Document Detail

Effects of subacute hypothyroidism on metabolism and growth-related molecules.
MedLine Citation:
PMID:  25079659     Owner:  NLM     Status:  In-Data-Review    
Thyroid hormones are crucial hormones that primarily regulate the metabolism of entire body cells. In this study, Sprague-Dawley rats were grouped into sham thyroidectomy (Sham Tx), thyroidectomy (Tx), Tx with thyroxine replacement (Tx + T4), and PTU injection (PTU) groups. Metabolic parameters were measured by means of metabolic cages for 14 days. After 14 days, the rats were sacrificed while the levels of plasma or serum TSH and growth-related molecules, such as active and total ghrelin, GH, and IGF-1, were assayed. The results revealed that hypothyroid rats tended to eat less food and experienced substantial body weight gain, whereas the rats with T4 replacement tended to eat more food while continuing to lose weight. In hypothyroid rats, the growth-related molecules, such as active ghrelin and total ghrelin secretion, were enhanced, and the ghrelin receptors were also up-regulated. However, circulating GH levels were not elevated and IGF-1 secretion was inhibited in hypothyroid rats. In the Tx + T4 group, the changes of active ghrelin, total ghrelin, GHS-R expression, and IGF-1 were reversed, whereas the GH secretion was higher than that of the Sham Tx group and hypothyroid groups. This study resulted in the novel finding that the ghrelin/GHS-R axis and GH/IGF-1 axis are interrupted in hypothyroid rats.
Yen-Jui Chang; Chii-Min Hwu; Chii-Chang Yeh; Paulus S Wang; Shyi-Wu Wang
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Publication Detail:
Type:  Journal Article     Date:  2014-07-30
Journal Detail:
Title:  Molecules (Basel, Switzerland)     Volume:  19     ISSN:  1420-3049     ISO Abbreviation:  Molecules     Publication Date:  2014  
Date Detail:
Created Date:  2014-08-01     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100964009     Medline TA:  Molecules     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  11178-95     Citation Subset:  IM    
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