Search Results
You are looking at 1 - 10 of 58 items for
- Abstract: Inflammation x
- Abstract: Cognition x
Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
Search for other papers by Reshma Aziz Merchant in
Google Scholar
PubMed
Search for other papers by Michael Wong Wai Kit in
Google Scholar
PubMed
Search for other papers by Jia Yi Lim in
Google Scholar
PubMed
Search for other papers by John E Morley in
Google Scholar
PubMed
Objective
To investigate the association of normal BMI with central obesity (CO), high BMI with CO, high BMI without CO, and normal BMI without CO, with function and cognition in older adults.
Methods
Cross-sectional study involving 754 participants ≥ 65 years. Data collected include demographics, cognition, and physical measurements.
Results
Females had a higher prevalence of high BMI with CO and a lower prevalence of high BMI without CO than males (61.0% vs 44.6% and 4.6% vs 15.0%, respectively). Within gender, CO groups, regardless of BMI, had lower mini-mental state examination (MMSE), handgrip strength (HGS), and longer timed-up-and-go (TUG) scores. Overall, the high BMI without CO group had the highest MMSE scores, HGS, and shortest TUG. Amongst males, HGS was significantly lower in the normal BMI with CO group (B −3.28, 95% CI −6.32 to −0.23, P = 0.04). CO, regardless of normal/high BMI, had significantly longer TUG time (B 2.65, 95% CI 0.45 to 4.84, P = 0.02; B 1.07, 95% CI 0.25 to 1.88, P = 0.01, respectively) than normal BMI without CO group. CO was associated with lower MMSE scores in both genders but significant only in males with normal BMI and CO (B −1.60, 95% CI −3.15 to −0.06, P = 0.04).
Conclusion
CO may be a better predictor of obesity and adverse outcomes in older adults. High BMI without CO was associated with better outcomes especially in males but require further validation. Prospective longitudinal studies are needed to ascertain the impact of BMI and/or CO on function, cognition, mortality, and gender differences.
TRIXY Center of Expertise, Leiden University Treatment and Expertise Centre (LUBEC), Sandifortdreef, Leiden, The Netherlands
Leiden Institute for Brain and Cognition, Leiden University, Wassenaarseweg, Leiden, The Netherlands
Search for other papers by Sophie van Rijn in
Google Scholar
PubMed
TRIXY Center of Expertise, Leiden University Treatment and Expertise Centre (LUBEC), Sandifortdreef, Leiden, The Netherlands
Leiden Institute for Brain and Cognition, Leiden University, Wassenaarseweg, Leiden, The Netherlands
Search for other papers by Kimberly Kuiper in
Google Scholar
PubMed
TRIXY Center of Expertise, Leiden University Treatment and Expertise Centre (LUBEC), Sandifortdreef, Leiden, The Netherlands
Department of Child and Adolescent Psychiatry/Psychology, Erasmus MC, Sophia Children’s Hospital, Dr. Molewaterplein, Rotterdam, The Netherlands
Search for other papers by Nienke Bouw in
Google Scholar
PubMed
TRIXY Center of Expertise, Leiden University Treatment and Expertise Centre (LUBEC), Sandifortdreef, Leiden, The Netherlands
Department of Clinical, Neuro, and Developmental Psychology, Vrije Universiteit Amsterdam, Van der Boechorststraat, Amsterdam, The Netherlands
Search for other papers by Evelien Urbanus in
Google Scholar
PubMed
TRIXY Center of Expertise, Leiden University Treatment and Expertise Centre (LUBEC), Sandifortdreef, Leiden, The Netherlands
Leiden Institute for Brain and Cognition, Leiden University, Wassenaarseweg, Leiden, The Netherlands
Search for other papers by Hanna Swaab in
Google Scholar
PubMed
Investigating sex chromosome trisomies (SCTs) may help in understanding neurodevelopmental pathways underlying the risk for neurobehavioral problems and psychopathology. Knowledge about the neurobehavioral phenotype is needed to improve clinical care and early intervention for children with SCT. This is especially relevant considering the increasing number of early diagnosed children with the recent introduction of noninvasive prenatal screening. The TRIXY Early Childhood Study is a longitudinal study designed to identify early neurodevelopmental risks in children with SCT, aged 1–7 years. This review summarizes the results from the TRIXY Early Childhood Study, focusing on early behavioral symptoms in areas of autism spectrum disorder, attention-deficit hyperactivity disorder, and communication disorders, and underlying neurocognitive mechanisms in domains of language, emotion regulation, executive functioning, and social cognition. Behavioral symptoms were assessed through structured behavior observation and parental questionnaires. Neurocognition was measured using performance tests, eyetracking, and psychophysiological measures of arousal. In total, 209 children aged 1–7 years were included: 107 children with SCT (33 XXX, 50 XXY, and 24 XYY) and 102 age-matched population controls. Study outcomes showed early behavioral symptoms in young children with SCT, and neurocognitive vulnerabilities, already from an early age onward. Neurobehavioral and neurocognitive difficulties tended to become more pronounced with increasing age and were rather robust, independent of specific karyotype, pre/postnatal diagnosis, or ascertainment strategy. A more longitudinal perspective on neurodevelopmental ‘at-risk’ pathways is warranted, also including studies assessing the effectiveness of targeted early interventions. Neurocognitive markers that signal differences in neurodevelopment may prove to be helpful in this. Focusing on early development of language, social cognition, emotion regulation, and executive functioning may help in uncovering early essential mechanisms of (later) neurobehavioral outcome, allowing for more targeted support and early intervention.
Search for other papers by Justyna Modrzynska in
Google Scholar
PubMed
Search for other papers by Christine F Klein in
Google Scholar
PubMed
Search for other papers by Kasper Iversen in
Google Scholar
PubMed
Search for other papers by Henning Bundgaard in
Google Scholar
PubMed
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Bolette Hartmann in
Google Scholar
PubMed
Search for other papers by Maike Mose in
Google Scholar
PubMed
Search for other papers by Nikolaj Rittig in
Google Scholar
PubMed
Search for other papers by Niels Møller in
Google Scholar
PubMed
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Jens J Holst in
Google Scholar
PubMed
Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Nicolai J Wewer Albrechtsen in
Google Scholar
PubMed
Objective
Glucagon and glucagon-like peptide-1 (GLP-1) originate from the common precursor, proglucagon, and their plasma concentrations have been reported to be increased during inflammatory conditions. Increased blood glucose levels are frequently observed in septic patients, and therefore we hypothesized that glucagon, but not GLP-1, is increased in individuals with inflammation.
Design
Prospective longitudinal cohort study.
Materials and methods
We measured glucagon and GLP-1 in plasma sampled consecutively in three cohorts consisting of patients with infective endocarditis (n = 16), urosepsis (n = 28) and post-operative inflammation following percutaneous aortic valve implantation or thoracic endovascular aortic repair (n = 5). Correlations between C-reactive protein (CRP), a marker of systemic inflammation, and glucagon and GLP-1 concentrations were investigated. Additionally, glucagon and GLP-1 concentrations were measured after a bolus infusion of lipopolysaccharide (LPS, 1 ng/kg) in nine healthy young males.
Results
Glucagon and CRP were positively and significantly correlated (r = 0.27; P = 0.0003), whereas no significant association between GLP-1 and CRP was found (r = 0.08, P = 0.30). LPS infusion resulted in acute systemic inflammation reflected by increased temperature, pulse, tumor necrosis factor-α (TNFα), interleukin-6 (IL-6) and concomitantly increased concentrations of glucagon (P < 0.05) but not GLP-1.
Conclusions
Systemic inflammation caused by bacterial infections or developed as a non-infected condition is associated with increased plasma concentration of glucagon, but not GLP-1. Hyperglucagonemia may contribute to the impaired glucose control in patients with systemic inflammatory diseases.
Search for other papers by Huiyuan Zhai in
Google Scholar
PubMed
Search for other papers by Dongxu Wang in
Google Scholar
PubMed
Search for other papers by Yong Wang in
Google Scholar
PubMed
Search for other papers by Hongwei Gu in
Google Scholar
PubMed
Search for other papers by Juan Jv in
Google Scholar
PubMed
Search for other papers by Liangliang Yuan in
Google Scholar
PubMed
Search for other papers by Chao Wang in
Google Scholar
PubMed
Search for other papers by Leiyao Chen in
Google Scholar
PubMed
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.
Search for other papers by Patricia Iozzo in
Google Scholar
PubMed
Search for other papers by Maria Angela Guzzardi in
Google Scholar
PubMed
The prevalence of obesity has reached epidemic proportions and keeps growing. Obesity seems implicated in the pathogenesis of cognitive dysfunction, Alzheimer’s disease and dementia, and vice versa. Growing scientific efforts are being devoted to the identification of central mechanisms underlying the frequent association between obesity and cognitive dysfunction. Glucose brain handling undergoes dynamic changes during the life-course, suggesting that its alterations might precede and contribute to degenerative changes or signaling abnormalities. Imaging of the glucose analog 18F-labeled fluorodeoxyglucose (18FDG) by positron emission tomography (PET) is the gold-standard for the assessment of cerebral glucose metabolism in vivo. This review summarizes the current literature addressing brain glucose uptake measured by PET imaging, and the effect of insulin on brain metabolism, trying to embrace a life-course vision in the identification of patterns that may explain (and contribute to) the frequent association between obesity and cognitive dysfunction. The current evidence supports that brain hypermetabolism and brain insulin resistance occur in selected high-risk conditions as a transient phenomenon, eventually evolving toward normal or low values during life or disease progression. Associative studies suggest that brain hypermetabolism predicts low BDNF levels, hepatic and whole body insulin resistance, food desire and an unfavorable balance between anticipated reward from food and cognitive inhibitory control. Emerging mechanistic links involve the microbiota and the metabolome, which correlate with brain metabolism and cognition, deserving attention as potential future prevention targets.
INSERM U1018, Université Paris Sud, Centre for Research in Epidemiology and Population Health, Hôpital Paul Brousse, Bât 15/16, 16 Avenue Paul Vaillant Couturier, 94807 Paris, Villejuif Cedex, France
Search for other papers by Richard H Tuligenga in
Google Scholar
PubMed
The aim of this meta-analysis was to compare the effect of intensive vs standard glycaemic control on cognitive decline in type 2 diabetic patients. A systematic search of PubMed and ALOIS was conducted from inception up to October 30, 2014. Randomised controlled trials (RCTs) of type 2 diabetic patients comparing the rate of change in cognitive function among participants assigned to intensive vs standard glycaemic control were included. An inverse-variance-weighted random effects model was used to calculate standardised mean differences (SMDs) and 95% CIs. A total of 24 297 patients from five RCTs were included in the meta-analysis. Follow-up ranged from 3.3 to 6.2 years. The result from the pooled analysis showed that intensive glycaemic control was not associated with a slower rate of cognitive decline in patients with type 2 diabetes, compared with standard glycaemic control (SMD=0.02; 95% CI=−0.03 to 0.08) although there was some heterogeneity across individual studies (I 2=68%, P for heterogeneity=0.01). There are few diabetes control trials including cognitive endpoints and a small number of trials comparing intensive and standard treatment strategies. Currently, intensive glycaemic control should not be recommended for prevention of cognitive decline in patients with type 2 diabetes because there is no evidence of its effectiveness. Moreover, the use of intensive diabetes treatment results in an increase of risk of hypoglycaemia, which is linked to a greater risk of poor cognition.
Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden
Search for other papers by Charlotte Höybye in
Google Scholar
PubMed
Search for other papers by Laia Faseh in
Google Scholar
PubMed
Department of Medicine, Karlstad Hospital, Karlstad, Sweden
Search for other papers by Christos Himonakos in
Google Scholar
PubMed
Search for other papers by Tomasz Pielak in
Google Scholar
PubMed
Search for other papers by Jesper Eugen-Olsen in
Google Scholar
PubMed
Growth hormone deficiency (GHD) syndrome is associated with adverse levels of several risk factors for cardiovascular diseases (CVD), including metabolic inflammation. However, the impact of GHD and GH treatment on low-grade inflammation is unknown. The aim of the study was to establish the level of the low-grade inflammation biomarker soluble urokinase plasminogen activator receptor (suPAR) in adults with GHD and the response to long-term GH treatment. Measurements of suPAR and CRP were performed in bio-bank serum samples from 72 adults, 34 males and 38 females, with GHD before and during at least 5 years of GH treatment. Mean age was 52.5 ± 15.5 years, BMI 27.3 ± 5 kg/m2. Clinical evaluations and blood sampling were performed at routine visits. Data on demography, anthropometry, lab results and clinical events were retrieved from post-marketing surveillance study databases and medical records. suPAR and high-sensitive (hs) CRP were analysed using ELISA and immunochemistry, respectively. At baseline blood pressure, lipid profile and fasting glucose were within the normal reference range. Baseline geometric mean and 95% CI of suPAR was 2.9 (2.7–3.3) ng/mL and of CRP 2.3 (0.6–4.0) mg/L. Mean follow-up was 8 ± 2 years. The suPAR levels remained stable during follow-up, although individual increases were seen on occurrence or presence of co-morbidities. In contrast, levels of CRP decreased. In conclusion, the decrease in CRP and indirectly the absence of an expected increase in suPAR over time indicates a favourable effect of GH on low-grade inflammation.
Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China
Search for other papers by Wentao Zhou in
Google Scholar
PubMed
Search for other papers by Tiantao Kuang in
Google Scholar
PubMed
Search for other papers by Xu Han in
Google Scholar
PubMed
Search for other papers by Wenqi Chen in
Google Scholar
PubMed
Search for other papers by Xuefeng Xu in
Google Scholar
PubMed
Search for other papers by Wenhui Lou in
Google Scholar
PubMed
Search for other papers by Dansong Wang in
Google Scholar
PubMed
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.
Search for other papers by Frederique Van de Velde in
Google Scholar
PubMed
Search for other papers by Marlies Bekaert in
Google Scholar
PubMed
Search for other papers by Anja Geerts in
Google Scholar
PubMed
Search for other papers by Anne Hoorens in
Google Scholar
PubMed
Search for other papers by Arsène-Hélène Batens in
Google Scholar
PubMed
Search for other papers by Samyah Shadid in
Google Scholar
PubMed
Institute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Duesseldorf, Germany
German Center for Diabetes Research (DZD), Munich-Neuherberg, Germany
Search for other papers by Margriet Ouwens in
Google Scholar
PubMed
Search for other papers by Yves Van Nieuwenhove in
Google Scholar
PubMed
Search for other papers by Bruno Lapauw in
Google Scholar
PubMed
Purpose
Obese subjects with nonalcoholic fatty liver disease (NAFLD) are more prone to develop additional metabolic disturbances such as systemic insulin resistance (IR) and type 2 diabetes. NAFLD is defined by hepatic steatosis, lobular inflammation, ballooning and stage of fibrosis, but it is unclear if and which components could contribute to IR.
Objective
To assess which histological components of NAFLD associate with IR in subjects with obesity, and if so, to what extent.
Methods
This cross-sectional study included 78 obese subjects (mean age 46 ± 11 years; BMI 42.2 ± 4.7 kg/m2). Glucose levels were analysed by hexokinase method and insulin levels with electrochemiluminescence. Homeostasis model assessment-estimated insulin resistance (HOMA-IR) was calculated. Liver biopsies were evaluated for histological components of NAFLD.
Results
A positive association between overall NAFLD Activity Score and HOMA-IR was found (r s = 0.259, P = 0.022). As per individual components, lobular inflammation and fibrosis stage were positively associated with HOMA-IR, glucose and insulin levels (P < 0.05), and HOMA-IR was higher in patients with more inflammatory foci or higher stage of fibrosis. These findings were independent of age, BMI, triglyceride levels, diabetes status and sex (all P < 0.043). In a combined model, lobular inflammation, but not fibrosis, remained associated with HOMA-IR.
Conclusion
In this group of obese subjects, a major contributing histological component of NAFLD to the relation between NAFLD severity and IR seems to be the grade of hepatic lobular inflammation. Although no causal relationship was assessed, preventing or mitigating this inflammatory response in obesity might be of importance in controlling obesity-related metabolic disturbances.
Search for other papers by Zhiwei Zhang in
Google Scholar
PubMed
Search for other papers by Hui Zhao in
Google Scholar
PubMed
Search for other papers by Aixia Wang in
Google Scholar
PubMed
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.
