Search Results

You are looking at 21 - 30 of 572 items for

  • Abstract: Aging x
  • Abstract: Autoimmune x
  • Abstract: Inflammation x
Clear All Modify Search
Sriharsha Gunna Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

Search for other papers by Sriharsha Gunna in
Google Scholar
PubMed
Close
,
Mahaveer Singh Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

Search for other papers by Mahaveer Singh in
Google Scholar
PubMed
Close
,
Rakesh Pandey Department of Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

Search for other papers by Rakesh Pandey in
Google Scholar
PubMed
Close
,
Rungmei S K Marak Department of Microbiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

Search for other papers by Rungmei S K Marak in
Google Scholar
PubMed
Close
,
Amita Aggarwal Department of Clinical Immunology and Rheumatology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

Search for other papers by Amita Aggarwal in
Google Scholar
PubMed
Close
,
Bibhuti Mohanta Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

Search for other papers by Bibhuti Mohanta in
Google Scholar
PubMed
Close
,
Liping Yu Barbara Davis Centre for Diabetes, School of Medicine University of Colorado, Aurora, Colorado, USA

Search for other papers by Liping Yu in
Google Scholar
PubMed
Close
, and
Eesh Bhatia Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

Search for other papers by Eesh Bhatia in
Google Scholar
PubMed
Close

The etiology, presentation and mortality of patients with primary adrenal insufficiency (PAI) in developing countries may differ from economically developed nations. However, information in this regard is scanty. The aim of this study was to determine the etiology and compare the clinical characteristics and mortality in infectious and autoimmune causes of PAI in Indian patients. All eligible (n = 89) patients (ages 15–83 years) diagnosed with PAI between 2006 and 2019 were studied. Patients were followed for a median duration of 5.9 (range 0.1–15.7) years. Eighty-six subjects underwent an abdominal computerized tomography scan or ultrasonography, and adrenal biopsy was performed in 60 patients. The most frequent etiologies of PAI were adrenal histoplasmosis (AH, 45%), adrenal tuberculosis (AT, 15%), autoimmunity (AI, 25%) and primary lymphoma (6%). Forty-two percent of patients presented with an acute adrenal crisis. AH and AT could not be differentiated on the basis of clinical features, except for a greater frequency of hepatomegaly–splenomegaly and type 2 diabetes mellitus (63% vs 15%, P < 0.01) in the former. Patients with an autoimmune etiology had a higher frequency of 21-hydroxylase antibodies (41% vs 3%) and autoimmune thyroid disease (46% vs 5%) vs those with infectious etiologies. Mortality was significantly higher in AH (45%) compared with AT (8%) or AI (5%) (P = 0.001). Causes of death included adrenal crises, progressive AH and unexplained acute events occurring at home. In conclusion, infections, especially AH, were the most frequent cause of PAI in north India. Despite appropriate therapy, AH had very high mortality as compared with AT and AI.

Open access
Hauke Thomsen Division of Molecular Genetic Epidemiology, German Cancer Research Centre (DKFZ), Heidelberg, Germany
Center for Primary Health Care Research, Lund University, Malmö, Sweden
GeneWerk GmbH, Heidelberg, Germany

Search for other papers by Hauke Thomsen in
Google Scholar
PubMed
Close
,
Xinjun Li Center for Primary Health Care Research, Lund University, Malmö, Sweden

Search for other papers by Xinjun Li in
Google Scholar
PubMed
Close
,
Kristina Sundquist Center for Primary Health Care Research, Lund University, Malmö, Sweden
Departments of Family Medicine and Community Health, Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, New York, USA
Center for Community-based Healthcare Research and Education (CoHRE), Department of Functional Pathology, School of Medicine, Shimane University, Shimane, Japan

Search for other papers by Kristina Sundquist in
Google Scholar
PubMed
Close
,
Jan Sundquist Center for Primary Health Care Research, Lund University, Malmö, Sweden
Departments of Family Medicine and Community Health, Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, New York, USA
Center for Community-based Healthcare Research and Education (CoHRE), Department of Functional Pathology, School of Medicine, Shimane University, Shimane, Japan

Search for other papers by Jan Sundquist in
Google Scholar
PubMed
Close
,
Asta Försti Division of Molecular Genetic Epidemiology, German Cancer Research Centre (DKFZ), Heidelberg, Germany
Center for Primary Health Care Research, Lund University, Malmö, Sweden
Hopp Children’s Cancer Center (KiTZ), Heidelberg, Germany
Division of Pediatric Neurooncology, German Cancer Research Centre (DKFZ), German Cancer Consortium (DKTK), Heidelberg, Germany

Search for other papers by Asta Försti in
Google Scholar
PubMed
Close
, and
Kari Hemminki Division of Molecular Genetic Epidemiology, German Cancer Research Centre (DKFZ), Heidelberg, Germany
Center for Primary Health Care Research, Lund University, Malmö, Sweden
Division of Cancer Epidemiology, German Cancer Research Centre (DKFZ), Heidelberg, Germany
Faculty of Medicine and Biomedical Center in Pilsen, Charles University in Prague, Pilsen, Czech Republic

Search for other papers by Kari Hemminki in
Google Scholar
PubMed
Close

Design

Addison’s disease (AD) is a rare autoimmune disease (AID) of the adrenal cortex, present as an isolated AD or part of autoimmune polyendocrine syndromes (APSs) 1 and 2. Although AD patients present with a number of AID co-morbidities, population-based family studies are scarce, and we aimed to carry out an unbiased study on AD and related AIDs.

Methods

We collected data on patients diagnosed with AIDs in Swedish hospitals and calculated standardized incidence ratios (SIRs) in families for concordant AD and for other AIDs, the latter as discordant relative risks.

Results

The number of AD patients was 2852, which accounted for 0.4% of all hospitalized AIDs. A total of 62 persons (3.6%) were diagnosed with familial AD. The SIR for siblings was remarkably high, reaching 909 for singleton siblings diagnosed before age 10 years. It was 32 in those diagnosed past age 29 years and the risk for twins was 323. SIR was 9.44 for offspring of affected parents. AD was associated with 11 other AIDs, including thyroid AIDs and type 1 diabetes and some rarer AIDs such as Guillain–Barre syndrome, myasthenia gravis, polymyalgia rheumatica and Sjögren’s syndrome.

Conclusions

The familial risk for AD was very high implicating genetic etiology, which for juvenile siblings may be ascribed to APS-1. The adult part of sibling risk was probably contributed by recessive polygenic inheritance. AD was associated with many common AIDs; some of these were known co-morbidities in AD patients while some other appeared to more specific for a familial setting.

Open access
Huiyuan Zhai Department of Pharmacy, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Affiliated with Nanjing University of Chinese Medicine, Nanjing, China

Search for other papers by Huiyuan Zhai in
Google Scholar
PubMed
Close
,
Dongxu Wang Department of Geriatrics, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Affiliated with Nanjing University of Chinese Medicine, Nanjing, China

Search for other papers by Dongxu Wang in
Google Scholar
PubMed
Close
,
Yong Wang Department of Pharmacy, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Affiliated with Nanjing University of Chinese Medicine, Nanjing, China

Search for other papers by Yong Wang in
Google Scholar
PubMed
Close
,
Hongwei Gu Central Laboratory, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Affiliated with Nanjing University of Chinese Medicine, Nanjing, China

Search for other papers by Hongwei Gu in
Google Scholar
PubMed
Close
,
Juan Jv Department of Cardiology, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Affiliated with Nanjing University of Chinese Medicine, Nanjing, China

Search for other papers by Juan Jv in
Google Scholar
PubMed
Close
,
Liangliang Yuan Department of Pharmacy, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Affiliated with Nanjing University of Chinese Medicine, Nanjing, China

Search for other papers by Liangliang Yuan in
Google Scholar
PubMed
Close
,
Chao Wang Department of Pharmacy, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Affiliated with Nanjing University of Chinese Medicine, Nanjing, China

Search for other papers by Chao Wang in
Google Scholar
PubMed
Close
, and
Leiyao Chen Department of Pharmacy, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Affiliated with Nanjing University of Chinese Medicine, Nanjing, China

Search for other papers by Leiyao Chen in
Google Scholar
PubMed
Close

Chronic inflammation induced by obesity plays a crucial role in the pathogenesis of insulin resistance. The infiltration of macrophages into adipose tissues contributes to adipose tissue inflammation and insulin resistance. Kaempferol, a flavonoid present in various vegetables and fruits, has been shown to possess remarkable anti-inflammatory properties. In this study, we used leptin receptor-deficient obese mice (db/db) as an insulin-resistant model and investigated the effects of kaempferol treatment on obesity-induced insulin resistance. Our findings revealed that the administration of kaempferol (50 mg/kg/day, for 6 weeks) significantly reduced body weight, fat mass, and adipocyte size. Moreover, it effectively ameliorated abnormal glucose tolerance and insulin resistance in db/db mice. In the adipose tissue of obese mice treated with kaempferol, we observed a reduction in macrophage infiltration and a downregulation of mRNA expression of M1 marker genes TNF-α and IL-1β, accompanied by an upregulation of Arg1 and IL-10 mRNA expression. Additionally, kaempferol treatment significantly inhibited the STING/NLRP3 signaling pathway in adipose tissue. In vitro experiments, we further discovered that kaempferol treatment suppressed LPS-induced inflammation through the activation of NLRP3/caspase 1 signaling in RAW 264.7 macrophages. Our results suggest that kaempferol may effectively alleviate inflammation and insulin resistance in the adipose tissue of db/db mice by modulating the STING/NLRP3 signaling pathway.

Open access
Mírian Romitti Thyroid Unit, Endocrine Division, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil

Search for other papers by Mírian Romitti in
Google Scholar
PubMed
Close
,
Vitor C Fabris Gynecological Endocrinology Unit, Endocrine Division, Hospital de Clínicas de Porto Alegre, and Department of Physiology, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil

Search for other papers by Vitor C Fabris in
Google Scholar
PubMed
Close
,
Patricia K Ziegelmann Postgraduate Program in Epidemiology and Department of Statistics, Institute of Mathematics, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil

Search for other papers by Patricia K Ziegelmann in
Google Scholar
PubMed
Close
,
Ana Luiza Maia Thyroid Unit, Endocrine Division, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil

Search for other papers by Ana Luiza Maia in
Google Scholar
PubMed
Close
, and
Poli Mara Spritzer Gynecological Endocrinology Unit, Endocrine Division, Hospital de Clínicas de Porto Alegre, and Department of Physiology, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil

Search for other papers by Poli Mara Spritzer in
Google Scholar
PubMed
Close

Polycystic ovary syndrome (PCOS) is the most prevalent endocrine disorder affecting women of reproductive age. PCOS has been associated with distinct metabolic and cardiovascular diseases and with autoimmune conditions, predominantly autoimmune thyroid disease (AITD). AITD has been reported in 18–40% of PCOS women, depending on PCOS diagnostic criteria and ethnicity. The aim of this systematic review and meta-analysis was to summarize the available evidence regarding the likelihood of women with PCOS also having AITD in comparison to a reference group of non-PCOS women. We systematically searched EMBASE and MEDLINE for non-interventional case control, cross-sectional or cohort studies published until August 2017. The Ottawa–Newcastle Scale was used to assess the methodological quality of studies. Statistical meta-analysis was performed with R. Thirteen studies were selected for the present analysis, including 1210 women diagnosed with PCOS and 987 healthy controls. AITD was observed in 26.03 and 9.72% of PCOS and control groups respectively. A significant association was detected between PCOS and chance of AITD (OR = 3.27, 95% CI 2.32–4.63). Notably, after geographical stratification, the higher risk of AITD in PCOS women persisted for Asians (OR = 4.56, 95% CI 2.47–8.43), Europeans (OR = 3.27, 95% CI 2.07–5.15) and South Americans (OR = 1.86, 95% CI 1.05–3.29). AIDT is a frequent condition in PCOS patients and might affect thyroid function. Thus, screening for thyroid function and thyroid-specific autoantibodies should be considered in patients with PCOS even in the absence of overt symptoms. This systematic review and meta-analysis is registered in PROSPERO under number CRD42017079676.

Open access
Elin Kahlert Clinic of Gastroenterology and Endocrinology, University Medical Center Goettingen, Goettingen, Germany

Search for other papers by Elin Kahlert in
Google Scholar
PubMed
Close
,
Martina Blaschke Clinic of Gastroenterology and Endocrinology, University Medical Center Goettingen, Goettingen, Germany
Endokrinologikum Goettingen, Goettingen, Germany

Search for other papers by Martina Blaschke in
Google Scholar
PubMed
Close
,
Knut Brockmann Interdisciplinary Pediatric Center for Children with Developmental Disabilities and Severe Chronic Disorders, University Medical Center Goettingen, Goettingen, Germany

Search for other papers by Knut Brockmann in
Google Scholar
PubMed
Close
,
Clemens Freiberg Interdisciplinary Pediatric Center for Children with Developmental Disabilities and Severe Chronic Disorders, University Medical Center Goettingen, Goettingen, Germany

Search for other papers by Clemens Freiberg in
Google Scholar
PubMed
Close
,
Onno E Janssen Endokrinologikum Hamburg, Hamburg, Germany

Search for other papers by Onno E Janssen in
Google Scholar
PubMed
Close
,
Nikolaus Stahnke Endokrinologikum Hamburg, Hamburg, Germany

Search for other papers by Nikolaus Stahnke in
Google Scholar
PubMed
Close
,
Domenika Strik Endokrinologikum Berlin, Berlin, Germany

Search for other papers by Domenika Strik in
Google Scholar
PubMed
Close
,
Martin Merkel Endokrinologikum Hannover, Hannover, Germany

Search for other papers by Martin Merkel in
Google Scholar
PubMed
Close
,
Alexander Mann Endokrinologikum Frankfurt, Frankfurt/Main, Germany

Search for other papers by Alexander Mann in
Google Scholar
PubMed
Close
,
Klaus-Peter Liesenkötter Endokrinologikum Berlin, Berlin, Germany

Search for other papers by Klaus-Peter Liesenkötter in
Google Scholar
PubMed
Close
, and
Heide Siggelkow Clinic of Gastroenterology and Endocrinology, University Medical Center Goettingen, Goettingen, Germany
Endokrinologikum Goettingen, Goettingen, Germany

Search for other papers by Heide Siggelkow in
Google Scholar
PubMed
Close

Objective

Turner syndrome (TS) is characterized by the complete or partial loss of the second sex chromosome and associated with a wide range of clinical manifestations. We aimed to assess the medical care of adult patients with TS in Germany.

Design

Retrospective multicenter observational study.

Methods

Data were collected from medical records of 258 women with TS treated between 2001 and 2017 in five non-university endocrinologic centers in Germany.

Results

Mean age was 29.8 ± 11.6 years, mean height 152 ± 7.7 cm, and mean BMI 26.6 ± 6.3 kg/m2. The karyotype was known in 50% of patients. Information on cholesterol state, liver enzymes, and thyroid status was available in 81–98% of women with TS; autoimmune thyroiditis was diagnosed in 37%. Echocardiography was performed in 42% and cardiac MRI in 8.5%, resulting in a diagnosis of cardiovascular disorder in 28%. Data on growth hormone therapy were available for 40 patients (15%) and data concerning menarche in 157 patients (61%).

Conclusion

In 258 women with TS, retrospective analysis of healthcare data indicated that medical management was focused on endocrine manifestations. Further significant clinical features including cardiovascular disease, renal malformation, liver involvement, autoimmune diseases, hearing loss, and osteoporosis were only marginally if at all considered. Based on this evaluation and in accordance with recent guidelines, we compiled a documentation form facilitating the transition from pediatric to adult care and further medical management of TS patients. The foundation of Turner Centers in March 2019 will improve the treatment of TS women in Germany.

Open access
John E M Midgley
Search for other papers by John E M Midgley in
Google Scholar
PubMed
Close
,
Rolf Larisch North Lakes Clinical, Department of Nuclear Medicine, Medical Department I, Ruhr Center for Rare Diseases (CeSER), 20 Wheatley Avenue, Ilkley LS29 8PT, UK

Search for other papers by Rolf Larisch in
Google Scholar
PubMed
Close
,
Johannes W Dietrich North Lakes Clinical, Department of Nuclear Medicine, Medical Department I, Ruhr Center for Rare Diseases (CeSER), 20 Wheatley Avenue, Ilkley LS29 8PT, UK
North Lakes Clinical, Department of Nuclear Medicine, Medical Department I, Ruhr Center for Rare Diseases (CeSER), 20 Wheatley Avenue, Ilkley LS29 8PT, UK

Search for other papers by Johannes W Dietrich in
Google Scholar
PubMed
Close
, and
Rudolf Hoermann North Lakes Clinical, Department of Nuclear Medicine, Medical Department I, Ruhr Center for Rare Diseases (CeSER), 20 Wheatley Avenue, Ilkley LS29 8PT, UK

Search for other papers by Rudolf Hoermann in
Google Scholar
PubMed
Close

Several influences modulate biochemical responses to a weight-adjusted levothyroxine (l-T4) replacement dose. We conducted a secondary analysis of the relationship of l-T4 dose to TSH and free T3 (FT3), using a prospective observational study examining the interacting equilibria between thyroid parameters. We studied 353 patients on steady-state l-T4 replacement for autoimmune thyroiditis or after surgery for malignant or benign thyroid disease. Peripheral deiodinase activity was calculated as a measure of T4–T3 conversion efficiency. In euthyroid subjects, the median l-T4 dose was 1.3 μg/kg per day (interquartile range (IQR) 0.94,1.60). The dose was independently associated with gender, age, aetiology and deiodinase activity (all P<0.001). Comparable FT3 levels required higher l-T4 doses in the carcinoma group (n=143), even after adjusting for different TSH levels. Euthyroid athyreotic thyroid carcinoma patients (n=50) received 1.57 μg/kg per day l-T4 (IQR 1.40, 1.69), compared to 1.19 μg/kg per day (0.85,1.47) in autoimmune thyroiditis (P<0.01, n=76) and 1.08 μg/kg per day (0.82, 1.44) in patients operated on for benign disease (P< 0.01, n=80). Stratifying patients by deiodinase activity categories of <23, 23–29 and >29 nmol/s revealed an increasing FT3–FT4 dissociation; the poorest converters showed the lowest FT3 levels in spite of the highest dose and circulating FT4 (P<0.001). An l-T4-related FT3–TSH disjoint was also apparent; some patients with fully suppressed TSH failed to raise FT3 above the median level. These findings imply that thyroid hormone conversion efficiency is an important modulator of the biochemical response to l-T4; FT3 measurement may be an additional treatment target; and l-T4 dose escalation may have limited success to raise FT3 appropriately in some cases.

Open access
Wentao Zhou The Research Institution of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China
Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Wentao Zhou in
Google Scholar
PubMed
Close
,
Tiantao Kuang The Research Institution of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Tiantao Kuang in
Google Scholar
PubMed
Close
,
Xu Han Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Xu Han in
Google Scholar
PubMed
Close
,
Wenqi Chen Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Wenqi Chen in
Google Scholar
PubMed
Close
,
Xuefeng Xu The Research Institution of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Xuefeng Xu in
Google Scholar
PubMed
Close
,
Wenhui Lou Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Wenhui Lou in
Google Scholar
PubMed
Close
, and
Dansong Wang The Research Institution of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China

Search for other papers by Dansong Wang in
Google Scholar
PubMed
Close

Objectives

Systemic inflammation markers have been demonstrated to be associated with prognosis in various tumors. In this study, we aimed to assess the value of neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio, lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammation index and the counts of lymphocyte, monocyte and neutrophil in predicting prognosis among patients with resected pancreatic neuroendocrine neoplasms (pNENs).

Methods

A total of 174 patients were included in the study. Univariate and multivariate analyses were performed to evaluate the predictive roles of inflammation markers for relapse-free survival (RFS) and overall survival (OS) in pNEN patients.

Results

The optimal cut-off values of NLR, LMR and lymphocyte count were 1.9, 5.0 and 1.4 × 109/L, respectively, determined by the X-tile software. RFS was found to be significantly longer in patients with NLR ≤1.9 (P = 0.041), LMR >5.0 (P < 0.001) and lymphocyte count >1.4 × 109/L (P = 0.002) in comparison to those with NLR >1.9, LMR ≤5.0 and lymphocyte count ≤1.4 × 109/L, respectively. Multivariate analysis revealed that LMR (hazard ratio 0.30, 95% CI 0.11–0.85, P = 0.023) was an independent predictor for RFS, but not NLR or lymphocyte count. For long-term survival analysis, patients with NLR ≤1.9 (P = 0.016) were found to be associated with favorable OS, but NLR was not an independent factor validated by multivariate analysis.

Conclusions

Preoperative LMR is an independent systemic inflammation marker to predict relapses in pNEN patients who underwent curative resections, whose clinical value needs to be verified in further large sample-based prospective studies.

Open access
Zhiwei Zhang Department of Obstetrics and Gynecology, Liaocheng People’s Hospital, Liaocheng, Shandong, China

Search for other papers by Zhiwei Zhang in
Google Scholar
PubMed
Close
,
Hui Zhao Department of Obstetrics and Gynecology, Liaocheng People’s Hospital, Liaocheng, Shandong, China

Search for other papers by Hui Zhao in
Google Scholar
PubMed
Close
, and
Aixia Wang Department of Obstetrics and Gynecology, Liaocheng People’s Hospital, Liaocheng, Shandong, China

Search for other papers by Aixia Wang in
Google Scholar
PubMed
Close

Background

Gestational diabetes mellitus (GDM) has a high incidence rate among pregnant women. The objective of the study was to assess the effect of plant-derived oleuropein in attenuating inflammatory and oxidative stress of GDM.

Methods

Oleuropein was administered to GDM mice at the doses of 5 or 10 mg/kg/day. Body weight, blood glucose, insulin and hepatic glycogen levels were recorded. To evaluate the effect of oleuropein in reducing oxidative stress, ELISA was used to measure the hepatic oxidative stress markers. The inflammation levels of GDM mice were evaluated by measuring serum levels of IL-6 and TNF-α by ELISA and mRNA levels of IL-1β, TNF-α and IL-6 by real-time PCR (RT-PCR). The AMP-activated protein kinase (AMPK) signaling pathway was assessed by Western blot. Gestational outcome was analyzed through comparing litter size and birth weight.

Results

Oleuropein attenuated the elevated body weight of GDM mice and efficiently reduced blood glucose, insulin and hepatic glycogen levels. Oxidative stress and inflammation were alleviated by oleuropein treatment. The AMPK signaling was activated by oleuropein in GDM mice. Gestational outcome was markedly improved by oleuropein treatment.

Conclusions

Our study suggests that oleuropein is effective in alleviating symptoms of GDM and improving gestational outcome in the mouse model. This effect is achieved by attenuating oxidative stress and inflammation, which is mediated by the activation of the AMPK signaling pathway.

Open access
Shaomin Shi Division of Nephrology, The First Affiliated Hospital of Yangtze University, Jingzhou, China

Search for other papers by Shaomin Shi in
Google Scholar
PubMed
Close
,
Xinghua Chen Division of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China

Search for other papers by Xinghua Chen in
Google Scholar
PubMed
Close
,
Wen Yu Department of Immunology, School of Medicine, Yangtze University, Jingzhou, China

Search for other papers by Wen Yu in
Google Scholar
PubMed
Close
,
Xiaolan Ke Division of Nephrology, The First Affiliated Hospital of Yangtze University, Jingzhou, China

Search for other papers by Xiaolan Ke in
Google Scholar
PubMed
Close
, and
Tean Ma Division of Nephrology, The First Affiliated Hospital of Yangtze University, Jingzhou, China

Search for other papers by Tean Ma in
Google Scholar
PubMed
Close

Protection of podocytes is one of the important means to delay the progression of diabetic nephropathy (DN), and glucagon-like peptide-1 (GLP-1) has been shown to have a protective effect on the kidney in DN models, but whether it has a protective effect on podocytes and the potential mechanisms of action remain largely unknown. In the present study, we established a type 2 diabetes mellitus (T2DM) mouse model by high-fat diet feeding combined with streptozotocin (STZ) induction and administered the intervention for 14 weeks. We found that liraglutide significantly ameliorated podocyte injury in DN mice. Mechanistically, we detected glucagon-like peptide-1 receptor (GLP-1R) protein expression levels in kidney tissues by immunohistochemical staining, immunofluorescence staining, and western blotting and found that podocytes could express GLP-1R and liraglutide treatment could restore GLP-1R expression in the kidney tissues of DN mice. Furthermore, we found that NLRP3-induced inflammation and pyroptosis were positively correlated with podocyte injury in DN mice, and liraglutide inhibited the expression of NLRP3-induced inflammation and pyroptosis-related proteins. Our results suggest that liraglutide protects DN mouse podocytes by regulating GLP-1R in renal tissues and by regulating NLRP3-induced inflammation and pyroptosis.

Open access
Zhengrong Jiang Department of Endocrinology, The Second affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China

Search for other papers by Zhengrong Jiang in
Google Scholar
PubMed
Close
,
Linghong Huang Department of Endocrinology, The Second affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China

Search for other papers by Linghong Huang in
Google Scholar
PubMed
Close
,
Lijun Chen Department of Endocrinology, The Second affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China

Search for other papers by Lijun Chen in
Google Scholar
PubMed
Close
,
Jingxiong Zhou Department of Endocrinology, The Second affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China

Search for other papers by Jingxiong Zhou in
Google Scholar
PubMed
Close
,
Bo Liang Department of Endocrinology, The Second affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China

Search for other papers by Bo Liang in
Google Scholar
PubMed
Close
,
Xuefeng Bai Department of Endocrinology, The Second affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China

Search for other papers by Xuefeng Bai in
Google Scholar
PubMed
Close
,
Lizhen Wu Department of Endocrinology, The Second affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China

Search for other papers by Lizhen Wu in
Google Scholar
PubMed
Close
, and
Huibin Huang Department of Endocrinology, The Second affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China

Search for other papers by Huibin Huang in
Google Scholar
PubMed
Close

Background

Graves’ disease is a common autoimmune disease. Cytokines and their signalling pathways play a major part in the pathogenesis of Graves’ disease; however, the underlying mechanism needs to be clarified.

Aims

The aim of this study was to explore whether circular RNAs participate in the immunological pathology of Graves’ disease via cytokine-related signalling pathways.

Methods

Bioinformatics analysis was performed to identify differentially expressed circular RNAs and their targets and associated pathways. A total of three patients with Graves’ disease and three sex- and age-matched healthy controls were enrolled for validation with microarray analysis and real-time quantitative PCR (qPCR). An additional 24 patients with Graves’ disease and 24 gender- and age-matched controls were included for validation by real-time fluorescent qPCR. Flow cytometry and CCK8 assays were used to detect the apoptotic and proliferative levels of Jurkat cells (T lymphocytes) with the silenced expression of circRNA. ELISA was performed to detect the growth and apoptosis-related proteins. The competition mechanism of endogenous RNA was explored by real-time fluorescence qPCR.

Results

A total of 366 significantly differentially expressed circular RNAs were identified in the Graves’ disease group compared to healthy controls. The level of hsa_circ_0090364 was elevated in Graves’ disease patients and positively correlated with thyroid-stimulating hormone receptor antibodies. Further analyses suggested that hsa_circ_0090364 may regulate the JAK-STAT pathway via the hsa-miR-378a-3p/IL-6ST/IL21R axis to promote cell growth.

Conclusions

These results provide novel clues into the pathophysiological mechanisms of Graves’ disease and potential targets for drug treatment.

Open access