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Thyroid-induced changes in the growth of the liver, kidney, and diaphragm of neonatal rats
J P Canavan1, J Holt, J Easton
1Department of Clinical Medicine, University of Leeds, England.
Insights
Thyroid hormones impact neonatal growth. Hypothyroidism stunts growth, while hyperthyroidism causes varied tissue responses, affecting protein turnover and organ size differently in liver, kidney, and diaphragm.
Area of Science:
- Endocrinology
- Developmental Biology
- Physiology
Background:
- Thyroid hormones (T3 and T4) are crucial for neonatal development.
- Postnatal thyroid hormone surges influence tissue growth and protein metabolism.
- Understanding tissue-specific responses to thyroid status is vital for developmental research.
Purpose of the Study:
- To investigate the effects of experimentally induced hypothyroidism and hyperthyroidism on neonatal rat tissues.
- To compare the impact of altered thyroid status on protein turnover and growth in the liver, kidney, and diaphragm.
- To determine tissue-specific thresholds of responsiveness to thyroid hormones during early development.
Main Methods:
- Hypothyroidism induced via propylthiouracil (PTU) in maternal drinking water.
- Hyperthyroidism induced by daily T4 injections in pups from day 3 postpartum.
- Quantification of protein synthesis and turnover rates in liver, kidney, and diaphragm tissues.
- Comparison with euthyroid control groups.
Main Results:
- Hypothyroidism decreased protein synthesis and growth in all studied tissues, leading to overall growth retardation.
- Hyperthyroidism did not affect hepatic protein synthesis or growth.
- Diaphragm showed increased protein synthesis and degradation, resulting in hypertrophy.
- Kidney exhibited increased protein turnover but underwent atrophy.
Conclusions:
- Thyroid hormones significantly influence neonatal tissue growth and protein dynamics.
- Individual tissues display distinct sensitivities and responses to varying thyroid hormone concentrations.
- The threshold for thyroid hormone responsiveness differs among the liver, kidney, and diaphragm.
Abstract:
Eu-, hypo- and hyper-thyroid rats were studied 12 days postpartum. Hypothyroidism was induced by administering propylthiouracil (PTU) via the mother's drinking water between late gestation and throughout lactation. This procedure effectively blocked the normal early postnatal surge of T3 and T4. In contrast, hyperthyroidism was induced in the young pups by daily injections of T4 from day 3 postpartum. The effects of these experimental manipulations of thyroid status on the rates of protein turnover and growth of the liver, kidney, and diaphragm were studied and compared with measurements made on appropriate euthyroid control tissues. Tissue rates of protein synthesis were decreased in response to hypothyroidism with consequent growth retardation of all three tissues and the whole animal. In contrast, the three body tissues responded very differently to the induction of hyperthyroidism. Hepatic rates of protein synthesis and growth were completely unaffected by thyroid excess. The response of the diaphragm was essentially the reverse of that seen with hypothyroidism, i.e., the enhanced rates of protein synthesis and protein degradation leading to muscle hypertrophy. The rates of protein turnover in the kidney were also increased, but unlike the diaphragm the net result was renal atrophy. Clearly, thyroid hormones influence the normal rapid growth of the neonate and its individual tissues. However, beyond a certain concentration the threshold of responsiveness to these hormones seems to vary between individual tissues.