A Comparison of the Effects of Altered Thyroid and Parathyroid Function on Reproduction in the Rat

Hendrich, C. E.; Porterfield, Susan P.; Henderson, Jennifer; Galton, Valerie Anne

doi:10.1055/s-0028-1093645

Cited by 9 publications

(5 citation statements)

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“…We have found that if hypothyroidism (Tx) is induced on day 1 of gestation in the laboratory rat, reproduc tive performance of these animals is greatly impaired [19]. The fetuses of these Tx mothers are small for gestational age and the numbers surviving to term are greatly diminished.…”

mentioning

confidence: 99%

Behavioral Testing of Progenies of Tx (Hypothyroid) and Growth Hormone-Treated Tx Rats: An Animal Model for Mental Retardation

Hendrich

Jackson

Porterfield³

1984

Neuroendocrinology

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Virgin Sprague-Dawley Holtzman rats were rendered Tx (hypothyroid) by radiothyroidectomy and maintained on 1.0 µg T4 (thyroxine) per 100 g BW until pregnant. One-half of these Tx animals were administered 0.5 IU of growth hormone (GH) during the last 10–11 days of gestation as GH secretion is especially deficient in Tx rats. Untreated, food restricted to the level consumed by the Tx-only rats, GH-treated euthyroid, and T4-treated until pregnant animals served as controls. The animals were allowed to go through parturition and each litter was reduced to no more than 6 pups by removing pups for tissue weights and protein analyses at 1 and 5 days of age. The pups were weaned at 22 days of age and 2 animals per litter were utilized for behavioral testing between 40 and 60 days of age. At the end of the behavioral testing period the 60-day-old offspring were sacrificed to obtain tissue weights and protein concentrations. The behavioral tests were based on the ability of the animals to learn a Lashley’s type 3 enclosed alley maze and their spontaneous activity was measured in stabilimeter cages. The animals were fasted overnight on alternate days and then given a food reward upon traversing the maze. This allowed for 10 separate trials in both the Lashley maze and the stabilimeters over the 20-day period from 40 to 60 days of age. Our previous studies have shown the fetuses and progenies of Tx-only mothers to have multiple metabolic defects including reduced rates of protein synthesis and tissue protein concentrations. The Tx mothers have poor reproductive performance and the surviving fetuses and early neonates are growth stunted. GH treatment of the Tx mother, during the latter part of gestation, corrects some of these parameters in their offspring. The progenies of Tx mothers used in this study were typical of those of our previous reports. The numbers of live 1 -day-old neonates, their body, brain, and liver weights were significantly reduced as compared to controls. Brain, liver, and serum protein concentrations were significantly depressed in 1, 5-, and 60-day-old offspring of Tx-only mothers as compared to those of GH-treated and offspring of the various control group mothers. These offspring of Tx-only mothers showed a total inability to learn the Lashley maze. None of the offspring of Tx-only mothers were able to traverse the maze on consecutive trials without committing errors as compared to 25–42% of the progenies of the control groups which learned the maze before the end of 10 trials. The time required, for the offspring of all maternal groups, to traverse the maze to obtain a food reward decreased significantly. However, the offspring of Tx-only mothers, even though they would try to traverse the maze rapidly, took significantly longer to traverse the maze than progenies of the control groups in trials 6–10 because of the errors committed. These same offspring of the Tx-only mothers had also significantly increased spontaneous movements in the stabilimeter cages as compared to progenies of control mothers...

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confidence: 99%

Behavioral Testing of Progenies of Tx (Hypothyroid) and Growth Hormone-Treated Tx Rats: An Animal Model for Mental Retardation

Hendrich

Jackson

Porterfield³

1984

Neuroendocrinology

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“…Besides, it is well known that how nutritional restrictions and some hormones such as glucocorticoid [22], leptin [23,24], and insulin [25,26] affect the fetal programming; however, little is known about the role played by a low intake of thyroid hormones in critical stages of development and its impact on adult life. In this sense, several studies have reported that hypothyroidism seriously affects the reproductive performance of the female rats [27,28], which compromises the number of pups per litter. Also, the hypothyroid offspring often presents lower body mass at birth and a delay in the maturation of the central nervous system denoted by an increased eye-opening time [20,29].…”

Section: Discussionmentioning

confidence: 99%

Maternal Thyroid Hormone Deficiency During Gestation and Lactation Alters Metabolic and Thyroid Programming of the Offspring in the Adult Stage

et al. 2019

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Environmental stimuli during critical developmental stages establish long-term physiological and structural patterns that “program” health during adult life. Little is known about how alterations in hormonal supply might have consequences in metabolic and thyroid programming. This work aims to prove that alterations in the supply of thyroid hormones during gestation and lactation have long-term consequences in the metabolic and thyroid programming of the offspring. Female Wistar rats were divided into euthyroid, hypothyroid, and hypothyroid with 20 μg/day of s.c. thyroxine (T4), replacement wet nurses. Rats were mating, and after birth, pups were grouped according to their wet nurses group. Milk quality of wet nurses was assessed on days 7, 14, and 21. Body mass gain and energy intake of the offspring were monitored for 28 weeks after weaning. At sacrifice, we extracted and weighed their thyroid gland and adipose reserves, and collected blood to measure its metabolic and thyroid profiles. Hypothyroid wet nurses presented a persistent low quality of milk, while both male and female hypothyroid offspring presented lower body mass gain, higher blood glucose, dyslipidemia, hyperinsulinemia, and hyperleptinemia, as well as lower total adipose reserves, but higher visceral reserve, diminished T3 and T4 concentrations, and lower weight of thyroid gland. Thyroxine replacement prevented all changes in both wet nurses and pups. We conclude that maternal thyroid hormone deficiency during congenital and lactation stages alters the metabolic and thyroid programming of the offspring, while the reestablishment of maternal thyroid status during critical periods of development can prevent these alterations.

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“…However, the source for the increased glycogen synthesis in GH-treated Tx animals does not appear to be glucose per se (Porterfield and Hendrich 1976). These observations have provided further evidence that the fetal maldevelopment associated with maternal hypothyroidism (Porterfield, Whittle and Hendrich 1975;Porterfield and Hendrich 1975;Porterfield and Hendrich 1916;Hendrich, Porterfield, Henderson and Galton 1976) is not due entirely to self-imposed undernutrition (Hendrich et al 1976). Preliminary studies have shown also that the transfer of leucine-U-14 C from mother to fetus and its uptake by brain is impaired in Tx mothers (Hendrich and Porterfield (1980).…”

Section: Introductionmentioning

confidence: 84%

Utilization of Alanine by Hypothyroid and Growth Hormone Treated Hypothyroid Rats, their Fetuses and Progeny

Ce¹,

Vt²,

Sp³

1982

Horm Metab Res

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Maternal thyroidectomy (Tx) results in decreased maternal and fetal liver glycogen and protein as well as fetal serum glucose and maternal and fetal serum protein on the 22nd day of gestation. Progeny of Tx mothers continue to show reduced serum and liver protein levels at 1, 5 and 30 days of age. Their serum glucose is also depressed at 1 and 5 days of age but is elevated over that of control progeny by 30 days of age; whereas, liver glycogen is elevated at 1 day of age but is similar to control progeny at 5 and 30 days of age. Growth hormone (GH) treatment of the Tx mother generally reverses these effects but does not correct reproductive performance of the Tx rat. These data on maternal and fetal tissue levels of glucose and glycogen confirm our previous observations.Alanine plays a major role in glucose as well as protein homeostasis. The utilization of alanine-U-14C was assessed by determining the amount converted to glucose-glycogen, the amount incorporated into protein, the serum and liver total alanine pool, the specific activity of the liver alanine pool and in 22 day pregnant rats, the amount of 14 C02 given off during the 30, 60 and 120 minute intervals. Maternal Tx depressed significantly the labeling of glycogen and protein in both maternal and fetal liver and reduced also the total 14 C02 formed. Surprisingly this effect was still present for the labeling of liver protein in 1, 5 and 30 day old progeny of Tx mothers. However, the labeling of liver glycogen was increased significantly in 1 day old progeny but was similar to control progeny in 5 and 30 day olds. The maternal serum alanine of Tx-GH treated rats was reduced significantly ; whereas, the fetal serum alanine of Tx only rats was decreased significantly. This was true also for the 1 and 5 day old progeny of Tx mothers. However, by 30 days of age the progeny of Tx mothers had elevated serum and reduced liver alanine levels. The rate of uptake of alanine-U-14 C was depressed in the livers of the Tx mothers, their fetuses and 1, 5 and 30 day old progeny. This resulted in an early (30 min) depression of the specific activity of their liver alanine pool and a late (60 or 120 min) elevation of the specific activity of their liver free alanine pool.GH-treatment of the Tx mother reversed these effects and labeled liver protein in fetuses and 1, 5 and 30 day old progeny was normal as was the rate of accumulation of labeled alanine in the liver and, therefore, the specific activity of the liver free alanine pool. However, liver glycogen labeling was increased 360% above controls in 22 day fetuses, remained elevated at 1 day but returned to normal at 5 and 30 days of age. The labeling of liver glycogen was essentially equal to the labeling of protein in these fetuses.It is concluded that maternal Tx results in long term metabolic alterations in their progeny and that this effect is at least in part due to the accompanying deficiency of GH secretion in the mothers. GH appears to stimulate increased gluconeogenesis and increased utilization of available ...

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A Comparison of the Effects of Altered Thyroid and Parathyroid Function on Reproduction in the Rat

Cited by 9 publications

References 12 publications

Behavioral Testing of Progenies of Tx (Hypothyroid) and Growth Hormone-Treated Tx Rats: An Animal Model for Mental Retardation

Behavioral Testing of Progenies of Tx (Hypothyroid) and Growth Hormone-Treated Tx Rats: An Animal Model for Mental Retardation

Maternal Thyroid Hormone Deficiency During Gestation and Lactation Alters Metabolic and Thyroid Programming of the Offspring in the Adult Stage

Utilization of Alanine by Hypothyroid and Growth Hormone Treated Hypothyroid Rats, their Fetuses and Progeny

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