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Submitted on July 22, 2004
Accepted on October 20, 2004
Departments of Psychiatry & Behavioral Science, Endocrinology, Metabolism and Molecular Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA; Neurobiology & Physiology, Howard Hughes Medical Institute, Northwestern University, Evanston, Illinois 60208, USA; The Jackson Laboratory, Bar Harbor, Maine 04609, USA; Current address: Wellcome Trust Centre for Human Genetics, Roosevelt Drive, Oxford OX3 7BN, United Kingdom
* To whom correspondence should be addressed. E-mail: e-redei{at}northwestern.edu.
Thyroid hormones are essential for the regulation of developmental and physiologic processes. The genetic factors underlying naturally occurring variability in mammalian thyroid function are, however, only partially understood. Genetic control of thyroid function can be studied with animal models such as the inbred Wistar-Kyoto (WKY) rat strain. Previous studies established that WKYs have elevated TSH, slightly elevated total T3, and normal total T4 levels compared with Wistar controls. The present study confirmed a persistent 24 h elevation of TSH in WKYs compared with the Fisher 344 (F344) rat, another inbred strain. Acute T3 challenge (25 µg/100 g body weight ip) suppressed serum TSH and T4 levels in both strains. Quantitative trait locus analysis of elevated TSH in a reciprocally bred WKYxF344 F2 population identified one highly significant locus on chromosome 6 (LOD=11.7, TSH-1) and one suggestive locus on chromosome 5 (LOD=2.3, TSH-2). The confidence interval of TSH-1 contains the TSH receptor and Type 2 deiodinase genes, and TSH-2 contains the Type 1 deiodinase gene. The WKY alleles of each gene contain sequence alterations but further studies are indicated to identify the specific gene or genes responsible for altered regulation of the thyroid axis. These findings suggest that one or more genetic alterations within the TSH-1 locus significantly contribute to the altered thyroid function tests of the WKY rat.
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