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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.

An ultramicroscopic study of brown adipose tissue (BAT) of rats treated with Ca-SANDOZ® (480 mg/l) for 3 days, revealed erythrocyte exovesiculation and migratory erythrocytic complexes from the capillaries to adipocyte cytoplasm and mitochondria. Two types of erythrocytic material transfer were observed: (i) numerous exocytic vesicles with electron dense material leaving the erythrocytes; (ii) furcated complexes with microholes, embedded in amorphous material. The content of red blood cell (RBC) complexes passed through the capillaries and transferred to the brown adipocytes where it was detectable in the cytoplasm and mitochondria. Light microscopy confirmed sphenoechinocytic transformation of the RBCs in the blood smears of the Ca-SANDOZ® treated rats.