This study was to evaluate the effect of androgen deficiency on thyroid immunoreactive C-cells and bone structure and function in a male orchidectomized middle-aged rat model. Fifteen-month-old male Wistar rats were divided into orchidectomized (Orx) and the sham-operated control (Sham) group. In the Orx group significant decreases (P < 0.05) were found in the volume of C cells (by 14%), their relative volume density (by 13%) and serum calcitonin concentration (by 54%) compared to the controls. Analyses of trabecular microarchitecture of the proximal tibia metaphysis showed that Orx induced marked decreases of cancellous bone area, trabecular thickness and trabecular number (by 52, 20 and 19% respectively; P < 0.05), whereas trabecular separation was increased by 27% (P < 0.05). In Orx rats, serum osteocalcin concentration was increased by 119% (P < 0.05), while serum calcium and phosphorus were 6 and 14% (P < 0.05) lower, respectively, compared to the levels in the Sham. In addition, urine calcium content was considerably higher (by 129%; P < 0.05) in Orx animals. These findings indicate that the androgen deficiency caused by Orx in middle-aged rats modulated the structure of C cells and diminished secretion of calcitonin. Histomorphometrical and biochemical analyses demonstrated a decrease of cancellous bone mass and increased bone turnover.

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 We examined whether isoflavones increase hepatic thyroid hormone concentrations and affect cholesterol metabolism in middle-aged rats  Serum T3 was not affected while hepatic T3 was almost doubled, which supports increased local T3 availability.  Obtained results are compatible with displacement of TH from TTR, major transport protein in rodent blood and human CSF.  Hepatic increase of T3 correlated with up-regulated expression of the Cyp7a1 gene and elevated 7α-hydroxycholesterol  IF also lowered 24-hydroxycholesterol and desmosterol in liver and serum, while the total cholesterol levels remained unchanged.

Androgen deficiency is one of the major factors leading to the development of osteoporosis in men. Since calcitonin (CT) is a potent antiresorptive agent, in the present study we investigated the effects of androgen deficiency and subsequent testosterone and estradiol treatment on CT-producing thyroid C cells, skeletal and hormonal changes in middle-aged orchidectomized (Orx) rats. Fifteen-month-old male Wistar rats were either Orx or sham-operated (SO). One group of Orx rats received 5 mg kg À1 b.w. testosterone propionate (TP) subcutaneously, while another group was injected with 0.06 mg kg À1 b.w. estradiol dipropionate (EDP) once a day for 3 weeks. A peroxidase-antiperoxidase method was applied for localization of CT in the C cells. The studies included ultrastructural microscopic observation of these cells. The metaphyseal region of the proximal tibia was measured histomorphometrically using an IMAGEJ public domain image processing program. TP or EDP treatment significantly increased C cell volume (Vc), volume densities (Vv) and serum CT concentration compared with the Orx animals. Administration of both TP and EDP significantly enhanced cancellous bone area (B.Ar), trabecular thickness (Tb.Th) and trabecular number (Tb.N) and reduced trabecular separation (Tb.Sp). Serum osteocalcin (OC) and urinary Ca concentrations were significantly lower after these treatments in comparison with Orx rats. These data suggest that testosterone and estradiol treatment in Orx middle-aged rats affect calcitonin-producing thyroid C cells, which may contribute to the bone protective effects of sex hormones in the rat model of male osteoporosis.

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