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Biomedical subjects

Arun Sinha

Publications and source records attributed to Arun Sinha.

3 recordsLinked to original sources

Evolutionary adaptation of a mammalian species to an environment severely depleted of iodide.

Lack of dietary iodine is associated with thyroid insufficiency and its dire consequences including cretinism, yet territories severely deficient in iodine are home to many species of wild animals. The premise of our work is that an adaptation must be in place in order to allow these animals to thrive. We collected phyllotine rodents of the genus Auliscomys from the Altiplanic region of North Chile, an area historically associated with goitre and other manifestations of iodine deficiency disorders. The iodide concentration in the stream water in this locality, at <1 micro g l(-1) would undoubtedly result in widespread thyroidal insufficiency in humans and domestic livestock. The animals we collected, identified as Auliscomys boliviensis, showed no evidence of thyroidal insufficiency. There was no enlargement of the thyroid glands; the serum concentrations of thyroid hormone (measured as T4) and thyroid-stimulating hormone were comparable to laboratory rats. Serum iodide concentration was about 40% of that measured in laboratory rats. We conclude that these animals have established a specialised adaptive mechanism, most probably at the level of the Na(+)/I(-) symporter, that acts to enhance the uptake of dietary iodide into the gut and again from the serum into the follicular cells of the thyroid gland.

Adaptation, Physiological↗

Thyroid hormone regulates the expression of alpha-internexin in neurons in culture.

Maternal hypothyroidism in the rat compromises alpha-internexin (alpha-IN) expression in early fetal brain. We have therefore examined whether 3,5,3'-triiodothyronine (T3) regulates alpha-IN expression in fetal brain neurons in culture. Cells expressed transcripts encoding T3 nuclear receptor isoforms in a T3-independent manner. alpha-IN protein abundance was increased in cultures treated with 0.1 and 1 nM T3 for 20 h (177 and 185% control, respectively) and in cultures treated with 1 nM T3 for 40 h (131% control). alpha-IN transcript abundance was unaffected by T3 treatment. In conclusion, T3 at a physiological level, stimulates alpha-IN protein, but not mRNA, levels in early differentiating neurons in culture. This supports the hypothesis that maternal thyroid hormone directly regulates early neuronal differentiation.

Animals↗