Search Results
Search for other papers by Tatsuya Kondo in
Google Scholar
PubMed
Search for other papers by Nobukazu Miyakawa in
Google Scholar
PubMed
Search for other papers by Sayaka Kitano in
Google Scholar
PubMed
Search for other papers by Takuro Watanabe in
Google Scholar
PubMed
Search for other papers by Rieko Goto in
Google Scholar
PubMed
Search for other papers by Mary Ann Suico in
Google Scholar
PubMed
Search for other papers by Miki Sato in
Google Scholar
PubMed
Search for other papers by Yuki Takaki in
Google Scholar
PubMed
Search for other papers by Masaji Sakaguchi in
Google Scholar
PubMed
Search for other papers by Motoyuki Igata in
Google Scholar
PubMed
Search for other papers by Junji Kawashima in
Google Scholar
PubMed
Search for other papers by Hiroyuki Motoshima in
Google Scholar
PubMed
Search for other papers by Takeshi Matsumura in
Google Scholar
PubMed
Search for other papers by Hirofumi Kai in
Google Scholar
PubMed
Search for other papers by Eiichi Araki in
Google Scholar
PubMed
Nonalcoholic fatty liver disease (NAFLD) is often accompanied by metabolic disorders such as metabolic syndrome and type 2 diabetes (T2DM). Heat shock response (HSR) is one of the most important homeostatic abilities but is deteriorated by chronic metabolic insults. Heat shock (HS) with an appropriate mild electrical stimulation (MES) activates HSR and improves metabolic abnormalities including insulin resistance, hyperglycemia and inflammation in metabolic disorders. To analyze the effects of HS + MES treatment on NAFLD biomarkers, three cohorts including healthy men (two times/week, n = 10), patients with metabolic syndrome (four times/week, n = 40), and patients with T2DM (n = 100; four times/week (n = 40) and two, four, seven times/week (n = 20 each)) treated with HS + MES were retrospectively analyzed. The healthy subjects showed no significant alterations in NAFLD biomarkers after the treatment. In patients with metabolic syndrome, many of the NAFLD steatosis markers, including fatty liver index, NAFLD-liver fat score, liver/spleen ratio and hepatic steatosis index and NAFLD fibrosis marker, aspartate aminotransferase/alanine aminotransferase (AST/ALT) ratio, were improved upon the treatment. In patients with T2DM, all investigated NAFLD steatosis markers were improved and NAFLD fibrosis markers such as the AST/ALT ratio, fibrosis-4 index and NAFLD-fibrosis score were improved upon the treatment. Thus, HS + MES, a physical intervention, may become a novel treatment strategy for NAFLD as well as metabolic disorders.
Search for other papers by Ling Zhou in
Google Scholar
PubMed
Search for other papers by Ruixue Zhang in
Google Scholar
PubMed
Search for other papers by Shuangyan Yang in
Google Scholar
PubMed
Search for other papers by Yaguang Zhang in
Google Scholar
PubMed
Search for other papers by Dandan Shi in
Google Scholar
PubMed
Background:
Our previous study revealed that astragaloside IV (AS-IV) effectively improved gestational diabetes mellitus (GDM) by reducing hepatic gluconeogenesis. Due to the importance of placental oxidative stress, we further explored the protective role of AS-IV on placental oxidative stress in GDM.
Methods:
First, non-pregnant mice were orally administrated with AS-IV to evaluate its safety and effect. Then GDM mice were orally administered with AS-IV for 20 days and its effect on the symptoms of GDM, placental oxidative stress, secretions of inflammatory cytokines, as well as toll-like receptor 4 (TLR4)/NF-κB signaling pathway, were evaluated.
Results:
AS-IV had no adverse effect on non-pregnant mice. On the other hand, AS-IV significantly attenuated the GDM-induced hyperglycemia, glucose intolerance, insulin resistance, placental oxidative stress, productions of inflammatory cytokines and the activation of TLR4/NF-κB pathway.
Conclusion:
AS-IV effectively protected against GDM by alleviating placental oxidative stress and inflammation, in which TLR4/NF-κB might be involved.
Department of Endocrinology, Zunyi Medical University, Zunyi, China
Search for other papers by Mengxue Yang in
Google Scholar
PubMed
Search for other papers by Bowen Sun in
Google Scholar
PubMed
Search for other papers by Jianhui Li in
Google Scholar
PubMed
Search for other papers by Bo Yang in
Google Scholar
PubMed
Search for other papers by Jie Xu in
Google Scholar
PubMed
Search for other papers by Xue Zhou in
Google Scholar
PubMed
Search for other papers by Jie Yu in
Google Scholar
PubMed
Search for other papers by Xuan Zhang in
Google Scholar
PubMed
Search for other papers by Qun Zhang in
Google Scholar
PubMed
Search for other papers by Shan Zhou in
Google Scholar
PubMed
Search for other papers by Xiaohua Sun in
Google Scholar
PubMed
Objectives
The pathogenesis of Graves’ disease (GD) remains unclear. In terms of environmental factors, GD development may be associated with chronic inflammation caused by alteration of the intestinal flora. This study explored the association of intestinal flora alteration with the development of GD among the Han population in southwest China.
Design and methods
Fifteen GD patients at the Affiliated Hospital of Zunyi Medical College between March 2016 and March 2017 were randomly enrolled. Additionally, 15 sex- and age-matched healthy volunteers were selected as the control group during the same period. Fresh stool samples were collected, and bacterial 16S RNA was extracted and amplified for gene sequencing with the Illumina MiSeq platform. The sequencing results were subjected to operational taxonomic unit-based classification, classification verification, alpha diversity analysis, taxonomic composition analysis and partial least squares-discriminant analysis (PLS-DA).
Results
The diversity indices for the GD group were lower than those for the control group. The GD group showed significantly higher abundances of Firmicutes, Proteobacteria and Actinobacillus and a higher Firmicutes/Bacteroidetes ratio than the control group. PLS-DA suggested the satisfactory classification of the flora between the GD group and the control group. The abundances of the genera Oribacterium, Mogibacterium, Lactobacillus, Aggregatibacter and Mogibacterium were significantly higher in the GD group than in the control group (P < 0.05).
Conclusions
The intestinal flora of GD patients was significantly different from that of the healthy population. Thus, alteration of intestinal flora may be associated with the development of GD.
Search for other papers by Angelo Maria Patti in
Google Scholar
PubMed
Search for other papers by Kalliopi Pafili in
Google Scholar
PubMed
Search for other papers by Nikolaos Papanas in
Google Scholar
PubMed
Search for other papers by Manfredi Rizzo in
Google Scholar
PubMed
Hormonal changes during pregnancy can trigger gestational diabetes (GDM), which is constantly increasing. Its main characteristic is pronounced insulin resistance, but it appears to be a multifactorial process involving several metabolic factors; taken together, the latter leads to silent or clinically evident cardiovascular (CV) events. Insulin resistance and central adiposity are of crucial importance in the development of metabolic syndrome, and they appear to correlate with CV risk factors, including hypertension and atherogenic dyslipidaemia. Hypertensive disease of pregnancy (HDP) is more likely to be an accompanying co-morbidity in pregnancies complicated with GDM. There is still inconsistent evidence as to whether or not co-existent GDM and HDP have a synergistic effects on postpartum risk of cardiometabolic disease; however, this synergism is becoming more accepted since both these conditions may promote endothelial inflammation and early atherosclerosis. Regardless of the presence or absence of the synergism between GDM and HDP, these conditions need to be dealt early enough, in order to reduce CV morbidity and to improve health outcomes for both women and their offspring.
Search for other papers by Clara Lundetoft Clausen in
Google Scholar
PubMed
Search for other papers by Åse Krogh Rasmussen in
Google Scholar
PubMed
Search for other papers by Trine Holm Johannsen in
Google Scholar
PubMed
Search for other papers by Linda Maria Hilsted in
Google Scholar
PubMed
Search for other papers by Niels Erik Skakkebæk in
Google Scholar
PubMed
Search for other papers by Pal Bela Szecsi in
Google Scholar
PubMed
Search for other papers by Lise Pedersen in
Google Scholar
PubMed
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Thomas Benfield in
Google Scholar
PubMed
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Anders Juul in
Google Scholar
PubMed
The hypothalamic–pituitary–thyroid hormone axis might be affected in COVID-19, but existing studies have shown varying results. It has been hypothesized that hyperinflammation, as reflected by the secretion of cytokines, might induce thyroid dysfunction among patients with COVID-19. We explored thyroid hormone involvement in the acute phase of symptomatic COVID-19 and its possible associations with cytokine levels and mortality risk. This was a single-center study of 116 consecutive patients hospitalized for moderate-to-severe COVID-19 disease. Serum concentrations of thyroid-stimulating hormone (TSH), free thyroxine (T4), and 45 cytokines/chemokines were measured in all patients within 3 days of admission. Data were extracted retrospectively through a manual review of health records. At admission, 95 (81.9%) were euthyroid; while 21 (18.1%) had biochemically thyroid dysfunction including subclinical thyrotoxicosis (n = 11), overt thyrotoxicosis (n = 2), hypothyroidism (n = 1), non-thyroidal illness (n = 2), and normal TSH but high free T4 (n = 5). TSH levels were inversely correlated with IL-8 (r s = –0.248), IL-10 (r s = –0.253), IL-15 (r s = –0.213), IP-10 (r s = –0.334), and GM-CSF (r s = –0.254). Moreover, IL-8 levels, IP-10, and GM-CSF were significantly higher in patients with serum TSH < 0.4 mIU/L. Lastly, a two-fold increment of IL-8 and IL-10 was associated with significantly higher odds of having TSH < 0.4 mIU/L (odds ratio 1.86 (1.11–3.10) and 1.78 (1.03–3.06)). Serum TSH was not associated with 30- or 90-day mortality. In conclusion, this study suggests that fluctuations of TSH levels in patients with COVID-19 may be influenced by circulating IL-8, IL-10, IL-15, IP-10, and GM-CSF as previously described in autoimmune thyroid diseases.
Search for other papers by Emmi Naskali in
Google Scholar
PubMed
Search for other papers by Katja Dettmer in
Google Scholar
PubMed
Search for other papers by Peter J Oefner in
Google Scholar
PubMed
Search for other papers by Pedro A B Pereira in
Google Scholar
PubMed
Search for other papers by Kai Krohn in
Google Scholar
PubMed
Search for other papers by Petri Auvinen in
Google Scholar
PubMed
Search for other papers by Annamari Ranki in
Google Scholar
PubMed
Search for other papers by Nicolas Kluger in
Google Scholar
PubMed
Objective
Intestinal autoimmunity with gastrointestinal (GI) dysfunction has been shown in patients with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED). Patients lack entero-endocrine (EE) cells and have circulating autoantibodies (Aabs) against critical enzymes in serotonin (5-HT) biosynthesis.
Design
We sought to determine the serum levels of 5-HT, tryptophan (Trp) metabolites and L-DOPA in 37 Finnish APECED patients and to correlate their abundance with the presence of TPH and AADC Aabs, GI dysfunction and depressive symptoms. We also performed an exploratory analysis of the gut microbiome.
Methods
Serum 5-HT, L-DOPA and Trp metabolite levels were determined by liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS/MS). TPH and AADC Aabs were measured by ELISA. Depression was assessed with a structured RBDI questionnaire. The V3–V4 regions of the bacterial 16S rRNA gene were sequenced for gut microbiome exploration.
Results
Serum 5-HT levels were significantly decreased (130 ± 131 nmol/L vs 686 ± 233 nmol/L, P < 0.0001) in APECED patients with TPH-1 (±AADC) Aabs compared to controls and patients with only AADC Aabs. Reduced 5-HT levels correlated with constipation. The genus Escherichia/Shigella was overrepresented in the intestinal microbiome. No correlation between serum Trp, 5-HT or l-DOPA levels and the RBDI total score, fatigue or sleep disorders was found.
Conclusions
This exploratory study found low serum levels of 5-HT to be associated with constipation and the presence of TPH-1 and AADC Aabs, but not with symptoms of depression. Hence, serum 5-HT, TPH1 and AADC Aabs should be determined in APECED patients presenting with GI symptoms.
Department of Immunology, Nanjing Medical University, Jiangsu, China
Search for other papers by Yun Hu in
Google Scholar
PubMed
Search for other papers by Na Li in
Google Scholar
PubMed
Search for other papers by Peng Jiang in
Google Scholar
PubMed
Search for other papers by Liang Cheng in
Google Scholar
PubMed
Search for other papers by Bo Ding in
Google Scholar
PubMed
Search for other papers by Xiao-Mei Liu in
Google Scholar
PubMed
Search for other papers by Ke He in
Google Scholar
PubMed
Search for other papers by Yun-Qing Zhu in
Google Scholar
PubMed
Search for other papers by Bing-li Liu in
Google Scholar
PubMed
Search for other papers by Xin Cao in
Google Scholar
PubMed
Search for other papers by Hong Zhou in
Google Scholar
PubMed
Search for other papers by Xiao-Ming Mao in
Google Scholar
PubMed
Objective
Thyroid nodules are usually accompanied by elevated thyroglobulin (Tg) level and autoimmune thyroid diseases (AITDs). However, the relationship between Tg and AITDs is not fully understood. Dysfunction of regulatory T cells (Tregs) plays an important role in the development of AITDs. We aimed to evaluate the effects of Tg on the function of Tregs in patients with thyroid nodules.
Methods
Tg levels and the functions of Tregs in peripheral blood and thyroid tissues of patients with thyroid nodules from Nanjing First Hospital were evaluated. The effects of Tg on the function of Tregs from healthy donors were also assessed in vitro. The function of Tregs was defined as an inhibitory effect of Tregs on the effector T cell (CD4+ CD25− T cell) proliferation rate.
Results
The level of Tg in peripheral blood correlated negatively with the inhibitory function of Tregs (R = 0.398, P = 0.03), and Tregs function declined significantly in the high Tg group (Tg >77 μg/L) compared with the normal Tg group (11.4 ± 3.9% vs 27.5 ± 3.5%, P < 0.05). Compared with peripheral blood, the function of Tregs in thyroid declined significantly (P < 0.01), but the proportion of FOXP3+ Tregs in thyroid increased (P < 0.01). High concentration of Tg (100 μg/mL) inhibited the function of Tregs and downregulated FOXP3, TGF-β and IL-10 mRNA expression in Tregs in vitro.
Conclusions
Elevated Tg level could impair the function of Tregs, which might increase the risk of AITDs in patient with thyroid nodules.
Search for other papers by Chenghao Piao in
Google Scholar
PubMed
Search for other papers by Xiaojie Wang in
Google Scholar
PubMed
Search for other papers by Shiqiao Peng in
Google Scholar
PubMed
Search for other papers by Xinyu Guo in
Google Scholar
PubMed
Search for other papers by Hui Zhao in
Google Scholar
PubMed
Search for other papers by Li He in
Google Scholar
PubMed
Search for other papers by Yan Zeng in
Google Scholar
PubMed
Search for other papers by Fan Zhang in
Google Scholar
PubMed
Search for other papers by Kewen Zhu in
Google Scholar
PubMed
Search for other papers by Yiwei Wang in
Google Scholar
PubMed
Objective
Gestational diabetes mellitus (GDM) is characterized by glucose intolerance during gestation. It is associated with a series of maternal and foetal complications. Interleukin (IL)-34 is a recently discovered pro-inflammatory cytokine that functions as a ligand for colony-stimulating factor-1 receptor (CSF-1R). The contribution of IL-34 in the development of multiple chronic inflammatory diseases and autoimmune diseases has been recently discovered. The aim of this study was to evaluate whether IL-34 participates in the pathogenesis of GDM.
Method
A total of 120 women were enrolled in this study, which included 60 GDM patients and age- and sex-matched healthy pregnant women. The expression of IL-34 in serum, cord blood and placental tissues was analysed by ELISA and Western blot assays. The association between IL-34 levels and clinical features was also studied. We additionally evaluated the effect of recombinant mouse IL-34 (rmIL-34) on apoptosis and pancreatic β cell function.
Results
We found that IL-34 expression is highly increased in serum, cord blood and placental tissues in patients with GDM. In addition, there was a positive association between serum IL-34 and insulin resistance and glucose concentrations. Our data also revealed that IL-34 contributes to the apoptosis of pancreatic β cells in GDM caused by CSF-1R. Furthermore, functional studies found that IL-34 inhibited pancreatic β cell function and cell viability, while CSF-1R inhibitor blocked this effect.
Conclusion
IL-34 plays a crucial role in the development of GDM by targeting CSF-1R, insulin production and β cell function.
Search for other papers by Yongping Liu in
Google Scholar
PubMed
Search for other papers by Shuo Wang in
Google Scholar
PubMed
Search for other papers by Qingling Guo in
Google Scholar
PubMed
Search for other papers by Yongze Li in
Google Scholar
PubMed
Search for other papers by Jing Qin in
Google Scholar
PubMed
Search for other papers by Na Zhao in
Google Scholar
PubMed
Search for other papers by Yushu Li in
Google Scholar
PubMed
Search for other papers by Zhongyan Shan in
Google Scholar
PubMed
Search for other papers by Weiping Teng in
Google Scholar
PubMed
Objective
Hashimoto’s thyroiditis (HT) is characterized by elevated specific auto-antibodies, including TgAb and TPOAb. Increasing evidence has demonstrated the essential role of Th17 cells in HT. However, the underlying mechanism is still unclear. Semaphorin 5A (Sema 5A) is involved in several autoimmune diseases through the regulation of immune cells. The aim of the present study was to explore the role of Sema 5A in HT.
Methods
We measured serum Sema 5A levels in HT (n = 92) and healthy controls (n = 111) by enzyme-linked immunosorbent assay (ELISA). RNA levels of Sema 5A and their receptors (plexin-A1 and plexin-B3), as well as several cytokines (IFN-γ, IL-4 and IL-17), were detected by real-time polymerase chain reaction in peripheral blood mononuclear cells from 23 patients with HT and 31 controls. In addition, we investigated the relationship between serum Sema 5A and HT.
Results
Serum Sema 5A in HT increased significantly compared with healthy controls (P < 0.001). Moreover, serum Sema 5A levels were positively correlated with TgAb (r = 0.511, P < 0.001), TPOAb (r = 0.423, P < 0.001), TSH (r = 0.349, P < 0.001) and IL-17 mRNA expression (r = 0.442, P < 0.001). Increased Sema 5A RNA expression was observed (P = 0.041) in HT compared with controls. In receiver-operating characteristic (ROC) analysis, serum Sema 5A predicted HT with a sensitivity of 79.35% and specificity of 96.40%, and the area under the curve of the ROC curve was 0.836 (95% CI: 0.778–0.884, P < 0.001).
Conclusions
These data demonstrated elevated serum Sema 5A in HT patients for the first time. Serum Sema 5A levels were correlated with thyroid auto-antibodies and IL-17 mRNA expression. Sema 5A may be involved in immune response of HT patients.
Search for other papers by Qing Zhu in
Google Scholar
PubMed
Search for other papers by Jianbin Su in
Google Scholar
PubMed
Search for other papers by Xueqin Wang in
Google Scholar
PubMed
Search for other papers by Mengjie Tang in
Google Scholar
PubMed
Search for other papers by Yingying Gao in
Google Scholar
PubMed
Search for other papers by Dongmei Zhang in
Google Scholar
PubMed
Graves’ disease (GD), an organ-specific autoimmune disease, is the most common cause of hyperthyroidism. Tumour necrosis factor-alpha (TNF-α) exhibits immunological and metabolic activities involved in the induction and maintenance of immune responses. We attempted to evaluate the relationship between GD and serum TNF-α and its soluble receptors (sTNFRs), soluble TNF receptor 1 and 2 (sTNF-R1 and sTNF-R2). A total of 72 GD patients and 72 matched healthy individuals were recruited for this study. Serum TNF-α and sTNFRs were measured by sandwich ELISA. In our study, no significant difference was observed in TNF-α, but sTNFRs were found to be significantly elevated in GD patients compared to healthy individuals. Serum sTNFR levels were positively correlated with free triiodothyronine (FT3) and free thyroxine (FT4), and TNF-α was negatively correlated with thyroid-stimulating hormone (TSH) in the GD group. It was also shown that thyrotropin receptor antibody (TRAb) was positively correlated with TNF-α and sTNFRs. Spearman’s correlation analysis showed that only sTNF-R1 was positively correlated with complement C3. Multiple linear regression analysis suggests that serum levels of sTNF-R1 and FT4 may play an important role in the serum level of FT3. According to the median value of FT3 level, GD patients were further divided into a high FT3 group and a low FT3 group. The serum levels of sTNF-R1 in the high FT3 GD group were significantly higher than those in the low FT3 GD group. In conclusion, sTNFRs may play an important role in anti-inflammatory and immune response in GD.
