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Influence of dietary iodine deficiency on the thyroid gland in Slc26a4- mutant mice.

Iwata T, Yoshida T, Teranishi M, Murata Y, Hayashi Y, Kanou Y, Griffith AJ, Nakashima T - Thyroid Res (2011)

Bottom Line: It is caused by loss-of-function mutations in the SLC26A4 (PDS) gene.However, direct evidence has not been shown to support this hypothesis.Even in Slc26a4- mice fed an iodine-deficient diet, the volume of the thyroid gland did not increase although the size of each epithelial cell increased with a concomitant decrease of thyroid colloidal area.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Otorhinolaryngology Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550, Japan. tsutomun@med.nagoya-u.ac.jp.

ABSTRACT

Background: Pendred syndrome (PDS) is an autosomal recessive disorder characterized by sensorineural hearing impairment and variable degree of goitrous enlargement of the thyroid gland with a partial defect in iodine organification. The thyroid function phenotype can range from normal function to overt hypothyroidism. It is caused by loss-of-function mutations in the SLC26A4 (PDS) gene. The severity of the goiter has been postulated to depend on the amount of dietary iodine intake. However, direct evidence has not been shown to support this hypothesis. Because Slc26a4- mice have deafness but do not develop goiter, we fed the mutant mice a control diet or an iodine-deficient diet to evaluate whether iodine deficiency is a causative environmental factor for goiter development in PDS.

Methods: We evaluated the thyroid volume in histological sections with the use of three-dimensional reconstitution software, we measured serum levels of total tri-iodothyronine (TT3) and total thyroxine (TT4) levels, and we studied the thyroid gland morphology by transmission electron microscopy.

Results: TT4 levels became low but TT3 levels did not change significantly after eight weeks of an iodine-deficient diet compared to levels in the control diet animals. Even in Slc26a4- mice fed an iodine-deficient diet, the volume of the thyroid gland did not increase although the size of each epithelial cell increased with a concomitant decrease of thyroid colloidal area.

Conclusions: An iodine-deficient diet did not induce goiter in Slc26a4- mice, suggesting that other environmental, epigenetic or genetic factors are involved in goiter development in PDS.

No MeSH data available.


Related in: MedlinePlus

Light microscopic findings of the thyroid gland. A, Slc26a4-/- control chow (CCD); B, Slc26a4+/- CCD; C, Slc26a4+/+ CCD; D, Slc26a4-/- iodine-deficient chow (ICD); E, Slc26a4+/- ICD; F, Slc26a4+/+ ICD. Scale bars: 30 μm.
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Figure 2: Light microscopic findings of the thyroid gland. A, Slc26a4-/- control chow (CCD); B, Slc26a4+/- CCD; C, Slc26a4+/+ CCD; D, Slc26a4-/- iodine-deficient chow (ICD); E, Slc26a4+/- ICD; F, Slc26a4+/+ ICD. Scale bars: 30 μm.

Mentions: Figure 2 demonstrates light microscopic observation of the thyroid gland of ICD and CCD groups for the three different Slc26a4 genotypes. The size and height of epithelial cells increased with a concomitant decrease of colloidal area in ICD thyroid glands as compared to those of CCD animals among all genotypes. Electron microscopic observations in Slc26a4-/- and Slc26a4+/- thyroid glands were consistent with these findings (Figure 3).


Influence of dietary iodine deficiency on the thyroid gland in Slc26a4- mutant mice.

Iwata T, Yoshida T, Teranishi M, Murata Y, Hayashi Y, Kanou Y, Griffith AJ, Nakashima T - Thyroid Res (2011)

Light microscopic findings of the thyroid gland. A, Slc26a4-/- control chow (CCD); B, Slc26a4+/- CCD; C, Slc26a4+/+ CCD; D, Slc26a4-/- iodine-deficient chow (ICD); E, Slc26a4+/- ICD; F, Slc26a4+/+ ICD. Scale bars: 30 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3141755&req=5

Figure 2: Light microscopic findings of the thyroid gland. A, Slc26a4-/- control chow (CCD); B, Slc26a4+/- CCD; C, Slc26a4+/+ CCD; D, Slc26a4-/- iodine-deficient chow (ICD); E, Slc26a4+/- ICD; F, Slc26a4+/+ ICD. Scale bars: 30 μm.
Mentions: Figure 2 demonstrates light microscopic observation of the thyroid gland of ICD and CCD groups for the three different Slc26a4 genotypes. The size and height of epithelial cells increased with a concomitant decrease of colloidal area in ICD thyroid glands as compared to those of CCD animals among all genotypes. Electron microscopic observations in Slc26a4-/- and Slc26a4+/- thyroid glands were consistent with these findings (Figure 3).

Bottom Line: It is caused by loss-of-function mutations in the SLC26A4 (PDS) gene.However, direct evidence has not been shown to support this hypothesis.Even in Slc26a4- mice fed an iodine-deficient diet, the volume of the thyroid gland did not increase although the size of each epithelial cell increased with a concomitant decrease of thyroid colloidal area.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Otorhinolaryngology Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550, Japan. tsutomun@med.nagoya-u.ac.jp.

ABSTRACT

Background: Pendred syndrome (PDS) is an autosomal recessive disorder characterized by sensorineural hearing impairment and variable degree of goitrous enlargement of the thyroid gland with a partial defect in iodine organification. The thyroid function phenotype can range from normal function to overt hypothyroidism. It is caused by loss-of-function mutations in the SLC26A4 (PDS) gene. The severity of the goiter has been postulated to depend on the amount of dietary iodine intake. However, direct evidence has not been shown to support this hypothesis. Because Slc26a4- mice have deafness but do not develop goiter, we fed the mutant mice a control diet or an iodine-deficient diet to evaluate whether iodine deficiency is a causative environmental factor for goiter development in PDS.

Methods: We evaluated the thyroid volume in histological sections with the use of three-dimensional reconstitution software, we measured serum levels of total tri-iodothyronine (TT3) and total thyroxine (TT4) levels, and we studied the thyroid gland morphology by transmission electron microscopy.

Results: TT4 levels became low but TT3 levels did not change significantly after eight weeks of an iodine-deficient diet compared to levels in the control diet animals. Even in Slc26a4- mice fed an iodine-deficient diet, the volume of the thyroid gland did not increase although the size of each epithelial cell increased with a concomitant decrease of thyroid colloidal area.

Conclusions: An iodine-deficient diet did not induce goiter in Slc26a4- mice, suggesting that other environmental, epigenetic or genetic factors are involved in goiter development in PDS.

No MeSH data available.


Related in: MedlinePlus