This study investigated the effects of type 1 diabetes (T1D), type 2 diabetes (T2D), and HT on the expression levels of SIRT1, SIRT3, and manganese superoxide dismutase (SOD2).
Similarly, expression of TRα-1, TRβ-1, TSHR, ERK1/2 and RAR proteins and mRNA in the uterus of non-treated hypothyroid rats also decreased (P < 0.05 when compared to euthyroid and thyroxine-treated hypothyroid rats).
Low T4 was observed in preterm infants irrespective of the cause of preterm birth, while maternal (TSH) and placental (DiO2, DiO3, and MCT10) compensatory responses were only activated in indicated preterm birth due to vascular complications.
COP subjects had a significantly higher risk for hypothyroidism than non-COP subjects (adjusted hazard ratio [AHR]: 3.8; 95% confidence interval [CI]: 3.2-4.7) after adjusting for age, sex, underlying comorbidities, and monthly income, and the AHR was particular higher in subjects with diabetes mellitus, hyperlipidemia, and mental disorder.
Male mice with a global (Dkk1fl/fl;Rosa26-CreERT2) or osteocyte-specific (Dkk1fl/fl;Dmp1:Cre) deletion of Dkk1 were pharmacologically rendered hypothyroid or hyperthyroid.
These findings suggested that both BDE-209 and DBDPE exposure could disrupt thyroid function in the direction of hypothyroidism and the underlying mechanism was likely to be oxidative stress and perturbations of HPT axis.
The patients with higher TIGIT mRNA levels had a greater prevalence of hypothyroidism, showing higher peak thyrotropin levels at diagnosis or at follow-up.
This study investigated the effects of type 1 diabetes (T1D), type 2 diabetes (T2D), and HT on the expression levels of SIRT1, SIRT3, and manganese superoxide dismutase (SOD2).
The opposing changes in mRNA expression levels of Ku-70 in patients with hypothyroidism indicate its potential as a prognostic marker for hypothyroidism induced by <sup>131</sup>I treatment.
Interestingly, in the hypothyroid state, CMNS caused concomitant activation of two signaling pathways that are usually reciprocally regulated - AMPK and mTOR signaling - which manifested as increased β-oxidation, MHC-I expression, and protein synthesis.
Mitochondrial content of coenzyme Q9 and Q10 was lower in hypothyroidism and higher in hyperthyroidism suggesting that the thyroid state-linked changes in the rates of H<sub>2</sub>O<sub>2</sub> production are due to changes in the ubiquinone mitochondrial content.
Influence of hypothyroidism on testicular mitochondrial oxidative stress by activating the p38 mitogen-activated protein kinase and c-Jun NH<sub>2</sub>-terminal kinase signaling pathways in rats.
In the male fish, transcriptions of corticotropin-releasing hormone (crh) and thyroid-stimulating hormone (tsh) in the brain were significantly up-regulated, probably as a compensation for hypothyroidism, but thyroglobulin (tg) and deiodinase 2 (dio2) were down-regulated in thyroid or liver.
In conclusion, a decrease in hepcidin concentration during the transition from the hypothyroid state to euthyroidism in patients with HT is associated with the observed dynamics in iron homeostasis, mainly reflected by improvement in RDW-CV and significant correlations between ferritin and hepcidin as well as between hepcidin and fT3.
Male mice with a global (Dkk1fl/fl;Rosa26-CreERT2) or osteocyte-specific (Dkk1fl/fl;Dmp1:Cre) deletion of Dkk1 were pharmacologically rendered hypothyroid or hyperthyroid.
Contemporaneous effects of diabetes mellitus and hypothyroidism on spermatogenesis and immunolocalization of Claudin-11 inside the seminiferous tubules of mice.
To verify our hypothesis that the MAPK pathway may function significantly in triclosan-induced hypothyroidism, Sprague-Dawley rats were gavaged with triclosan for 31 consecutive days; Nthy-ori 3-1 cells were treated with triclosan in the presence/absence of NAC, inhibitors (SB203580 and SB202474), or TRHr siRNA.
Previous studies indicate that Dnajc17 as a candidate modifier gene for hypothyroidism, since it is expressed in the thyroid bud, interacts with NKX2.1 and PAX8 and it has been associated to the hypothyroid phenotype in mice carrying a single Nkx2.1 and Pax8 genes (double heterozygous knock-out).
Ten proteins were more abundant in the hypothyroid vs. euthyroid state: complement C2, serotransferrin, complement C3, Ig κ chain C region, α-1-antichymotrypsin, complement C4-A, haptoglobin, fibrinogen α chain, apolipoprotein A-I, and Ig α-1 chain C region.