Influence of thyroid hormones and temperature on adipose tissue development and lung maturation

Symonds, Michael; Clarke, L.

doi:10.1079/pns19960048

Cited by 15 publications

(10 citation statements)

References 49 publications

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“…The maturation of the fetal lung is dependent on an intact fetal adrenal and thyroid gland (Symonds & Clarke, 1996; Fowden et al 1998). Potential glucocorticoid and thyroid response elements have also been identified in the promoter region of human UCP2 (Tu et al 1999), suggesting that the developmental ontogeny of UCP2 mRNA expression in the sheep lung could be directly or indirectly regulated by glucocorticoids and thyroid hormones, as is the case for brown adipose tissue‐specific UCP1 (Mostyn et al 2003 b ).…”

Section: Discussionmentioning

confidence: 99%

Ontogeny and nutritional programming of uncoupling protein‐2 and glucocorticoid receptor mRNA in the ovine lung

Gnanalingham

Mostyn

Dandrea

et al. 2005

The Journal of Physiology

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This study investigated the developmental and nutritional programming of uncoupling protein-2 (UCP2), glucocorticoid receptor (GR) and 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) mRNA in the sheep lung from the time of uterine attachment to 6 months of age. The effect of maternal nutrient restriction on lung development was determined in early to mid gestation (i.e. 28-80 days gestation, period of maximal placental growth, and embryonic and pseudoglandular stages of fetal lung development) and late gestation (i.e. 110-147 days gestation, period of maximal fetal growth, and canalicular and saccular stages of fetal lung development). Fetal lungs were sampled at 80 and 140 days (term ∼148 days) gestation, and sheep lungs at 1, 7, 30 days and 6 months. GR and 11βHSD1 mRNA were maximal at 140 days gestation, whereas UCP2 mRNA peaked at 1 day of age and then declined with postnatal age. Maternal nutrient restriction in both early-to-mid and late gestation had no effect on lung weight, but increased UCP2, GR and 11βHSD1 mRNA abundance at every sampling age. These findings suggest that the developmental ontogeny of UCP2 mRNA in the ovine lung is under local glucocorticoid hormone action and that maternal nutrient restriction has long-term consequences for UCP2 and GR mRNA abundance in the lung irrespective of its timing.

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Section: Discussionmentioning

confidence: 99%

Ontogeny and nutritional programming of uncoupling protein‐2 and glucocorticoid receptor mRNA in the ovine lung

Gnanalingham

Mostyn

Dandrea

et al. 2005

The Journal of Physiology

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“…18,19 Reduced maternal food consumption is also likely to impact on maternal thyroid status 21 that can be important in determining postnatal outcomes. 22 In the present study therefore the extent to which maternal dexamethasone administration may effect both the maternal metabolic and hormonal environment, in particular her thyroid status, as well as her food intake was also examined.…”

Section: Research Papermentioning

confidence: 99%

Maternal dexamethasone administration and the maturation of perirenal adipose tissue of the neonatal sheep

Gnanalingham

Hyatt²,

Bispham

et al. 2008

Organogenesis

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Maternal dexamethasone administration promotes fetal maturation such that thermoregulation is improved following premature delivery and is thus comparable with a full term birth. In the present study we determined the impact of dexamethasone on both the mothers' metabolic status together with adipose tissue function in the newborn. Glucocorticoid action, adipokine gene expression and mitochondrial protein abundance were measured in perirenal adipose tissue of neonatal sheep that were born into either a warm (30˚C) or cool (15˚C) ambient temperature at 140 days of gestation (dGA; term ~147 dGA), either two days after maternal dexamethasone administration, or at 146 dGA for controls. Dexamethasone administration resulted in a reduction in maternal food intake in conjunction with raised plasma cortisol and free triiodothyronine. In offspring of dexamethasone administered mothers, plasma cortisol was lower and non-esterified fatty acids (NEFA) higher than controls. Glucocorticoid receptor (GR), 11β-hydroxysteroid dehydrogenase (11β-HSD1), interleukin-6 and uncoupling protein (UCP)1 and 2 mRNA together with voltage dependent anion channel, cytochrome c protein and UCP1 abundance were all increased by dexamethasone administration and being born into a cool ambient temperature. Gene expression of tumor necrosis factor α, adiponectin and peroxisome proliferator-activated receptor transcription factor γ were unaffected by dexamethasone. The abundance of mRNA for the GR, 11β-HSD1, UCP1 and 2 mRNA together with each protein were positively correlated to plasma NEFA and negatively correlated to plasma cortisol. In conclusion, despite reduced maternal food intake dexamethasone promotes maturation of glucocorticoid action and mitochondrial protein abundance in the newborn, an adaptation dependent on delivery temperature.

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“…Thyroid hormones play crucial roles in growth and normal CNS maturation, neuronal and glial cell differentiation and migration, synaptogenesis, and myelination (Koibuchi and Chin, 2000;Oppenheimer and Schwartz, 1997). Additionally, thyroid hormones affect adipocyte development and lipid accretion, O 2 consumption, as well as maturation of the renin-angiotensin system and cardiovascular function in fetuses (Chen et al, 2005;Hausman, 1999;Symonds and Clarke, 1996).…”

Section: Introductionmentioning

confidence: 99%

Unbiased stereological estimation of the rat fetal pituitary volume and of the total number and volume of TSH cells after maternal dexamethasone application

Manojlović‐Stojanoski¹,

Nestorović²,

Ristić³

et al. 2010

Microscopy Res & Technique

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Glucocorticoids have an inhibitory influence on proliferation activity of the pituitary cells while stimulating apoptosis. Therefore, it was hypothesized that the synthetic glucocorticoid, dexamethasone (DX), has an inhibitory influence on the number of thyroid-stimulating hormone (TSH) cells during fetal development. The effects of maternal administration of DX on stereological parameters of TSH cells, and TSH serum concentration were investigated in 21-day-old rat fetuses. On day 16 of pregnancy, the experimental dams received 1.0 mg DX/kg b.w. subcutaneously, followed by 0.5 mg DX/kg b.w./day on days 17 and 18 of gestation. The control gravid females received the same volume of saline vehicle. TSH cells were stained immunocytochemically by the peroxidase-antiperoxidase (PAP) method. The fetal pituitary volumes were estimated using Cavalieri's principle. A physical disector counting technique in combination with the fractionator sampling method was used for estimation of pituitary TSH cell number. Cell and nuclear volumes were measured with a planar rotator. Maternal DX application was found to cause a significant decrease of pituitary volume and number of TSH cells per pituitary in 21-day-old fetuses in comparison with the control fetuses. TSH cell number expressed per body weight unit declined significantly after maternal DX administration. These results indicate an inhibitory DX influence on proliferative activity of precursors and likely differentiated TSH cells and increased apoptotic prevalence. The histological appearance, volume of TSH cells and TSH serum concentration suggest intensive synthetic activity in TSH cells of DX exposed fetuses.

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Influence of thyroid hormones and temperature on adipose tissue development and lung maturation

Cited by 15 publications

References 49 publications

Ontogeny and nutritional programming of uncoupling protein‐2 and glucocorticoid receptor mRNA in the ovine lung

Ontogeny and nutritional programming of uncoupling protein‐2 and glucocorticoid receptor mRNA in the ovine lung

Maternal dexamethasone administration and the maturation of perirenal adipose tissue of the neonatal sheep

Unbiased stereological estimation of the rat fetal pituitary volume and of the total number and volume of TSH cells after maternal dexamethasone application

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