Effects of methimazole-induced hypothyroidism on immunohistochemical, stereomorphometric and some ultrastructural characteristics of pancreatic β-cells

M. Ukropina, R. Glišić, K. Veličković, M. Markelić, I. Golić, M. Čakić-Milošević and V. Koko
Archives of Biological Sciences, 64 (2012), 943-951.

Abstract. The function of pancreatic β-cells is to produce and secrete insulin, a crucial hormone in carbohydrate metabolism. The transcription factor PDX1 is required for insulin gene transcription and mature β-cell function. Since this factor is regulated by triiodothyronine, a disturbance in insulin biosynthesis and/or secretion is usually related to a deficiency of this hormone. In the present study, we used methods of immunohistochemistry, stereology and electron microscopy to explore the correlation between altered thyroid status and insulin synthesis/secretion in a model of methimazole-induced hypothyroidism in rats. In hypothyroid animals fewer functional PDX1-positive β-cells were detected in the islets of Langerhans, while insulin immunostaining was stronger. Stereological analysis of β-cell granules revealed more numerous immature insulin granules in hypothyroid rats. Taken together, these data suggest that the applied treatment caused impaired insulin synthesis and secretion. Rare cells with granules characteristic for both α- and β-cells observed in hypothyroid animals could provide functional compensation for diminished insulin synthesis.

Keywords: pancreas, hypothyroidism, PDX1, β-cell granules

IF: 0.791
IF5: 0.747
MNTR classification: M23

BibTeX:

@article{ukropina2012-abs,
  title = {Effects of methimazole-induced hypothyroidism on immunohistochemical, stereomorphometric and some ultrastructural characteristics of pancreatic $\beta$-cells},
  author = {Ukropina, Mirela and Glisic, Radmila and Velickovic, Ksenija and Markelic, Milica and Golic, Igor and Cakic-Milosevic, Maja and Koko, Vesna},
  journal = {Archives of Biological Sciences},
  volume = {64},
  number = {3},
  pages = {943--951},
  year = {2012}
}