachul, P., Witkowski, P., & Hara, M. (2019). Pancreatic beta cell/islet mass and body mass index. Islets, 11(1), 1-9. https://doi.org/10.1080/19382014.2018.1557486
Abramov, A. V., Tikhonovskaya, M. A., & Kolesnik, Yu. M. (2004). Osobennosti vliyaniya khronicheskogo prenatal'nogo stressa na strukturno-funktsional'nuyu organizatsiyu beta-endokrinotsitov [Features of the influence of chronic prenatal stress on the structural and functional organization of beta-endocrinocytes]. Klinichna ta eksperymentalna patolohiia, 3(2), 176-179. [in Russian].
Ivanenko, T. V. (2011). Vliyanie gipoksicheskikh trenirovok na funktsiyu beta-kletok pankreaticheskikh ostrovkov [Effect of hypoxic training on functioning of pancreatic islet beta-cells]. Aktualni problemy suchasnoi medytsyny:Visnyk Ukrainskoi medychnoi stomatolohichnoi akademii, 11(4), 82-84. [in Russian].
Abramova, T. V. (2016). The distribution of the islets of Langerhans in pancreas of euglycemic spontaneously hypertensive rats. Pathologia, 13(1), 19-21. https://doi.org/10.14739/2310-1237.2016.1.72359
Abramova, T. V., & Kolesnyk, Yu. M. (2016). The features of beta-cells organization in the pancreas of spontaneously hypertensive rat (SHR). Pathologia, 13(3), 4-8. https://doi.org/10.14739/2310-1237.2016.3.86931
Abramova, T. V., & Kolesnyk, Yu. M. (2017). Osobennosti organizatsii populyatsii al'fa-kletok v podzheludochnoi zheleze u krys so spontannoi gipertenzii (SHR) [Features of the alpha-cell population organization in pancreas of spontaneously hypertensive rats (SHR)]. Pathologia, 14(2), 124-128. [in Russian]. https://doi.org/10.14739/2310-1237.2017.2.109249
Kim, A., Miller, K., Jo, J., Kilimnik, G., Wojcik, P., & Hara, M. (2009). Islet architecture: A comparative study. Islets, 1(2), 129-136. https://doi.org/10.4161/isl.1.2.9480
Naya, F. J., Huang, H. P., Qiu, Y., Mutoh, H., DeMayo, F. J., Leiter, A. B., & Tsai, M. J. (1997). Diabetes, defective pancreatic morphogenesis, and abnormal enteroendocrine differentiation in BETA2/neuroD-deficient mice. Genes & development, 11(18), 2323-2334. https://doi.org/10.1101/gad.11.18.2323
Hussain, M. A., Miller, C. P., & Habener, J. F. (2002). Brn-4 transcription factor expression targeted to the early developing mouse pancreas induces ectopic glucagon gene expression in insulin-producing beta cells. The Journal of biological chemistry, 277(18), 16028-16032. https://doi.org/10.1074/jbc.M107124200
Unger, R. H., & Cherrington, A. D. (2012). Glucagonocentric restructuring of diabetes: a pathophysiologic and therapeutic makeover. The Journal of clinical investigation, 122(1), 4-12. https://doi.org/10.1172/JCI60016
Ivanenko, T. V., & Vynokurova, A. V. (2021) Kliuchovi molekuliarno-henetychni rehuliatory dyferentsiiuvannia endokrynotsytiv pidshlunkovoi zalozy [Key molecular genetic regulators of pancreatic endocrinocyte differentiation]. Klinichna ta eksperymentalna patolohiia, 20(4), 112-117. [in Ukrainian]. https://doi.org/10.24061/1727-4338.XX.4.78.2021.15
Gosmain, Y., Masson, M. H., & Philippe, J. (2013). Glucagon: the renewal of an old hormone in the pathophysiology of diabetes. Journal of diabetes, 5(2), 102-109. https://doi.org/10.1111/1753-0407.12022
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