Sex-specific changes in thyroid gland function and circulating thyroid hormones in nestling American kestrels (Falco sparverius) following embryonic exposure to polybrominated diphenyl ethers by maternal transfer

2016 ◽  
Vol 35 (8) ◽  
pp. 2084-2091 ◽  
Author(s):  
Kim J. Fernie ◽  
Sarah C. Marteinson
2012 ◽  
Vol 47 (No. 7) ◽  
pp. 199-210 ◽  
Author(s):  
Huszebucza GY ◽  
M. Kulcszr ◽  
P. Rudas

After briefly introducing the basec steps in production and metabolism of thyroid hormones, the author gives an overview of nutritional, metabolic and disease related factors and endocrine interactions influencing thyroid gland function in ruminants, particularly in the postpartum dairy cow. Involvement of thyroid hormonal regulation of seasonal patterns of reproduction as well as ovarian endocrine function are discussed.


2000 ◽  
Vol 83 (5) ◽  
pp. 3101-3112 ◽  
Author(s):  
Marlies Knipper ◽  
Christoph Zinn ◽  
Hannes Maier ◽  
Mark Praetorius ◽  
Karin Rohbock ◽  
...  

Both a genetic or acquired neonatal thyroid hormone (TH) deficiency may result in a profound mental disability that is often accompanied by deafness. The existence of various TH-sensitive periods during inner ear development and general success of delayed, corrective TH treatment was investigated by treating pregnant and lactating rats with the goitrogen methimazole (MMI). We observed that for the establishment of normal hearing ability, maternal TH, before fetal thyroid gland function on estrus days 17–18, is obviously not required. Within a crucial time between the onset of fetal thyroid gland function and the onset of hearing at postnatal day 12 ( P12), any postponement in the rise of TH-plasma levels, as can be brought about by treating lactating mothers with MMI, leads to permanent hearing defects of the adult offspring. The severity of hearing defects that were measured in 3- to 9-mo-old offspring could be increased with each additional day of TH deficiency during this critical period. Unexpectedly, the active cochlear process, assayed by distortion product otoacoustic emissions (DPOAE) measurements, and speed of auditory brain stem responses, which both until now were not thought to be controlled by TH, proved to be TH-dependent processes that were damaged by a delay of TH supply within this critical time. In contrast, no significant differences in the gross morphology and innervation of the organ of Corti or myelin gene expression in the auditory system, detected as myelin basic protein (MBP) and proteolipid protein (PLP) mRNA using Northern blot approach, were observed when TH supply was delayed for few days. These classical TH-dependent processes, however, were damaged when TH supply was delayed for several weeks. These surprising results may suggest the existence of different TH-dependent processes in the auditory system: those that respond to corrective TH supply (e.g., innervation and morphogenesis of the organ of Corti) and those that do not, but require T3 activity during a very tight time window (e.g., active cochlear process, central processes).


PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e113699 ◽  
Author(s):  
Xijin Xu ◽  
Junxiao Liu ◽  
Xiang Zeng ◽  
Fangfang Lu ◽  
Aimin Chen ◽  
...  

2020 ◽  
Author(s):  
Elena V. Kozlova ◽  
Bhuvaneswari D. Chinthirla ◽  
Pedro A. Pérez ◽  
Nicholas V. DiPatrizio ◽  
Donovan A. Argueta ◽  
...  

AbstractPolybrominated diphenyl ethers (PBDEs) are brominated flame retardant chemicals and environmental contaminants with endocrine-disrupting properties that are associated with diabetes and metabolic syndrome in humans. However, their diabetogenic actions are not completely characterized or understood. In this study, we investigated the effects of DE-71, a commercial penta-mixture of PBDEs, on glucose regulatory parameters in a perinatal exposure model using female C57Bl/6 mice. Results from in vivo glucose and insulin tolerance tests and ex vivo analyses showed that DE-71 produced fasting hyperglycemia, glucose intolerance, reduced sensitivity and delayed glucose clearance after insulin challenge, and exaggerated hepatic endocannabinoid tone in F1 offspring exposed to 0.1 mg/kg DE-71 relative to control. DE-71 effects on F0 dams were more limited indicating that indirect exposure to developing offspring is more detrimental. Other ex vivo glycemic correlates occur more generally in exposed F0 and F1, i.e., reduced plasma insulin and altered glucoregulatory endocrines, exaggerated sympathoadrenal activity, decreased thermogenic brown adipose tissue mass and reduced hepatic glutamate dehydrogenase enzymatic activity. Hepatic PBDE congener analysis indicated maternal transfer of BDE-28 and −153 to F1 at a collective level of 200 ng/g lipid, in range with maximum values detected in serum of human females. Given the persistent diabetogenic phenotype, especially pronounced in female offspring after developmental exposure to environmentally relevant levels of DE-71, additional animal studies should be conducted that further characterize PBDE-induced diabetic pathophysiology and identify critical developmental time windows of susceptibility. Longitudinal human studies should also be conducted to determine the risk of long-lasting metabolic consequences after maternal transfer of PBDEs during early-life development.


2011 ◽  
Vol 24 (2) ◽  
pp. 377-386 ◽  
Author(s):  
A.V. Sakellaropoulou ◽  
M.N. Hatzistilianou ◽  
M.N. Emporiadou ◽  
V.TH. Aivazis ◽  
I. Rousso ◽  
...  

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