Proliferation and transdifferentiation of endocrinocytes of the rat during experimental diabetes

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Abstract

Some studies have found an increase number of α-cells in experimental diabetes, which may cause rising of blood glucose levels, along with the lack of insulin. But the mechanism of increasing the amount of glucagon-positive cells is still unknown. The aim of the study was to investigate the proliferative activity and the possibility of differentiation of α- and β-cells of the islets of Langerhans of pancreas during experimental diabetes in rats The work was performed on 33 white mongrel male rats. After alloxan injection, blood glucose levels were measured by glucose oxidase method and the expression of insulin, glucagon, and proliferating cell nuclear antigen was studied. Isolated proliferating glucagon-positive cells were found only on day 14 of the experiment. At the same time of the experiment bigormonal cells were found that synthesize insulin and glucagon. The results of the double staining for PCNA and glucagon showed that the increasing number of glucagon-positive cells in early stages of experimental diabetes is not related to their proliferation Probably it is due to differentiation of the progenitor cells of the islets in pancreas

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About the authors

M. S Kaligin

Email: mfkaligin@mail.ru
Kazan (Volga Region) Federal University Kazan, Russia

M. O Mavlikeev

Kazan (Volga Region) Federal University Kazan, Russia

A. A Titova

Kazan (Volga Region) Federal University Kazan, Russia

A. S Plushkina

Kazan (Volga Region) Federal University Kazan State Medical University Kazan, Russia

M. A Titova

Kazan (Volga Region) Federal University Kazan, Russia

A. A Gumerova

Kazan (Volga Region) Federal University Kazan, Russia

A. P Kiassov

Kazan (Volga Region) Federal University Kazan State Medical University Kazan, Russia

References

  1. Whiting D.R., Guariguata L., Weil C. et al. IDF diabetes atlas: global estimates of the prevalence of diabetes for 2011 and 2030. Diabetes Res. Clin. Pract. 2011; 94(3): 311-21.
  2. Плюшкина А.С., Калигин М.С., Андреева Д.И. и др. C-kit-позитивные клетки островков поджелудочной железы крысы как клетки-предшественницы эндокриноцитов при аллоксановом диабете. Клеточная трансплантология и тканевая инженерия 2012; VIIC3): 138-41.
  3. Калигин М.С., Плюшкина А.С., Титова А.А. и др. С-kit и десмин-позитивные клетки в регенерации островков поджелудочной железы при экспериментальном диабете у крыс. Клеточная трансплантология и тканевая инженерия 2013; VIII (3): 113-5.
  4. Habener J. F., Stanojevic V. α-cell role in β-cell generation and regeneration. Islets 2012; 4(3): 188-98.
  5. Алеева Г.Н., Киясов А.П., Миннебаев М.М. и др. Динамика В- и А-клеточной популяций поджелудочной железы и содержания глюкозы в крови крыс при аллоксановом диабете. Бюл. эксперим. биол. мед. 2002; 133(2): 151-3.
  6. Ye L., Robertson M.A., Hesselson D. et al. Glucagon is essential for alpha cell transdifferentiation and beta cell neogenesis. Dev. 2015; 142(8): 1407-17.
  7. Thorel F., Nepote V., Avril I. et al. Conversion of adult pancreatic alpha-cells to beta-cells after extreme beta-cell loss. Nature 2010; 464(7292): 1149-54.
  8. Орехович В.Н. Современные методы в биохимии. М. : Наука; 1977, 392.
  9. Калигин М.С., Титова А.А., Плюшкина А.С. Пролиферация клеток поджелудочной железы при экспериментальном диабете Гены и Клетки 2014; 9 (3): 85-8.
  10. Lenzen S. The mechanisms of alloxan- and streptozotocin-induced diabetes. Diabetologia 2008; 51(2): 216-26.
  11. Калигин М.С., Гумерова А.А., Титова М.А. и др. C-kit маркёр стволовых клеток эндокриноцитов поджелудочной железы Морфология 2011; 140 (4): 32-7.
  12. Li W.C., Horb M.E., Tosh D. et al. In vitro transdifferentiation of hepatoma cells into functional pancreatic cells. Mech. Dev. 2005; 122(6): 835-47.
  13. Fodor A., Harel C., Fodor L. et al. Adult rat liver cells transdifferentiated with lentiviral IPF1 vectors reverse diabetes in mice: an ex vivo gene therapy approach. Diabetologia 2007; 50(1): 121-30.
  14. Zhou Q., Brown J., Kanarek A. et al. In vivo reprogramming of adult pancreatic exocrine cells to beta-cells. Nature 2008; 455(7213): 627-32.
  15. Chakrabarti S.K., James J.C., Mirmira R.G. Quantitative assessment of gene targeting in vitro and in vivo by the pancreatic transcription factor, Pdx1 Importance of chromatin structure in directing promoter binding. J. Biol. Chem. 2002; 277(15): 13286-93.
  16. Schisler J.C, Jensen P.B., Taylor D.G. et al. The Nkx6. 1 homeodomain transcription factor suppresses glucagon expression and regulates glucose-stimulated insulin secretion in islet beta cells. PNAS USA 2005; 102(20): 7297-302.
  17. Collombat P., Mansouri A., Hecksher-Sorensen J. et al. Opposing actions of Arx and Pax4 in endocrine pancreas development. Genes Dev. 2003; 17(20): 2591-603.
  18. Jonsson J., Carlsson L., Edlund T. et al. Insulin-promoterfactor 1 is required for pancreas development in mice. Nature 1994; 371: 606-9.
  19. Collombat P., Hecksher-S0rensen J., Serup P., Mansouri A. Specifying pancreatic endocrine cell fates. Mech. Dev. 2006; 123; 501-12.

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