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Serum growth hormone levels in hypothyroid and GH-treated thyroidectomized rats and their progenies
C E Hendrich1, S P Porterfield
1Department of Physiology and Endocrinology, Medical College of Georgia, Augusta 30912.
Insights
Growth hormone (GH) is ineffective in preventing developmental deficits in hypothyroid rat offspring. Adequate thyroid hormones are crucial for GH
Area of Science:
- Endocrinology
- Developmental Biology
- Neuroscience
Background:
- Thyroid hormones are essential for normal fetal and postnatal development.
- Growth hormone (GH) plays a critical role in growth and development.
- Maternal hypothyroidism can impact fetal development and offspring neurodevelopment.
Purpose of the Study:
- To investigate the role of growth hormone (GH) in the context of maternal hypothyroidism.
- To determine if GH administration can mitigate developmental deficits in offspring of hypothyroid mothers.
- To examine the interplay between thyroid hormones and GH during gestation and postnatal development.
Main Methods:
- Measurement of serum GH levels in control, thyroidectomized (Tx), and GH-treated Tx rats and their fetuses/progenies at various gestational and postnatal ages.
- Assessment of GH secretion patterns during critical developmental periods.
- Comparison of GH levels between different experimental groups.
Main Results:
- Maternal GH levels were depressed in Tx and GH-treated Tx rats during gestation.
- Fetal GH levels were affected by maternal thyroid status, with GH levels altered in fetuses of Tx and GH-treated Tx mothers.
- Postnatal GH levels were elevated in progenies of Tx mothers, normalizing by 75 days of age.
- GH administration to Tx mothers did not fully normalize fetal GH levels.
- Offspring of Tx mothers exhibited disrupted pituitary-thyroid axis and persistent deficits in thyroid hormone levels.
Conclusions:
- Growth hormone (GH) alone is insufficient to prevent learning and memory deficits in offspring exposed to thyroid hormone deficiency in utero.
- Adequate thyroid hormone levels are necessary for GH to be effective in preventing developmental abnormalities.
- The study highlights the critical importance of the thyroid hormone-GH axis for normal neurodevelopment.
Abstract:
Growth hormone (GH) was measured in the sera of control, hypothyroid (thyroidectomized [Tx]) and GH-treated Tx rats and their fetuses on Days 19, 20, 21, and 22 of gestation and in their progenies on postnatal Days 1, 5, 30, and 75. Maternal endogenous serum GH increased dramatically between the 19th and 20th days of gestation and remained elevated through the 22nd day in control rats, but was depressed significantly in Tx and GH-treated Tx rats during this period. GH was not always detected in the sera of 19-day-old fetuses. On Day 20, GH was depressed in fetuses of Tx mothers as compared with those form controls or GH-treated Tx mothers. GH was elevated in sera of fetuses from GH-treated Tx rats over fetuses of control and Tx only rats on the 22nd day of gestation. In postnatal rats, those from GH-treated mothers continued to show elevated serum GH on Day 1 as compared with those from Tx only mothers. On postnatal Days 5 and 30, progenies of Tx mothers had significantly elevated GH as compared with progenies of control mothers. At 75 days of age, the GH levels of these progenies had normalized. We have shown previously that the hormonal secretions of the pituitary-thyroid axis are badly disrupted in the progenies of Tx and GH-treated Tx mothers and that even as adults these animals have tissue (brain and liver) deficits of active thyroid hormones. Although the onset of GH secretion is mildly delayed in fetuses of Tx but not GH-treated Tx mothers, the serum GH levels of both groups of progenies are elevated during most of the neonatal period through the time of puberty. It is, therefore, concluded that GH in the absence of adequate levels of thyroid hormones is ineffective in preventing many of the learning and memory deficits induced in the progenies of Tx mothers.
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