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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

archives of biological sciences

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