scholarly journals Inflammatory Markers and Plasma Fatty Acids in Predicting WBC Level Alterations in Association With Glucose-Related Markers: A Cross-Sectional Study

2020 ◽  
Vol 11 ◽  
Author(s):  
Gurum Shin ◽  
Kyunghye Jang ◽  
Minjoo Kim ◽  
Jong Ho Lee ◽  
Hye Jin Yoo
Keyword(s):  
Fatty Acids ◽  
Inflammatory Markers ◽  
Cross Sectional Study ◽  
Sectional Study ◽  
Cross Sectional ◽  
Plasma Fatty Acids

Association of plasma fatty acids pattern with omentin gene expression in human adipose tissues: A cross-sectional study

2020 ◽  
Author(s):  
Mohammad Nosrati-Oskouie ◽  
Emad Yuzbashian ◽  
Maryam Zarkesh ◽  
Nazanin sadat Aghili-Moghadam ◽  
Mehdi Hedayati ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Cross Sectional Study ◽  
Sectional Study ◽  
Cross Sectional ◽  
Adipose Tissues ◽  
Plasma Fatty Acids

scholarly journals Polymorphisms of the TNF-α gene interact with plasma fatty acids on inflammatory biomarker profile: a population-based, cross-sectional study in São Paulo, Brazil

2017 ◽  
Vol 117 (12) ◽  
pp. 1663-1673 ◽  
Author(s):  
Erica Oki ◽  
Marina N. Norde ◽  
Antônio A. F. Carioca ◽  
José M. P. Souza ◽  
Inar A. Castro ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Population Based ◽  
Cross Sectional Study ◽  
Sao Paulo ◽  
Inflammatory Biomarkers ◽  
Sectional Study ◽  
Cross Sectional ◽  
Plasma Fatty Acids ◽  
Inflammatory Biomarker ◽  
Tnf Α

AbstractThe aim of the present study was to investigate the relationship of four TNF-α SNP with inflammatory biomarkers and plasma fatty acids (FA), and the interaction among them in a population-based, cross-sectional study in São Paulo, Brazil. A total of 281 subjects, aged >19 and <60 years, participated in a cross-sectional, population-based study performed in Brazil. The following SNP spanning the TNF-α gene were genotyped: -238G/A (rs361525), -308G/A (rs1800629), -857C/T (rs1799724) and -1031T/C (rs1799964). In all, eleven plasma inflammatory biomarkers and plasma FA profile were determined. To analyse the interaction between TNF-α SNP and plasma FA, a cluster analysis was performed to stratify individuals based on eleven inflammatory biomarkers into two groups used as outcome: inflammatory (INF) and non-inflammatory clusters. The -238A allele carriers had higher TNF-α (P=0·033), IL-6 (P=0·013), IL-1β (P=0·037), IL-12 (0·048) and IL-10 (P=0·010) than the GG genotype. The -308A allele carriers also had lower levels of plasma palmitoleic acid (P=0·009), oleic acid (P=0·039), total MUFA (P=0·014), stearoyl-CoA desaturase (SCD) activity index-16 (P=0·007), SCD-18 (P=0·020) and higher levels of PUFA (P=0·046) and DHA (P=0·044). Significant interactions modifying the risk of belonging to the INF cluster were observed with inflammatory cluster as outcome between -857C/T and plasma α-linolenic acid (P=0·026), and also between -308G/A and plasma stearic acid (P=0·044) and total SFA (P=0·040). Our study contributes to knowledge on TNF-α SNP and their association with inflammatory biomarker levels, plasma FA and the interaction among them, of particular interest for the Brazilian population.

scholarly journals Heart rate variability and long chain n-3 PUFA in patients with chronic kidney disease commencing haemodialysis: a cross-sectional study

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Ana Pinto ◽  
Helen MacLaughlin ◽  
Robert Gray ◽  
Wendy Hall
Keyword(s):  
Chronic Kidney Disease ◽  
Fatty Acids ◽  
Heart Rate ◽  
Cardiac Death ◽  
Autonomic Function ◽  
Cross Sectional Study ◽  
Cardiac Autonomic Function ◽  
Sectional Study ◽  
Cross Sectional ◽  
Long Chain

AbstractThe risk of sudden cardiac death (SCD) is doubled when a patient with chronic kidney disease (CKD) stage 5 starts haemodialysis. Low heart rate variability (HRV) has been reported to be independently associated with increased risk of SCD and all cardiac death in haemodialysis patients. Long chain n-3 polyunsaturated fatty acids (LC n-3 PUFA; 20:5n-3, EPA and 22:6n-3, DHA) may exert anti-arrhythmic effects on cardiac myocytes. Haemodialysis patients have lower serum LC n-3 PUFA levels compared to populations without CKD. Few studies have investigated the relationship between LC n-3 PUFA and HRV in patients with CKD. This study aimed to characterise the variability of LC n-3 PUFA status in patients who recently commenced haemodialysis, and to investigate relationships between LC n-3 PUFA status and HRV. A cross-sectional study was conducted in adults aged 40–80 years with CKD commencing haemodialysis (within 6–10 weeks) (NRES research ethics committee ref: 14/LO/0186). At 2 separate study days, pre-dialysis blood samples were taken to measure fatty acid composition by GC, and HRV monitors (Actiheart, CamNtech Ltd, UK) were fitted after dialysis had started to monitor parameters of cardiac autonomic function during dialysis, during the night, and for a total of 24 h. Forty-five patients (mean age 58 y, SD 9, 20 females/25 males) completed data collection at least once; 91% presented hypertension and 39% had type 2 diabetes. Sample mean omega-3 index (O3I; EPA + DHA as a % of fatty acids in erythrocyte membranes) was very low (3.45%, SD 1.25; median 3.26 %, IQR 1.32); only 2 individuals had O3I > 5%. Variability in erythrocyte EPA (median 0.66 %, IQR 0.42) and DHA (median 2.40 %, IQR 1.32) was limited. Most HRV parameters did not significantly correlate with O3I following adjustment (e.g. age, BMI, β-blockers). Plasma EPA significantly positively correlated with overall and longer phase components of HRV and significantly negatively correlated with beat-to-beat variability over 24 h after full adjustment for confounders. This suggests that although higher circulating EPA concentrations were associated with better cardiac responsivity to environmental stimulations over 24 h, they were also associated with poorer parasympathetic tone (the predominant influence on beat-to-beat HRV). No correlations were observed between plasma DHA and HRV. The divergent pattern of relationships between plasma EPA versus DHA and HRV raises the theory that patients commencing haemodialysis may have compromised conversion of EPA to DHA which may impair vagally-mediated regulation of cardiac autonomic function, a potential mechanism for high risk of SCD.

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