Search Results
You are looking at 41 - 50 of 572 items for
- Abstract: Aging x
- Abstract: Autoimmune x
- Abstract: Inflammation x
Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina
Search for other papers by Fernando Aprile-Garcia in
Google Scholar
PubMed
Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina
Search for other papers by María Antunica-Noguerol in
Google Scholar
PubMed
Search for other papers by Maia Ludmila Budziñski in
Google Scholar
PubMed
Search for other papers by Ana C Liberman in
Google Scholar
PubMed
Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina
Search for other papers by Eduardo Arzt in
Google Scholar
PubMed
Inflammatory responses are elicited after injury, involving release of inflammatory mediators that ultimately lead, at the molecular level, to the activation of specific transcription factors (TFs; mainly activator protein 1 and nuclear factor-κB). These TFs propagate inflammation by inducing the expression of cytokines and chemokines. The neuroendocrine system has a determinant role in the maintenance of homeostasis, to avoid exacerbated inflammatory responses. Glucocorticoids (GCs) are the key neuroendocrine regulators of the inflammatory response. In this study, we describe the molecular mechanisms involved in the interplay between inflammatory cytokines, the neuroendocrine axis and GCs necessary for the control of inflammation. Targeting and modulation of the glucocorticoid receptor (GR) and its activity is a common therapeutic strategy to reduce pathological signaling. Poly (ADP-ribose) polymerase 1 (PARP1) is an enzyme that catalyzes the addition of PAR on target proteins, a post-translational modification termed PARylation. PARP1 has a central role in transcriptional regulation of inflammatory mediators, both in neuroendocrine tumors and in CNS cells. It is also involved in modulation of several nuclear receptors. Therefore, PARP1 and GR share common inflammatory pathways with antagonic roles in the control of inflammatory processes, which are crucial for the effective maintenance of homeostasis.
Search for other papers by A Rouland in
Google Scholar
PubMed
INSERM Unit, LNC-UMR 1231, University of Burgundy, Dijon, France
Search for other papers by J-C Chauvet-Gelinier in
Google Scholar
PubMed
INSERM Unit, LNC-UMR 1231, University of Burgundy, Dijon, France
Search for other papers by A-L Sberna in
Google Scholar
PubMed
Search for other papers by E Crevisy in
Google Scholar
PubMed
Search for other papers by P Buffier in
Google Scholar
PubMed
Search for other papers by T Mouillot in
Google Scholar
PubMed
INSERM Unit, LNC-UMR 1231, University of Burgundy, Dijon, France
Search for other papers by J-M Petit in
Google Scholar
PubMed
INSERM Unit, LNC-UMR 1231, University of Burgundy, Dijon, France
Search for other papers by B Vergès in
Google Scholar
PubMed
Objective
The Type A personality, characterized by impatience, strong career ambition and competitiveness, is associated with greater sensitivity to external stress. Type 1 diabetes (T1D) is an auto-immune disease, which is potentially influenced by stress, unlike type 2 diabetes (T2D). The aim of this study was to assess whether individuals with T1D and T2D exhibited significant differences on the Type A personality scale. We also assessed personality in patients with thyroid auto-immune diseases to validate potential links between auto-immune disease and Type A personality.
Design and methods
The Bortner questionnaire was used to assess Type A personality in 188 patients with T1D, 430 patients with T2D and 85 patients with auto-immune thyroid disease (Graves’ disease or Hashimoto’s thyroiditis).
Results
Type A Bortner scores were significantly higher in T1D patients than in T2D patients (188 ± 34 vs 177 ± 36, P < 0.0001). Patients with auto-immune thyroid diseases and T1D patients had similar Type A Bortner scores (189 ± 33 vs 188 ± 34, P = 0.860).
Conclusion
Patients with auto-immune T1D have higher Type A scores than T2D patients. Furthermore, patients with auto-immune thyroid disease also have elevated Type A scores similar to those observed in type 1 diabetes, suggesting that an elevated Type A score in T1D is potentially related to its auto-immune origin. This suggests a possible link between Type A personality and auto-immune diseases via stress-triggering psychobiological pathways. The different personality score between T1D and T2D is an important factor, which could influence self-care coping strategies in diabetes and long-term prognosis.
Search for other papers by Karim Gariani in
Google Scholar
PubMed
Diabetes Center, Faculty of Medicine, University of Geneva, Geneva, Switzerland
Search for other papers by François R Jornayvaz in
Google Scholar
PubMed
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the industrialized world. NAFLD encompasses a whole spectrum ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis. The latter can lead to hepatocellular carcinoma. Furthermore, NASH is the most rapidly increasing indication for liver transplantation in western countries and therefore represents a global health issue. The pathophysiology of NASH is complex and includes multiple parallel hits. NASH is notably characterized by steatosis as well as evidence of hepatocyte injury and inflammation, with or without fibrosis. NASH is frequently associated with type 2 diabetes and conditions associated with insulin resistance. Moreover, NASH may also be found in many other endocrine diseases such as polycystic ovary syndrome, hypothyroidism, male hypogonadism, growth hormone deficiency or glucocorticoid excess, for example. In this review, we will discuss the pathophysiology of NASH associated with different endocrinopathies.
Search for other papers by Nese Cinar in
Google Scholar
PubMed
Search for other papers by Alper Gurlek in
Google Scholar
PubMed
Adipose tissue secretes a variety of active biological substances, called adipocytokines, that act in an autocrine, paracrine, and endocrine manner. They have roles in appetite control, thermogenesis, and thyroid and reproductive functions. All these molecules may lead to local and generalized inflammation, mediating obesity-associated vascular disorders including hypertension, diabetes, atherosclerosis, and insulin resistance. Thyroid dysfunction is associated with changes in body weight, thermogenesis, and energy expenditure. The connections between cardiovascular risk factors such as dyslipidemia, impaired glucose tolerance, insulin resistance, atherosclerosis, and thyroid dysfunction have been reported in several studies. The adipocytokines serve as causative or protective factors in the development of these disorders in the states of thyroid dysfunction. Abnormal levels of adipocytokines (adiponectin (ADP), leptin, resistin, vaspin, and visfatin) in hypo- and hyperthyroidism have been reported with controversial results. This review aims to update the implication of novel adipokines ADP, vaspin, and visfatin in thyroid dysfunction.
Search for other papers by Ruixin Hu in
Google Scholar
PubMed
Search for other papers by Yanting Yuan in
Google Scholar
PubMed
Search for other papers by Chaolong Liu in
Google Scholar
PubMed
Search for other papers by Ji Zhou in
Google Scholar
PubMed
Search for other papers by Lixia Ji in
Google Scholar
PubMed
Search for other papers by Guohui Jiang in
Google Scholar
PubMed
In patients with type 2 diabetes mellitus (T2DM), the intestinal flora is out of balance and accompanied by leaky gut. The flora is characterized by an increase in mucus-degrading bacteria and a decrease in fiber-degrading bacteria. Short-chain fatty acids (SCFAs), as the major fiber-degrading bacteria fermentation, not only ameliorate the leaky gut, but also activate GPR43 to increase the mass of functional pancreatic β-cells and exert anti-inflammation effect. At present, the gut microbiota is considered as the potential target for anti-diabetes drugs, and how to reverse the imbalance of gut microbiota has become a therapeutic strategy for T2DM. This review briefly summarizes the drugs or compounds that have direct or potential therapeutic effects on T2DM by modulating the gut microbiota, including biguanides, isoquinoline alkaloids, stilbene and C7N-aminocyclic alcohols.
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China
Search for other papers by Wenqi Yang in
Google Scholar
PubMed
Search for other papers by Ling Liu in
Google Scholar
PubMed
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China
Search for other papers by Yuan Wei in
Google Scholar
PubMed
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China
Search for other papers by Chunlu Fang in
Google Scholar
PubMed
Search for other papers by Fu Zhou in
Google Scholar
PubMed
Search for other papers by Jinbao Chen in
Google Scholar
PubMed
Search for other papers by Qinghua Han in
Google Scholar
PubMed
Search for other papers by Meifang Huang in
Google Scholar
PubMed
Search for other papers by Xuan Tan in
Google Scholar
PubMed
Search for other papers by Qiuyue Liu in
Google Scholar
PubMed
Search for other papers by Qiang Pan in
Google Scholar
PubMed
Search for other papers by Lu Zhang in
Google Scholar
PubMed
Search for other papers by Xiaojuan Lei in
Google Scholar
PubMed
Key Laboratory of Sports Technique, Tactics and Physical Function of General Administration of Sport of China, Scientific Research Center, Guangzhou Sport University, Guangzhou, China
Search for other papers by Liangming Li in
Google Scholar
PubMed
Objective
The protective effects of exercise against glucose dysmetabolism have been generally reported. However, the mechanism by which exercise improves glucose homeostasis remains poorly understood. The FGF21–adiponectin axis participates in the regulation of glucose metabolism. Elevated levels of FGF21 and decreased levels of adiponectin in obesity indicate FGF21–adiponectin axis dysfunction. Hence, we investigated whether exercise could improve the FGF21–adiponectin axis impairment and ameliorate disturbed glucose metabolism in diet-induced obese mice.
Methods
Eight-week-old C57BL/6J mice were randomly assigned to three groups: low-fat diet control group, high-fat diet group and high-fat diet plus exercise group. Glucose metabolic parameters, the ability of FGF21 to induce adiponectin, FGF21 receptors and co-receptor levels and adipose tissue inflammation were evaluated after 12 weeks of intervention.
Results
Exercise training led to reduced levels of fasting blood glucose and insulin, improved glucose tolerance and better insulin sensitivity in high-fat diet-induced obese mice. Although serum FGF21 levels were not significantly changed, both total and high-molecular-weight adiponectin concentrations were markedly enhanced by exercise. Importantly, exercise protected against high-fat diet-induced impaired ability of FGF21 to stimulate adiponectin secretion. FGF21 co-receptor, β-klotho, as well as receptors, FGFR1 and FGFR2, were upregulated by exercise. We also found that exercise inhibited adipose tissue inflammation, which may contribute to the improvement in the FGF21–adiponectin axis impairment.
Conclusions
Our data indicate exercise protects against high-fat diet-induced FGF21–adiponectin axis impairment, and may thereby exert beneficial effects on glucose metabolism.
Department of Clinical Research, University of Basel, Basel, Switzerland
Search for other papers by Clara Odilia Sailer in
Google Scholar
PubMed
Department of Biomedicine, University of Basel, Basel, Switzerland
Search for other papers by Sophia Julia Wiedemann in
Google Scholar
PubMed
Search for other papers by Konrad Strauss in
Google Scholar
PubMed
Search for other papers by Ingeborg Schnyder in
Google Scholar
PubMed
Medical Department III, Endocrinology, Nephrology, Rheumatology, University Hospital of Leipzig, Leipzig, Germany
Search for other papers by Wiebke Kristin Fenske in
Google Scholar
PubMed
Department of Clinical Research, University of Basel, Basel, Switzerland
Search for other papers by Mirjam Christ-Crain in
Google Scholar
PubMed
Osmotic stimulus or stress results in vasopressin release. Animal and human in vitro studies have shown that inflammatory parameters, such as interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α), increase in parallel in the central nervous system and bronchial, corneal or intestinal epithelial cell lines in response to osmotic stimulus. Whether osmotic stimulus directly causes a systemic inflammatory response in humans is unknown. We therefore investigated the influence of osmotic stimulus on circulatory markers of systemic inflammation in healthy volunteers. In this prospective cohort study, 44 healthy volunteers underwent a standardized test protocol with an osmotic stimulus leading into the hyperosmotic/hypernatremic range (serum sodium ≥150 mmol/L) by hypertonic saline infusion. Copeptin – a marker indicating vasopressin activity – serum sodium and osmolality, plasma IL-8 and TNF-α were measured at baseline and directly after osmotic stimulus. Median (range) serum sodium increased from 141 mmol/L (136, 147) to 151 mmol/L (145, 154) (P < 0.01), serum osmolality increased from 295 mmol/L (281, 306) to 315 mmol/L (304, 325) (P < 0.01). Median (range) copeptin increased from 4.3 pg/L (1.1, 21.4) to 28.8 pg/L (19.9, 43.4) (P < 0.01). Median (range) IL-8 levels showed a trend to decrease from 0.79 pg/mL (0.37, 1.6) to 0.7 pg/mL (0.4, 1.9) (P < 0.09) and TNF-α levels decreased from 0.53 pg/mL (0.11, 1.1) to 0.45 pg/mL (0.12, 0.97) (P < 0.036). Contrary to data obtained in vitro, circulating proinflammatory cytokines tend to or decrease in human plasma after osmotic stimulus. In this study, osmotic stimulus does not increase circulating markers of systemic inflammation.
Search for other papers by Simon Schimmack in
Google Scholar
PubMed
Department of General Surgery, Xiangya Hospital, Central South University, Changsha, China
Department of Burns and Plastic Surgery, The Third Xiangya Hospital, Central South University, Changsha, China
Search for other papers by Yongchao Yang in
Google Scholar
PubMed
Search for other papers by Klaus Felix in
Google Scholar
PubMed
Search for other papers by Markus Herbst in
Google Scholar
PubMed
Search for other papers by Yixiong Li in
Google Scholar
PubMed
Search for other papers by Miriam Schenk in
Google Scholar
PubMed
Search for other papers by Frank Bergmann in
Google Scholar
PubMed
Search for other papers by Thilo Hackert in
Google Scholar
PubMed
Search for other papers by Oliver Strobel in
Google Scholar
PubMed
Objective
Elevated pre-operative C-reactive protein (CRP) serum values have been reported to be associated with poor overall survival for patients with pancreatic neuroendocrine neoplasms (pNEN). The aim of this study was to identify mechanisms linking CRP to poor prognosis in pNEN.
Methods
The malignant properties of pNENs were investigated using the human pNEN cell-lines BON1 and QGP1 exposed to CRP or IL-6. Analyses were performed by ELISA, Western blot, flow cytometry and immunocytochemistry as well as invasion and proliferation assays. To compare cytokine profiles and CRP levels, 76 serum samples of pNEN patients were analyzed using Luminex technology. In parallel, the expression of CRP and growth signaling pathway proteins was assessed on cell lines and paraffin-embedded primary pNEN.
Results
In BON1 and QGP1 cells, inflammation (exposure to IL-6) significantly upregulated CRP expression and secretion as well as migratory properties. CRP stimulation of BON1 cells increased IL-6 secretion and invasion. This was accompanied by activation/phosphorylation of the ERK, AKT and/or STAT3 pathways. Although known CRP receptors – CD16, CD32 and CD64 – were not detected on BON1 cells, CRP uptake of pNEN cells was shown after CRP exposure. In patients, increased pre-operative CRP levels (≥5 mg/L) were associated with significantly higher serum levels of IL-6 and G-CSF, as well as with an increased CRP expression and ERK/AKT/STAT3 phosphorylation in pNEN tissue.
Conclusion
The malignant properties of pNEN cells can be stimulated by CRP and IL-6 promoting ERK/AKT/STAT pathways activation as well as invasion, thus linking systemic inflammation and poor prognosis.
Search for other papers by Gregory Knowles in
Google Scholar
PubMed
Search for other papers by Emily Warmington in
Google Scholar
PubMed
Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK
Search for other papers by Lisa M Shepherd in
Google Scholar
PubMed
Institute of Applied Health Research, University of Birmingham, Birmingham, UK
Search for other papers by Jonathan M Hazlehurst in
Google Scholar
PubMed
Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK
Search for other papers by Anne de Bray in
Google Scholar
PubMed
Search for other papers by Helena Gleeson in
Google Scholar
PubMed
Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK
Medical Research Council London Institute of Medical Sciences, London, UK
Search for other papers by Wiebke Arlt in
Google Scholar
PubMed
Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK
NIHR Birmingham Biomedical Research Centre, University of Birmingham and University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK
Search for other papers by Alessandro Prete in
Google Scholar
PubMed
Objective
Patients with primary adrenal insufficiency (PAI) are thought to be particularly vulnerable to coronavirus disease 2019 (COVID-19); however, little is known about its true impact on this group. We assessed morbidity and health promotion attitudes during the pandemic amongst a large cohort of patients with PAI.
Design
Cross-sectional, single-centre study.
Methods
In May 2020, COVID-19 advice on social distancing and sick-day rules was distributed to all patients with PAI registered with a large secondary/tertiary care centre. A semi-structured questionnaire was used to survey patients in early 2021.
Results
Of 207 contacted patients, 162 responded (82/111 with Addison’s disease, AD; 80/96 with congenital adrenal hyperplasia, CAH). Patients with AD were older than those with CAH (median age 51 vs 39 years; P < 0.001) and had more comorbidities (Charlson comorbidity index ≥2 47.6% vs 10.0%; P< 0.001). By the time of the survey, 47 patients (29.0%) had been diagnosed with COVID-19, the second commonest cause of sick-day dosing during the study and the leading trigger of adrenal crises (4/18 cases). Patients with CAH had a higher risk of COVID-19 compared to AD (adjusted odds ratio 2.53 (95% CI 1.07–6.16), P= 0.036), were less inclined to have the COVID-19 vaccine (80.0% vs 96.3%; P = 0.001), and were less likely to have undergone hydrocortisone self-injection training (80.0% vs 91.5%; P = 0.044) or wear medical alert jewellery (36.3% vs 64.6%; P = 0.001).
Conclusions
COVID-19 was a principal trigger for adrenal crises and sick-day dosing in patients with PAI. Despite a higher risk of COVID-19, patients with CAH showed less engagement with self-protective attitudes.
Significance statement
We conducted a cross-sectional study on a large and well-characterised group of patients with PAI and demonstrated that COVID-19 was a leading cause of morbidity during the early phases of the pandemic. Patients with AD were older and had a greater burden of comorbidity than those with CAH, including non-adrenal autoimmune disorders. However, patients with CAH were more likely to develop COVID-19 and demonstrated reduced engagement with healthcare services and health promotion strategies.
Search for other papers by W N H Koek in
Google Scholar
PubMed
Search for other papers by N Campos-Obando in
Google Scholar
PubMed
Search for other papers by B C J van der Eerden in
Google Scholar
PubMed
Search for other papers by Y B de Rijke in
Google Scholar
PubMed
Search for other papers by M A Ikram in
Google Scholar
PubMed
Department of Epidemiology, Erasmus MC, Rotterdam, the Netherlands
Search for other papers by A G Uitterlinden in
Google Scholar
PubMed
Search for other papers by J P T M van Leeuwen in
Google Scholar
PubMed
Search for other papers by M C Zillikens in
Google Scholar
PubMed
Background
Sex differences in calcium and phosphate have been observed. We aimed to assess a relation with age.
Methods
We used the laboratory values of serum calcium, phosphate and albumin from three different samples ( 2005, 2010 and 2014 years) using the hospital information system of Erasmus MC, Rotterdam. The samples were divided into three age groups: 1–17, 18–44 and ≥45 years. Sex differences in calcium and phosphate were analyzed using ANCOVA, adjusting for age and serum albumin. Furthermore, sex by age interactions were determined and we analyzed differences between age groups stratified by sex.
Results
In all three samples there was a significant sex × age interaction for serum calcium and phosphate, whose levels were significantly higher in women compared to men above 45 years. No sex differences in the younger age groups were found. In men, serum calcium and phosphate levels were highest in the youngest age group compared to age groups of 18–44 and ≥45 years. In women, serum calcium levels were significantly higher in the age group 1–17 and the age group ≥45 years compared to the 18–44 years age group. In women, serum phosphate was different between the three different age groups with highest level in the group 1–17 years and lowest in the group 18–44 years.
Conclusion
There are age- dependent sex differences in serum calcium and phosphate. Furthermore, we found differences in serum calcium and phosphate between different age groups. Underlying mechanisms for these age- and sex- differences are not yet fully elucidated.
