Thyroid‐induced changes in the growth of the Liver, Kidney, and Diaphragm of Neonatal Rats

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.

The influence of thyroid hormones on the growth of the atria and ventricles of the heart in immature rats

“…at 20 days (Table 3). These changes in the heart contrast with the lack of growth enhancement found in the lungs (Holt et al 1993) or hver (Canavan et al 1994) of the same hyperthyroid neonate. Although the excess T3 and T4 could be acting directly on the myocardial tissue, indirect haemodynamic effects (Klein & Hong 1986, Coleman et al 1989) could possibly be responsible for much of the accelerated growth and increased protein synthesis, especially in the ventricles.…”

“…Both the atria and ventricles of these animals were clearly growth retarded. The extent of the growth suppression was similar to that experienced by the whole animal (34%; Holt et al 1993) whilst this varied more widely in other body tissues such as the diaphragm (48%), liver (28%) (Canavan et al 1994) and lungs (18%; Holt et al 1993).…”

Impact Of Continuous Treatment With Propylthiouracil On Renal And Hepatic Functions In Rabbits

“…Histopathological studies ruled out the effect of thyroid hormone deficiency on the renal cortex and outer renal medulla. The proximal and distal convoluted tubules and medullary part of the ascending lobe of Henle were primary and severely affected in rats (Canavan et al, 1994). PTU, which found to induce a direct effect on the thyroid gland causing hypothyroidism, was indirectly affected the renal function and structure such effect may be mediated by an associated deficiency of thyroid hormone (T 3 and T 4 ).…”

The Renal Manifestations of Thyroid Disease

“…[4][5][6] In neonatal rats, hypothyroidism decreases kidney size and weight, tubule length and diameter, and, to a lesser extent, glomerular volume. [7][8][9] These changes invariably reverse with thyroid hormone replacement. Hypothyroidism also blunts compensatory hypertrophy after unilateral nephrectomy in remnant kidney models.…”