Endocrine Abstracts

Thyroid hormones (TH) are required for normal postnatal growth development in mammals. The physiological importance of TH becomes evident under the conditions of congenital–neonatal hypothyroidism (CH). If not treated immediately, CH has a profound impact on physiology and can permanently imprint neurological and endocrine systems, which, in turn, led to mental retardation, growth arrest, and metabolic disturbances. A delayed growth development or long-lasting influence of CH on somatotropic-related liver functions could be related with GH resistance. GH resistance has been shown in rat models of sepsis, uremia or in small rats for gestational age. In these models, GH resistance has been associated with increased expression of suppressors of cytokine signalling (SOCS) proteins which contribute to impair GH–JAK–STAT signaling. Here, we studied expression of SOCS genes in liver from rats previously exposed to CH. Pregnant rats were given anti-thyroid drug methimazole (MMI) from Gestational Day 12 until postnatal day (PND) 30 to induce CH in male offspring. Growth defects due to CH were evident as a reduction in body weight and tail length from the second week of life. Once the growth inhibiting condition (MMI) was discontinued on PND30, significant catch-up growth was evident in CH rats. On PND80, significant reduction in body mass, tail length, and circulating IGF1 remained in CH rats. Serum levels of thyroid hormones, cholesterol, and triglycerides showed no significant differences. However, we observed down-regulation of female-predominant (e.g. CYP2C7) together with induction of male-predominant genes (e.g. CYP2C11) which suggested that a male pattern of gene expression was enhanced in CH rat liver. Finally, we observed an impaired somatic growth followed by catch-up growth in rats previously exposed to CH that was associated with increased expression of SOCS (SOCS2 and CIS), a phenomena that requires further research.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.