Effects of methimazole-induced hypothyroidism on immunohistochemical, stereomorphometric and some ultrastructural characteristics of pancreatic β-cells
Author(s) -
Mirela Ukropina,
Radmila Glišić,
Ksenija Veličković,
Milica Markelić,
Igor Golić,
Maja Čakić-Milošević,
Vesna Koko
Publication year - 2012
Publication title -
archives of biological sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.217
H-Index - 25
eISSN - 1821-4339
pISSN - 0354-4664
DOI - 10.2298/abs1203943u
Subject(s) - endocrinology , medicine , insulin , hormone , immunostaining , pdx1 , biology , thyroid , immunohistochemistry , islet
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
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