Serum Thyroid Hormone Levels Research Articles

The Thyroid Condition and Residual Clinical Signs in 31 Existing Endemic Neurological Cretins After 42 Years of Iodine Supplementation in China.

BackgroudEndemic cretinism is the most severe manifestation among the iodine deficiency-related disorders. The clinical status of the cretins may be modified subsequently by the duration and severity of the disease. We aimed to reassess the clinical status and thyroid function of 31 surviving “neurological cretins” after 42 years of iodine supplementation in a historically severely iodine deficiency area of China.MethodsIt was a cross-sectional study in design and we investigated all 31 surviving neurological cretins and 85 controls. A detailed neurological examination was conducted on each patients. All the participants were given a questionnaire and underwent B-mode ultrasonography of the thyroid. The serum levels of thyroid hormones, thyroid antibodies, serum iodine concentration (SIC) and urine iodine concentration (UIC) were measured.ResultsThe neurological cretins had shorter stature than that of the control. Neurological damage is still present in patients with cretinism. The prevalence of subclinical hypothyroidism and thyroid nodule in the cretins was significantly higher (χ2 =4.766, P=0.029 and χ2 =17.077, P<0.0001, respectively) compared with the control. After adjusting for confounding factors, endemic neurocretinism was found to be an independent risk factor for subclinical hypothyroidism (OR=4.412; 95% CI: 1.358–14.334; P=0.014) and thyroid nodule (OR=6.433; 95% CI: 2.323–17.816; P<0.0001).ConclusionsIodine supplementation after birth does not reverse the neurological damage that results from maternal/foetal hypothyroidism in utero and is subsequently manifested as neurological cretinism. There is a cross-sectional association between endemic neurocretinism and subclinical hypothyroidism and thyroid nodule.

Mediation effects of thyroid function in the associations between phthalate exposure and lipid metabolism in adults

Phthalates are a group of industrial chemicals widely used in everyday products including cosmetics, food packaging and containers, plastics, and building materials. Previous studies have indicated that urinary phthalate metabolites are associated with metabolic effects including those on lipid metabolism, but the results are mixed. Furthermore, whether thyroid function mediates the association between phthalate exposure and lipid metabolism remains unclear. In the present study, we explored whether changes in thyroid function markers mediate the associations between phthalate exposure and lipid metabolism indicators in Taiwanese adults. The cross-sectional data were obtained from the Taiwan Environmental Survey for Toxicants conducted in 2013. Levels of 11 urinary phthalate metabolites, levels of 5 thyroid hormones, and 8 indicators of lipid metabolism were assessed in 222 Taiwanese adults. The relationships of urinary phthalate metabolite levels with serum thyroid hormone levels and lipid metabolism indicators were explored using multiple regression models. Mediation analysis was conducted to evaluate the role of thyroid function in the association between phthalate exposure and lipid metabolism. The metabolite of di(− 2-ethylhexyl) phthalate (∑DEHPm) exhibited a significant positive association with the lipid metabolite indicator of high-density lipoprotein cholesterol (HDL-C; β = 0.059, 95% confidence interval [CI] = 0.009, 0.109) in adults, and the thyroid function indicator thyroxine (T4) had a significant negative association with the metabolite ∑DEHPm (β = − 0.059, 95% CI = − 0.101, − 0.016) and a significant negative association with HDL-C (β = − 0.284, 95% CI = − 0.440, − 0.128). The T4 indirect effect was 0.015 (95% CI = − 0.0087, 0.05), and the mediation effect was 32.2%. Our results support the assumption that exposure to phthalates influences the homeostasis of lipid metabolism by interfering with thyroid function.

Evaluation of lipid profile in postmenopausal breast cancer patients and its association with serum level of thyroid hormones, vitamin D and estrogen

The aim of the present research is to evaluate the lipid profile in postmenopausal breast cancer patients and its association with serum level of thyroid hormones, vitamin D, and estrogen level. In this research, 45 postmenopausal women with breast cancer (BC group) and 45 postmenopausal healthy women (control group) were participated. Serum level of cholesterol, triglyceride, and HDL were measured using spectrophotometry. Serum level of LDL and VLDL was estimated by formula and serum level of TSH, T3, T4, fT4, 25 (OH) D3 and estrogen hormone were determined by the ELISA technique. The obtained results show that the concentrations of HDL-C in BC subgroup (Pvalue less than 0.05) were substantially lower than the healthy group. Although other lipid profile including TC, TG, LDL and VLDL in the BC group was higher than in the healthy group, however, this difference was not significant. Also, T3 level in the BC group was significantly higher than the healthy group (P&lt; 0.05). Finally, the serum concentration of 25-OH- D3 was considerably lower in the BC group (P 0.05) than in the healthy group and the serum concentration of estrogen in the BC group was significantly higher than the healthy group (P &lt; 0.05). A significant positive correlation was observed between T4 and HDL (r=0.33, P=0.02). Also T4 had a significant negative correlation with TG (r= -0.37, p=0.01) and VLDL (r= -0.37, P=0.01). Based on these findings, it can be concluded that thyroid dysfunction, vitamin D deficiency, lipid profile disorders, and high level of estrogen can be considered as risk factors for breast cancer in postmenopausal women. Therefore, routine screening of these parameters in the postmenopausal period is recommended to reduce the incidence of breast cancer.

Evaluation of lipid profile in postmenopausal breast cancer patients and its association with serum level of thyroid hormones, vitamin D and estrogen

Evaluation of lipid profile in postmenopausal breast cancer patients and its association with serum level of thyroid hormones, vitamin D and estrogen

Molecular Cloning and Expression Analysis of Thyrotropin-Releasing Hormone, and Its Possible Role in Gonadal Differentiation in Rice Field eel Monopterus albus.

Simple SummaryThyrotropin-releasing hormone (TRH) is an important upstream regulator in the hypothalamus-pituitary-thyroid (HPT) axis in mammals. In this study, we isolated and characterized trh gene from a protogynous hermaphrodite fish rice field eel Monopterus albus. TRH had no significant effect on serum thyroid hormone levels in rice field eel. However, we found that TRH was involved in the regulation gonadal differentiation-related gene expression and serum sex steroid hormone secretion. Our results indicated that TRH may play a novel role in gonadal differentiation in rice field eel.Rice field eel (Monopterus albus), a protogynous hermaphrodite fish, is a good model for the research of sex determination and gonadal differentiation in teleosts. In this study, we cloned the full-length cDNA sequence of trh, which encoded a predicted protein with 270 amino acids. Trh mainly expressed in the brain, followed by the ovary, testis, muscle and pituitary, and had low levels in other peripheral tissues. During natural sex reversal, trh mRNA expression levels exhibited a significant increase at the late intersexual stage in the hypothalamus. In the gonad, trh mRNA expression levels showed a trend of increase followed by decrease, and only increased significantly at the middle intersexual stage. No matter static incubation or intraperitoneal (IP) injection, TRH had no significant effect on trh and thyroid-stimulating hormone β subunit (tshβ) mRNA expression levels, and serum T3, T4 and TRH release. After static incubation of ovarian fragments by TRH, the expression of gonadal soma derived factor (gsdf) was up-regulated significantly at both the doses of 10 and 100 nM. IP injection of TRH stimulated the expression of gsdf, and inhibited the expression of ovarian aromatase gene (cyp19a1a), accompanied by the increase of serum 11-KT levels. The results indicated that TRH may play a novel role in gonadal differentiation by the regulation of gonadal differentiation-related gene expression and sex steroid hormone secretion in rice field eel.

Association of Thyroid Hormones with Oxidative Stress Markers in Patient with Hyperthyroidism

Background: Biomarkers for diagnosing the occurrence and development of hyperthyroidism constitute a major worldwide clinical scrutiny. Evidence is continuing in an investigation about the most relevant biomarkers in developing the disease.Objective: To discover and correlate the most dependent biomarkers in developing hyperthyroidism in both genders.Patients and Methods: In the present study, two groups were included, the first group: forty males and females with chronic hyperthyroidism were enrolled. Serum levels of thyroid hormones, lipid profile, oxidative stress marker, blood glucose, and renal function markers were measured and compared with euthyroid subjects. Results: The present study revealed that referral biomarkers were varied between genders with a remarkable association of hyperthyroidism with serum cholesterol, triglycerides, and low-density lipoproteins in females, while nitrites and creatinine and MDA were significantly correlated in male patients. Conclusion: In this study, we found that indicating biomarkers for hyperthyroidism could be differentially changed in different genders that help in understanding the progression and development of the disease. Keywords: Hyperthyroidism, oxidative stress, malondialdehyde, creatinine, nitrite.

Helicobacter pylori Infection Is Associated With Thyroid Dysfunction in Children With Congenital Hypothyroidism.

Helicobacter pylori (H. pylori) infection leads to a systemic low-grade inflammatory state and has been associated causally with a diverse spectrum of extra-gastric disorders. Among them, the infection has been involved in the pathogenesis of autoimmune thyroid disease (ATD), but only one study had evaluated children. Therefore, a cross-sectional study was conducted in a cohort of 142 children and adolescents, randomly assessed among those followed up for thyroid diseases in a university pediatric endocrinology service: 106 with congenital hypothyroidism (CH) and 36 with ATD. All children were asymptomatic, under strict control on levothyroxine replacement, and reported no other diseases or use of drugs. Helicobacter pylori status was evaluated by the 13C-Urea Breath Test (13C-UBT). Antithyroid antibodies (ATPO, antiTg, and TRAb) and serum thyroid hormones (TSH, free T4, and T3) were assessed by standard assays. Data were analyzed in logistic models by the SPSS statistical software package, and a p-value ≤ 0.05 was considered statistically significant. The prevalence of H. pylori infection was 19.44% in children with ATD. Neither the gender nor the serum levels of thyroid hormones and antithyroid antibodies were associated with the H. pylori-positive status. Thirty-seven (34.90%) children with CH were infected with H. pylori. The mean T3 serum level (3.59 ± 0.84) was significantly lower (p = 0.001) in the infected children than in those free from the infection (3.95 ± 0.89), association that remained after adjustment for the other variables in the multivariate analysis. Because no difference was observed in the levels of TSH and T4, the results indicate that the infection may lead to impairment in the thyroid hormonal balance, but not in the hypothalamic-pituitary-thyroid axis function. In as much as H. pylori infection is highly widespread and the prevalence of CH is also not negligible, additional studies are required to confirm our results and to identify the involved mechanisms.

Sublethal effects of acrylamide on thyroid hormones, complete blood count and micronucleus frequency of vertebrate model organism (Cyprinus carpio)

Abstract Objectives Acrylamide, a widely used chemical in industry, clinical laboratory and waste treatment plants, is considered a carcinogen in humans. The present study examined the hormonal, hematologic, and genotoxic responses in the invertebrate model common carp Cyprinus carpio after exposure to sublethal acrylamide. Methods Fish were exposed to acrylamide at 10 and 50 mg/L for 96 h, along with the respective control group. Serum levels of cortisol and thyroid hormones were measured using diagnostic ELISA direct immunoenzymatic kits. For micronucleus (MN) frequency assay, thin smears of the peripheral blood of fish were prepared. Results Serum levels of cortisol in both treatment groups considerably increased, which proposed that acrylamide caused a stress reaction of acrylamide exposed fish (p&lt;0.05). Fish demonstrated significant decreases in triiodothyronine (T3), free thyroxine (FT4), and free triiodothyronine (FT3) concentrations in a dose-dependent manner after acrylamide exposure (p&lt;0.05). However, serum thyroxine (T4) concentrations did not alter significantly in the treatment groups. Mean MN frequencies of fish erythrocytes increased significantly in acrylamide exposed groups suggesting that acrylamide is genotoxic in common carp (p&lt;0.05). The hematocrit, hemoglobin, and erythrocyte numbers of carp increased significantly in exposure groups (p&lt;0.05). Conclusions These results suggested that acrylamide can significantly affect the hemopoietic system. Furthermore, this study confirmed that the widespread use of acrylamide, even in sublethal concentrations, could affect the survival of non-target organisms, especially fish, in aquatic environments.

The Clinical Value of Thyroid Hormone Levels and Correlation with Severity of Liver Cirrhosis.

Background The aims of this study were to expound the effect of thyroid hormone on the occurrence of liver cirrhosis and the severity classification of liver cirrhosis with meta-analysis. Methods A comprehensive search of PubMed, EMbase, The Cochrane Library, Web of Science, Google Scholar, CNKI, and WanFang Data databases and reference lists of retrieved articles was performed since the inception of each database until September 2021. Two reviewers independently screened literature, extracted data, and assessed the risk of bias by RevMan 5.3 software. In continuous variable analysis, the standardized mean difference (SMD) and 95% confidence interval (95% CI) were calculated through a random-effect model. Results Eighteen case-control studies involving 3336 subjects were included for review. The results of the meta-analysis showed free triiodothyronine (FT3) and free thyroxine (FT4) levels in the liver cirrhosis group were lower than the control group (SMD = −1.29, 95% CI [−1.85, −0.74], P < 0.001), (SMD = −0.61, 95% CI [−0.96, −0.26], P < 0.001), thyroid-stimulating hormone (TSH) levels in liver cirrhosis group were higher than the control group (SMD = 0.34, 95%CI [0.06, 0.63], P < 0.001) and that FT3 levels in Child-Pugh A VS B and Child-Pugh B VS C group were higher than the control group (SMD = 1.08, 95%CI [0.80, 1.37], P = 0.008), (SMD = 0.68, 95%CI [0.38, 0.98], P < 0.001). Conclusions Cirrhosis has decreased FT3 and FT4 levels and increased TSH levels. FT3 levels correlate negatively with the Child-Pugh score, and it is a measure of the severity of liver cirrhosis dysfunction. FT3 serum levels of thyroid hormones are a prognostic marker in liver cirrhosis.

Health impact assessment of pet cats caused by organohalogen contaminants by serum metabolomics and thyroid hormone analysis

Companion animals are in close contact with the human surroundings, and there is growing concern about the effects of harmful substances on the health of pet cats. In this study, we investigated the potential health effects of organohalogen compounds (OHCs) on thyroid hormone (TH) homeostasis and metabolomics in Japanese pet cats. There was a significant negative correlation between concentrations of several contaminants, such as polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs), hydroxylated PCBs (OH-PCBs), hydroxylated PBDEs (OH-PBDEs), and THs in cat serum samples. These results suggested that exposure to OHCs causes a decrease in serum TH levels in pet cats.In this metabolomics study, each exposure level of parent compounds (PCBs and PBDEs) and their hydroxylated compounds (OH-PCBs and OH-PBDEs) were associated with their own unique primary metabolic pathways, suggesting that parent and phenolic compounds exhibit different mechanisms of action and biological effects. PCBs were associated with many metabolic pathways, including glutathione and purine metabolism, and the effects were replicated in in-vivo cat PCB administration studies. These results demonstrated that OHC exposure causes chronic oxidative stress in pet cats. PBDEs were positively associated with alanine, aspartate, and glutamate metabolism. Due to the chronic exposure of cats to mixtures of these contaminants, the combination of their respective metabolic pathways may have a synergistic effect.

Protective effects of curcumin against thyroid hormone imbalance after gas explosion-induced traumatic brain injury via activation of the hypothalamic-pituitary-thyroid axis in male rats.

Gas explosion (GE)-induced traumatic brain injury (TBI) can affect thyroid hormone (TH) homeostasis in miners. This study evaluated the effects of hepatic transthyretin and hypothalamic-pituitary-thyroid (HPT) axis on thyroids and explored the protective effect and mechanism of curcumin on GE-induced TBI. Thirty rats were randomly divided into three groups (10 per group): first group (control group)-rats received GE treatment once; second group (GE group)-rats received GE treatment (200m from the source of the explosion once); third group (GE + Cur group)-rats received curcumin (Cur) by lavage at a dose of 100mg/kg/day once every other day for 7days after receiving GE. After GE, the pathological changes were analyzed by hemotoxylin and eosin staining, and the levels of serum reactive oxygen species (ROS), urine iodine (UI), THs, nuclear factor-kappa B (NF-κB), superoxide dismutase (SOD), glutathione peroxidase (Gpx), and malondialdehyde (MDA) were analyzed using ELISA. Expression of proteins in the HPT axis of rats was examined by immunohistochemistry and Western blotting. We found that GE could induce pathologic changes in rat thyroid and liver. Serum levels of THs, NF-κB and serum redox state became unbalanced in rats after GE. GE could inhibit the biosynthesis and biotransformation of THs by affecting key HPT axis proteins. Additionally, GE reduced the level of hepatic transthyretin. Serum THs levels and thyroid sections were almost recovered to normal after curcumin treatment. The aforementioned key HPT axis proteins in the curcumin group showed opposite expression trends. In summary, GE affected THs balance while curcumin can protect against these injury effects by affecting TH biosynthesis, biotransformation, and transport, and inducing oxidative stress and inflammatory responses.

Regulation of PTU-induced hypothyroidism in rats by caffeic acid primarily by activating thyrotropin receptors and by inhibiting oxidative stress

BackgroundEarlier, nothing was known on the thyroid-regulatory potential of caffeic acid (CA). We investigated its role in 6-propyl-thiouracil (PTU)-induced hypothyroid rats and also worked out the possible involvement of 5’-deiodinase I (5’-DI) and thyrotropin receptor (TSHR) in its mode of action. MethodsA pre-standardized dose (100 mg/kg) of CA was orally administered to PTU-induced rats for 30 days and its effects were evaluated on the alterations in the levels of serum triiodothyronine (T3), thyroxine (T4), thyrotropin (TSH) and hepatic 5’-D1activity; expression of thyroid TSHR, aspartate transaminase (AST), alanine transaminase (ALT), tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), total cholesterol (CHOL), triglycerides (TG) and hepatic lipid peroxidation (LPO). For the first time an interaction of CA with TSHR was studied in silico. ResultsPTU significantly reduced serum levels of thyroid hormones (TH), hepatic 5’-D1 and antioxidant activities as well as TSHR expression, but increased the serum TSH, AST, ALT, TNF-α, IL-6, CHOL, TG and hepatic LPO. However, CA treatment ameliorated all these PTU-induced alterations near to normal levels. Further, the distorted histo-architecture of thyroid gland by PTU was corrected by this compound. The molecular docking study indicated that CA possesses a high binding free energy with target TSHR. These results were comparable to that of a standard pro-thyroid drug, thyroxine. ConclusionCA potentially stimulated thyroid function by increasing TH levels, hepatic 5’-D1 activity and upregulation of TSHR protein expression. In addition, it attenuated the increase in oxidative stress markers, liver markers, lipids and improved the thyroid histo-architecture, thus protected from PTU-induced adverse effects. In silico studies suggested the interaction of CA with TSHR that yielded the binding energy (-6.51 kcal/mol) as compared to thyroxine (-6.10 kcal/mol) suggesting it as a highly potent thyro-stimulatory drug.

Maternal Exercise Before and During Pregnancy Facilitates Embryonic Myogenesis by Enhancing Thyroid Hormone Signaling.

Background: Maternal exercise (ME) improves fetal and offspring muscle development, but mechanisms remain to be established. Since the thyroid hormone (TH) is critical for cell differentiation during embryonic development, we hypothesized that ME elevates TH receptor (THR) signaling in embryos, which promotes embryonic myogenesis. Methods: Female mice were exercised daily on a treadmill or received a daily TH, triiodothyronine (T3) injection. Embryos (embryonic day 12.5 [E12.5]) and P19 cells were used for studying effects of TH on embryonic myogenesis. TH levels in serum and embryos after ME or T3I were analyzed. Expression of TH signaling related genes and myogenic genes was assessed. THRα binding to the promoters of myogenic genes was investigated by chromatin immunoprecipitation-qantitative polymerase chain reaction (ChIP-qPCR). A CRISPR/CAS9 plasmid was utilized to knock out THRα in P19 cells. Results: ME elevated TH levels in both maternal circulation and embryos, which were correlated with enhanced TH signaling and myogenesis. At E12.5, both myogenic determinants (Pax3, Pax7) and myogenic regulatory factors (Myf5, Myod) were upregulated in ME embryos. ME increased THRα content and elevated messenger RNA (mRNA) expression of TH transporter Slc16a2 and deiodinase Dio2. In addition, the THRα binding to the promoters of Pax3/7 was increased. In P19 embryoid bodies, T3 promoted myogenic differentiation, which was abolished by ablating THRα. Furthermore, maternal daily injection of T3 at a level matching exercised mothers promoted embryonic myogenesis. Conclusions: ME promotes TH delivery to the embryos and enhances embryonic myogenesis, which is partially mediated by enhanced TH signaling in ME embryos.

Thyroid function in children with Prader-Willi syndrome in Southern China: a single-center retrospective case series

BackgroundTo investigate hypothalamic-pituitary-thyroid function in children of different ages, nutritional phases, and genotypes that were diagnosed with Prader-Willi syndrome (PWS), as well as the effects of recombinant human growth hormone (rhGH) treatment on thyroid hormones in PWS patients.MethodsOne hundred and thirty PWS patients (87 boys and 43 girls) aged from newborn to 15 years (y) (median 1.25 y, mean, SD: 2.95 ± 3.45 y), were surveyed in this study. Serum thyroid hormone levels were examined at least once per3-6 months during the 2 years follow-up study. Central hypothyroidism (C-HT) was identified as low/normal thyroid-stimulating hormone (TSH) and low free thyroxine 4 (FT4).ResultsAll study participants had normal neonatal TSH screening test results. The prevalence of C-HT is 36.2% (47/130). No C-HT cases were diagnosed in PWS either below 1 month (m) or above 12 y. The prevalence of C-TH would be increased with age before 3 y until reaching the peak, followed by a gradual decline over the years. The prevalence of C-HT varies significantly at different ages (Pearson's χ2 = 19.915; p < 0.01). However, there is no correlation between the C-HT prevalence and nutritional phases (Pearson's χ2 = 4.992; p = 0.288), genotypes (Pearson's χ2 = 0.292; p = 0.864), or rhGH therapy (Pearson's χ2 = 1.799; p = 0.180).ConclusionsThis study suggests the prevalence of C-TH was increased with the age before 3 y, and reached the peak in the 1 to 3 y group, then gradually declined over the years. There is no correlation between C-HT prevalence and nutritional phases, genotypes, or rhGH treatment.

Cold exposure prevents fat accumulation in striped hamsters refed a high-fat diet following food restriction

BackgroundIn mammals, body mass lost during food restriction is often rapidly regained, and fat is accumulated when ad libitum feeding is resumed. Studies in small cold-acclimated mammals have demonstrated significant mobilization of fat deposits during cold exposure to meet the energy requirements of metabolic thermogenesis. However, no studies to our knowledge have examined the effect of cold exposure on fat accumulation during body mass recovery when refed ad libitum. In this study, striped hamsters restricted to 80% of their regular food intake were then refed ad libitum and exposed to one of three conditions: Intermittent cold temperature (5 °C) for 2 h per day (ICE-2 h/d), intermittent cold temperature (5 °C) for 12 h per day (ICE-12 h/d), or persistent cold exposure (PCE) for four weeks. We measured energy intake, fat deposit mass, serum thyroid hormone levels, and uncoupling protein 1 expression in brown adipose tissue.ResultsThere was no significant effect of intermittent or persistent cold exposure on body mass regain, whereas energy intake increased significantly and total fat deposit decreased in the ICE-12 h/d and PCE groups compared to the ICE-2 h/d group and control group maintained at 23 °C (CON). In the ICE-12 h/d and PCE groups, hamsters had 39.6 and 38.3% higher serum 3,3′,5-triiodothyronine levels, respectively, and 81.6 and 71.3% up-regulated expression of uncoupling protein 1, respectively, in brown adipose tissue compared to their counterparts in the CON group. The rate of mitochondrial state III and state IV respiration O2 consumption and the activity of cytochrome c oxidase in BAT and liver were significantly higher in the ICE-12 h/d and PCE groups than in the ICE-2 h/d and CON groups.ConclusionsOur findings suggest thyroid hormone-mediated heat production in brown adipose tissue and liver may be involved in preventing fat accumulation during refeeding in animals frequently or persistently exposed to cold conditions.

244 Physiological Response of Nursery Pigs Fed Cold-Pressed Canola Cake-Based Diets with Soluble Fiber Source or Feed Additives

Abstract This study was conducted to evaluate the effects of soluble fiber source or feed additives on physiological response of nursery pigs fed cold-pressed canola cake (CPCC) based diets. A total of 24 nursery pigs [initial body weight (BW) = 7.29 kg] were housed in 24 metabolic crates and fed 6 diets (4 pigs/diet) in a completely randomized design. The diets were a corn-soybean meal (SBM)-based diet and corn-SBM-CPCC (30%)-based diets without or with barley, acidifier, encapsulated butyric acid, and probiotics. The diets were formulated to meet or exceed NRC (2012) nutrient recommendations for nursery pigs and were fed for 2 weeks. Pig BW and feed intake were measured on day 0 and d 14. On d 14, blood samples were collected for measuring serum concentrations of triiodothyronine (T3) and tetraiodothyronine (T4), then all pigs were euthanized for measuring organ weights and pH of digesta in the gastrointestinal tract. Pigs fed corn-SBM based diet had greater (P &amp;lt; 0.05) gain to feed ratio compared with pigs fed CPCC diet by 24%. Dietary acidifier increased (P &amp;lt; 0.05) average daily gain (ADG) of pigs fed CPCC diet by 45.6% and had no difference from that of pigs fed corn-SBM based diet. There were no differences in weight of the thyroid gland, liver, and heart relative to BW. Dietary treatments did not affect serum T3 and T4 concentrations of pigs fed CPCC diets. Dietary barley, acidifier, or butyric acid had no influence on digesta pH of duodenum, jejunum, ileum, cecum, proximal colon, and distal colon in pigs fed CPCC diets. However, dietary probiotics increased (P &amp;lt; 0.05) pH of distal colonic digesta (6.62) compared with pigs fed corn-SBM diet (6.15) and CPCC diet (6.13). Supplementation of acidifier in 30% CPCC diet increased average daily gain of nursery pigs while maintaining normal metabolic organ weights and serum thyroid hormones level.

Body Composition and Serum Concentration of Thyroid Hormones in Euthyroid Men and Women from General Population.

Body composition, especially an increased amount of fat mass and decreased lean body mass, is connected with metabolic complications. Thyroid hormones can influence body composition pattern. To date, scarce data defining the relationships between thyroid hormones and parameters of body composition using dual-energy X-ray absorptiometry (DXA), especially in cohort studies, are available. Therefore, the aim of the present study was to investigate the relationships among serum concentrations of (thyroid-stimulating hormone (TSH), thyroid hormones, and distribution of fat tissue assessed using the DXA method in a euthyroid cohort from the Białystok PLUS study. We examined 582 euthyroid subjects who were divided into lean (body mass index (BMI) < 25 kg/m2) and overweight/obese (BMI ≥ 25 kg/m2) (84 lean men, 182 overweight/obese men, 160 lean women, and 156 overweight/obese women). Serum concentrations of TSH, free T3 (fT3), and free T4 (fT4) were assessed, and DXA was performed. We observed lower serum levels of fT4 (p = 0.03) and higher serum levels of fT3 (p = 0.04) in overweight/obese vs. lean men, whereas serum levels of TSH did not differ between these groups (p = 0.38). In lean men, we only observed a relationship between serum levels of TSH and visceral adipose tissue (VAT) (r = −0.24, p = 0.02). In overweight/obese men, we found that serum levels of fT3 were positively connected with total fat mass (r = 0.16, p = 0.02), android fat mass (r = 0.15, p = 0.03), and gynoid fat mass (r = 0.17, p = 0.01), but not with VAT (r = 0.03, p = 0.63). We did not observe differences in serum levels of TSH, fT3, and fT4 between lean and overweight/obese women. Additionally, we did not notice relationships between serum levels of thyroid hormones and fat in different regions estimated by DXA in lean and overweight/obese women (all p > 0.05). We concluded that the serum concentration of TSH is connected with VAT in lean men, whereas, in overweight/obese men, higher fT3 is connected with an increased fat amount. These associations are absent in women.

Environmentally relevant concentrations of mercury inhibit the growth of juvenile silver carp (Hypophthalmichthys molitrix): Oxidative stress and GH/IGF axis

Mercury (Hg) is a global environmental contaminant, and excessive mercury levels in water can adversely affect the growth of fish. Silver carp (Hypophthalmichthys molitrix) is one of the important freshwater aquaculture fish in China, and its natural resources have been critically declining. However, the effects of Hg2+ exposure on the growth hormone/insulin-like growth factor (GH/IGF) axis and its toxic mechanism are still unclear. In this study, we systematically evaluated the bioaccumulation, histomorphology, antioxidant status, hormone levels, and GH/IGF axis toxicity of juvenile silver carp after exposure to environmental-related concentrations of Hg2+ (0, 0.05, 0.5, 5, and 50 µg/L) for 28 days. Results showed that the Hg2+ bioaccumulation in the liver increased with a rise in Hg2+ concentration and time of exposure. The body length (BL), body weight (BW), weight growth rate (WGR) and specific growth rate (SGR) all decreased after Hg2+ exposure. The serum levels of growth hormones (GH and IGF) and thyroid hormones (T3 and T4) were significantly decreased, and the expressions of GH/IGF axis-related genes were significantly downregulated after 7, 14, and 28 days of Hg2+ exposure. Correlations between the growth parameters and growth hormones or expression of genes in GH/IGF axis further suggested that environmentally relevant concentrations of Hg2+ could have adverse effects on growth. In addition, with increasing Hg2+ exposure, superoxide activities of dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST)and levels of reduced glutathione (GSH) and malondialdehyde (MDA) were significantly increased, whereas the activity of glutathione peroxidase (GPx) significantly decreased and oxidative stress-related gene significantly changed. Liver lesions were mainly characterized by inflammatory cell infiltration, hepatocyte necrosis and fat vacuolation after exposure to Hg2+. Taken together, the results indicate that Hg2+ exposure leads to growth inhibition and oxidative stress in juvenile silver.

Effects of mobile phone radiation and noise pollution on serum levels of LDH, thyroid hormones, liver enzymes, cortisol, and reproductive system in male Wistar rats

The expansion of mobile phones and noise pollution in the human environment has given rise to dangerous outcomes. In this study, the effects of exposure to traffic noise and cell phone radiation on the serum levels of LDH, thyroid hormones, liver enzymes, cortisol, and reproductive system function and testicular histology of male rats have been analyzed. Male Wistar rats were exposed to mobile radiation (930 MHz) and noise pollution (100 dB, 700 to 5700 Hz). After eight weeks of exposure, serum levels of LDH, thyroid hormones, liver enzymes, cortisol, and male reproductive hormones were measured using the enzyme-linked fluorescence assay method. Testicular tissue was also examined by H&amp;E staining. Data were analyzed using ANOVA. The results showed that prolonged exposure to cell phone radiation and noise pollution increased the LDH levels, reduced the T3, T4, glutamic-pyruvic transaminase, cortisol, testosterone, LH, FSH levels, and decreased the number of spermatogonia and spermatocytes, serum glutamic-pyruvic transaminase and alkaline phosphatase. Conclusively, long term exposure to mobile phone radiation and noise pollution leads to increased LDH, decreased T3, T4 and SGPT level, and had destructive effects on testicular tissue leading to decreased serum testosterone level as well as decreased spermatogonia, spermatocyte and Sertoli cells count..

Ageing related thyroid deficiency increases brain-targeted transport of liver-derived ApoE4-laden exosomes leading to cognitive impairment

Alzheimer’s disease (AD) is the prevalent cause of dementia in the ageing world population. Apolipoprotein E4 (ApoE4) allele is the key genetic risk factor for AD, although the mechanisms linking ApoE4 with neurocognitive impairments and aberrant metabolism remains to be fully characterised. We discovered a significant increase in the ApoE4 content of serum exosomes in old healthy subjects and AD patients carrying ApoE4 allele as compared with healthy adults. Elevated exosomal ApoE4 demonstrated significant inverse correlation with serum level of thyroid hormones and cognitive function. We analysed effects of ApoE4-containing peripheral exosomes on neural cells and neurological outputs in aged or thyroidectomised young mice. Ageing-associated hypothyroidism as well as acute thyroidectomy augmented transport of liver-derived ApoE4 reach exosomes into the brain, where ApoE4 activated nucleotide-binding oligomerisation domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome by increasing cholesterol level in neural cells. This, in turn, affected cognition, locomotion and mood. Our study reveals pathological potential of exosomes-mediated relocation of ApoE4 from the periphery to the brain, this process can represent potential therapeutic target.