Publications by authors named "N P Riksen"

170 Publications

Superficial versus Deep Subcutaneous Adipose Tissue: Sex-Specific Associations with Hepatic Steatosis and Metabolic Traits.

J Clin Endocrinol Metab 2021 Jun 17. Epub 2021 Jun 17.

Department of Internal Medicine, Division of Vascular Medicine, Radboud university medical center, Nijmegen, The Netherlands.

Objective: Subcutaneous adipose tissue (SAT) is not homogeneous, as the fascia scarpa separates the deep SAT (dSAT) from the superficial SAT (sSAT). The aim of this study was to evaluate the sex-specific associations of sSAT and dSAT with hepatic steatosis and the metabolic syndrome in overweight individuals.

Methods: We recruited 285 individuals with a BMI≥27 kg/m 2, aged 55-81 years. Abdominal magnetic resonance imaging was performed around level L4-L5 to measure VAT, dSAT and sSAT volumes. The amount of hepatic fat was quantified by MR spectroscopy.

Results: Men had significantly higher volumes of VAT (122.6 cm 3 versus 98.7 cm 3, p<0.001) and had only half of the volume of sSAT compared to women adjusted for BMI (50.3 cm 3 in men versus 97.0 cm 3 in women, p<0.001). dSAT correlated significantly with hepatic fat content in univariate analysis (stand. β=0.190, p<0.05), while VAT correlated significantly with hepatic steatosis in a multivariate model, adjusted for age, alcohol use and other abdominal fat compartments (stand. β=0.184, p=0.037). Moreover, dSAT in men correlated negatively with HDL-c (stand. β=-0.165, p=0.038) in multivariate analyses. In women with a BMI between 30-40 kg/m 2, in a multivariate model adjusted for age, alcohol use and other abdominal fat compartments, VAT correlated positively (stand. β=-0.404, p=0.003), and sSAT negatively (stand. β=-0.300, p=0.04) with hepatic fat content.

Conclusions: In men, dSAT is associated with hepatic steatosis and adverse metabolic traits, such as lower HDL-cholesterol levels; while in women with obesity sSAT shows a beneficial relation with respect to hepatic fat content.
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http://dx.doi.org/10.1210/clinem/dgab426DOI Listing
June 2021

Oral Microbiome in Relation to Periodontitis Severity and Systemic Inflammation.

Int J Mol Sci 2021 May 30;22(11). Epub 2021 May 30.

Department of Internal Medicine and Radboud Institute for Molecular Life Science (RIMLS), Radboud University Medical Center, 6525 GA Nijmegen, The Netherlands.

Systemic inflammation induced by periodontitis is suggested to be the link between periodontitis and cardiovascular disease. The aim of this work was to explore the oral microbiome in periodontitis in relation to disease severity and systemic inflammation. The saliva and subgingival microbiome from periodontal pocket samples of patients with severe (n = 12) and mild periodontitis (n = 13) were analyzed using metagenomic shotgun sequencing. The taxa and pathways abundances were quantified. The diversity was assessed and the abundances to phenotype associations were performed using ANCOM and linear regression. A panel of inflammatory markers was measured in blood and was associated with taxa abundance. The microbial diversity and species richness did not differ between severe and mild periodontitis in either saliva or periodontal pockets. However, there were significant differences in the microbial composition between severe and mild periodontitis in the subgingival microbiome (i.e., pocket samples) and, in a lower grade, in saliva, and this is positively associated with systemic inflammatory markers. The "red complex" and "cluster B" abundances in periodontal pockets were strongly associated with inflammatory markers interleukin-6 and the white blood cell count. Our data suggest that systemic inflammation in severe periodontitis may be driven by the oral microbiome and may support the indirect (inflammatory) mechanism for the association between periodontitis and cardiovascular disease.
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http://dx.doi.org/10.3390/ijms22115876DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8199296PMC
May 2021

Pro-inflammatory Monocyte Phenotype During Acute Progression of Cerebral Small Vessel Disease.

Front Cardiovasc Med 2021 13;8:639361. Epub 2021 May 13.

Department of Internal Medicine, Radboud Institute for Molecular Life Science, Radboud University Medical Center, Nijmegen, Netherlands.

The etiology of cerebral small vessel disease (SVD) remains elusive, though evidence is accumulating that inflammation contributes to its pathophysiology. We recently showed retrospectively that pro-inflammatory monocytes are associated with the long-term progression of white matter hyperintensities (WMHs). In this prospective high-frequency imaging study, we hypothesize that the incidence of SVD progression coincides with a pro-inflammatory monocyte phenotype. Individuals with SVD underwent monthly magnetic resonance imaging (MRI) for 10 consecutive months to detect SVD progression, defined as acute diffusion-weighted imaging-positive (DWI+) lesions, incident microbleeds, incident lacunes, and WMH progression. Circulating inflammatory markers were measured, cytokine production capacity of monocytes was assessed after stimulation, and RNA sequencing was performed on isolated monocytes in a subset of participants. 13 out of 35 individuals developed SVD progression (70 ± 6 years, 54% men) based on incident lesions ( = 7) and/or upper quartile WMH progression ( = 9). Circulating E-selectin concentration ( < 0.05) and the cytokine production capacity of interleukin (IL)-1β and IL-6 ( < 0.01) were higher in individuals with SVD progression. Moreover, RNA sequencing revealed a pro-inflammatory monocyte signature including genes involved in myelination, blood-brain barrier, and endothelial-leukocyte interaction. Circulating monocytes of individuals with progressive SVD have an inflammatory phenotype, characterized by an increased cytokine production capacity and a pro-inflammatory transcriptional signature.
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http://dx.doi.org/10.3389/fcvm.2021.639361DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8155247PMC
May 2021

Neuroinflammation in cognitive decline post-cardiac surgery (the FOCUS study): an observational study protocol.

BMJ Open 2021 05 11;11(5):e044062. Epub 2021 May 11.

Department of Intensive Care Medicine, Radboud university medical center, Nijmegen, The Netherlands

Introduction: Postoperative cognitive dysfunction occurs frequently after coronary artery bypass grafting (CABG). The underlying mechanisms remain poorly understood, but neuroinflammation might play a pivotal role. We hypothesise that systemic inflammation induced by the surgical trauma could activate the innate immune (glial) cells of the brain. This could lead to an exaggerated neuroinflammatory cascade, resulting in neuronal dysfunction and loss of neuronal cells. Therefore, the aims of this study are to assess neuroinflammation in vivo presurgery and postsurgery in patients undergoing major cardiac surgery and investigate whether there is a relationship of neuroinflammation to cognitive outcomes, changes to brain structure and function, and systemic inflammation.

Methods And Analysis: The FOCUS study is a prospective, single-centre observational study, including 30 patients undergoing elective on-pump CABG. Translocator protein (TSPO) positron emission tomography neuroimaging will be performed preoperatively and postoperatively using the second generation tracer F-DPA-714 to assess the neuroinflammatory response. In addition, a comprehensive cerebral MRI will be performed presurgery and postsurgery, in order to discover newly developed brain and vascular wall lesions. Up to 6 months postoperatively, serial extensive neurocognitive assessments will be performed and blood will be obtained to quantify systemic inflammatory responses and peripheral immune cell activation.

Ethics And Dissemination: Patients do not benefit directly from engaging in the study, but imaging neuroinflammation is considered safe and no side effects are expected. The study protocol obtained ethical approval by the Medical Research Ethics Committee region Arnhem-Nijmegen. This work will be published in peer-reviewed international medical journals and presented at medical conferences.

Trial Registration Number: NCT04520802.
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http://dx.doi.org/10.1136/bmjopen-2020-044062DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8118022PMC
May 2021