This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints, Permissions and Rights Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by OKAMURA, K. Articles by KRULICH, L. Search for Related Content PubMed PubMed Citation Articles by OKAMURA, K. Articles by KRULICH, L.

Hypothyroidism in Severely Iodine-Deficient Rats^*

KEN OKAMURA, ALVIN TAUROG and LADISLAV KRULICH

Departments of Pharmacology and Physiology, University of Texas Health Science Center, Dallas, Texas 75235

Address requests for reprints to: Dr. Alvin Taurog, Department of Pharmacology, University of Texas Health Science Center, Dallas, Texas 75235.

Abstract

The thyroid status of severely iodine-deficient rats was assessed by measurement of the resting metabolic rate (RMR) and liver mitochondrial -glycerophosphate dehydrogenase (-GPD). Rats maintained on the iodine-deficient diet for 2 or 3 months showed significantly reduced RMR and - GPD, compared to rats on the same diet supplemented with KI in the drinking water. They also displayed markedly reduced serum T₄ levels, slightly reduced serum T₃ levels, and highly elevated serum TSH levels.

A significant decrease in liver -GPD was observed 29 days after the rats were placed on the iodine-deficient diet. However, the decrease in RMR in the same animals was not statistically significant. These results suggest that measurement of liver - GPD may be a more sensitive index of impending hypothyroidism than measurement of O₂ consumption.

The present study demonstrates that a hypothyroid state can be induced in rats exposed to a severely iodine-deficient diet. In severe iodine deficiency, the compensatory mechanisms of increased TSH stimulation and preferential T₃ secretion from the thyroid are insufficient to prevent a fall in serum T₃. The hypothyroid state results from the inability to maintain a normal serum T₃ level and possibly also from the very low levels of serum T₄.

Footnotes

^* This work was supported by USPHS Grants AM-03612 and AM- 10073.

Permanent address: Department of Internal Medicine, Kyushu University, Fukuoka, Japan.

USPHS career research awardee

Received December 24, 1980.

This article has been cited by other articles:

				A. C. Bianco, D. Salvatore, B. Gereben, M. J. Berry, and P. R. Larsen Biochemistry, Cellular and Molecular Biology, and Physiological Roles of the Iodothyronine Selenodeiodinases Endocr. Rev., February 1, 2002; 23(1): 38 - 89. [Abstract] [Full Text] [PDF]

				R. Peeters, C. Fekete, C. Goncalves, G. Legradi, H. M. Tu, J. W. Harney, A. C. Bianco, R. M. Lechan, and P. R. Larsen Regional physiological adaptation of the central nervous system deiodinases to iodine deficiency Am J Physiol Endocrinol Metab, July 1, 2001; 281(1): E54 - E61. [Abstract] [Full Text] [PDF]