Serum- and HDL3-serum amyloid A and HDL3-LCAT activity are influenced by increased CVD-burden

McEneny, Jane; McKavanagh, Peter; York, Edmund; Nadeem, Nida; Harbinson, Mark; Stevenson, Michael R.; Ball, Peter; Lusk, Lisa; Trinick, Thomas R.; McKay, Gareth J.; Donnelly, Patrick

doi:10.1016/j.atherosclerosis.2015.11.018

Cited by 10 publications

(8 citation statements)

References 31 publications

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“…SAA may be transiently associated with HDL decline during acute inflammation. This acute-phase protein may displace ApoA-I, leading to increased catabolism of HDL ( McEneny et al, 2016 ). Our results show that following hypoxia, lipoprotein pattern shifts toward a more atherogenic lipid profile by lowering total HDL-C and HDL2-C sub-fraction.…”

Section: Discussionmentioning

confidence: 99%

Effects of Hypoxia and Bed Rest on Markers of Cardiometabolic Risk: Compensatory Changes in Circulating TRAIL and Glutathione Redox Capacity

et al. 2018

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In chronic diseases, hypoxia and physical inactivity are associated with atherosclerosis progression. In contrast, a lower mortality from coronary artery disease and stroke is observed in healthy humans residing at high altitude in hypoxic environments. Eleven young, male volunteers completed the following 10-day campaigns in a randomized order: hypoxic ambulatory, hypoxic bed rest and normoxic bed rest. Before intervention, subjects were evaluated in normoxic ambulatory condition. Normobaric hypoxia was achieved in a hypoxic facility simulating 4000 m of altitude. Following hypoxia, either in bed rest or ambulatory condition, markers of cardiometabolic risk shifted toward a more atherogenic pattern consisting of: (a) lower levels of total HDL cholesterol and HDL2 sub-fraction and decreased hepatic lipase; (b) activation of systemic inflammation, as determined by C-reactive protein and serum amyloid A; (c) increased plasma homocysteine; (d) decreased delta-5 desaturase index in cell membrane fatty acids, a marker of insulin sensitivity. Bed rest and hypoxia additively decreased total HDL and delta-5 desaturase index. In parallel to the pro-atherogenic effects, hypoxia activated selected anti-atherogenic pathways, consisting of increased circulating TNF-related apoptosis-inducing ligand (TRAIL), a protective factor against atherosclerosis, membrane omega-3 index and erythrocyte glutathione availability. Hypoxia mediated changes in TRAIL concentrations and redox glutathione capacity (i.e., GSH/GSSG ratio) were greater in ambulatory conditions (+34 ± 6% and +87 ± 31%, respectively) than in bed rest (+17 ± 7% and +2 ± 27% respectively). Hypoxia-induced cardiometabolic risk is blunted by moderate level of physical activity as compared to bed rest. TRAIL and glutathione redox capacity may contribute to the positive interaction between physical activity and hypoxia.Highlights:– Hypoxia and bed rest activate metabolic and inflammatory markers of atherogenesis.– Hypoxia and physical activity activate selected anti-atherogenic pathways.– Hypoxia and physical activity positive interaction involves TRAIL and glutathione.

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Section: Discussionmentioning

confidence: 99%

Effects of Hypoxia and Bed Rest on Markers of Cardiometabolic Risk: Compensatory Changes in Circulating TRAIL and Glutathione Redox Capacity

et al. 2018

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“…Plasma activities of CETP, LCAT, and PLTP were assessed using fluorescence assay kits (Roar Biomedical, Inc., New York, NY, USA) with the fluorescence spectrophotometer SpectraMax M2 (Molecular Devices, LLC, Sunnyvale, CA, USA). The procedures of plasma CETP, PLTP, and LCAT activity measurements were according to the manufacturers’ instructors, and the procedures and mechanisms of the assays were described by others [ 18 , 19 ]. The assay of LCAT activity was based on the ratio of the levels of the hydrolyzed (390-nm peak) to the non-hydrolyzed (470-nm peak) phosphatidylcholine (as the substrate reagent).…”

Section: Methodsmentioning

confidence: 99%

Capsaicin Supplementation Improved Risk Factors of Coronary Heart Disease in Individuals with Low HDL-C Levels

et al. 2017

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Low high-density lipoprotein cholesterol (HDL-C) is associated with an increased risk of coronary heart disease (CHD). This study aimed to evaluate the effects of capsaicin intervention on the serum lipid profile in adults with low HDL-C. In a randomized, double-blind, controlled clinical trial, 42 eligible subjects were randomly assigned to the capsaicin (n = 21, 4 mg of capsaicin daily) or to the control group (n = 21, 0.05 mg of capsaicin daily) and consumed two capsaicin or control capsules, which contained the powder of the skin of different peppers, twice daily for three months. Thirty-five subjects completed the trial (18 in the capsaicin group and 17 in the control group). The baseline characteristics were similar between the two groups. Compared with the control group, fasting serum HDL-C levels significantly increased to 1.00 ± 0.13 mmol/L from 0.92 ± 0.13 mmol/L in the capsaicin group (p = 0.030), while levels of triglycerides and C-reactive protein and phospholipid transfer protein activity moderately decreased (all p < 0.05). Other lipids, apolipoproteins, glucose, and other parameters did not significantly change. In conclusion, capsaicin improved risk factors of CHD in individuals with low HDL-C and may contribute to the prevention and treatment of CHD.

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“…This was unsurprising, given serum SAA levels have been shown to correlate with HDL SAA levels and may suggest that individuals with the SAA 1.5 allele have HDL particles with a higher affinity for SAA. We and others have previously reported that increased SAA levels within HDL fractions may compromise the functionality of the HDL particle reducing its cardioprotective properties [15,16].…”

Section: Discussionmentioning

confidence: 90%

“…A significant but modest correlation between SAA with age and estimated glomerular filtration rate (eGFR) (r = 0.15, p = 0.03 and r = − 0.19, p < 0.001, respectively) was detected. Females tended to have higher serum SAA levels than males (30 mg/L (25,36) vs. 19 mg/L (16,23); p < 0.001).…”

Section: Subject Characteristicsmentioning

confidence: 91%

“…When released, SAA readily associates with high-density lipoprotein (HDL), becoming the major carrier of this protein in the circulation [13,14]. HDL is traditionally considered to be atheroprotective; however, evidence suggests its association with SAA causes a change in the protein and lipid composition of HDL which negates some of its anti-atherogenic properties as it transitions to a proatherogenic state [13,15,16]. SAA has been detected in foam cells within atherosclerotic lesions and may lead to plaque instability [6,[17][18][19].…”

Section: Introductionmentioning

confidence: 99%

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Serum amyloid A levels are associated with polymorphic variants in the serum amyloid A 1 and 2 genes

Griffiths¹,

Maxwell²,

McCarter³

et al. 2019

Ir J Med Sci

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Background Serum amyloid A (SAA) is secreted by liver hepatocytes in response to increased inflammation whereupon it associates with high-density lipoprotein (HDL) and alters the protein and lipid composition of HDL negating some of its antiatherogenic properties. Aims To identify variants within the SAA gene that may be associated with SAA levels and/or cardiovascular disease (CVD). Methods We identified exonic variants within the SAA genes by deoxyribonucleic acid (DNA) Sanger sequencing. We tested the association between SAA variants and serum SAA levels in 246 individuals with and without CVD. Results Increased SAA was associated with rs2468844 (beta [β] = 1.73; confidence intervals [CI], 1.14-1.75; p = 0.01), rs1136747 (β = 1.53 (CI, 1.11-1.73); p = 0.01) and rs149926073 (β = 3.37 (CI, 1.70-4.00); p = 0.02), while rs1136745 was significantly associated with decreased SAA levels (β = 0.70 (CI, 0.53-0.94); p = 0.02). Homozygous individuals with the SAA1.3 haplotype had significantly lower levels of SAA compared with those with SAA1.1 or SAA1.5 (β = 0.43 (CI, 0.22-0.85); p = 0.02) while SAA1.3/1.5 heterozygotes had significantly higher SAA levels compared with those homozygous for SAA1.1 (β = 2.58 (CI, 1.19-5.57); p = 0.02). Conclusions We have identified novel genetic variants in the SAA genes associated with SAA levels, a biomarker of inflammation and chronic disease. The utility of SAA as a biomarker for inflammation and chronic disease may be influenced by underlying genetic variation in baseline levels.

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Serum- and HDL3-serum amyloid A and HDL3-LCAT activity are influenced by increased CVD-burden

Cited by 10 publications

References 31 publications

Effects of Hypoxia and Bed Rest on Markers of Cardiometabolic Risk: Compensatory Changes in Circulating TRAIL and Glutathione Redox Capacity

Effects of Hypoxia and Bed Rest on Markers of Cardiometabolic Risk: Compensatory Changes in Circulating TRAIL and Glutathione Redox Capacity

Capsaicin Supplementation Improved Risk Factors of Coronary Heart Disease in Individuals with Low HDL-C Levels

Serum amyloid A levels are associated with polymorphic variants in the serum amyloid A 1 and 2 genes

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