Association between serum amyloid A and obesity: a meta-analysis and systematic review

Zhao, Yulan; He, Xuelian; Shi, Xiang; Huang, Can; Liu, Jie; Zhou, Shuli; Heng, Chew‐Kiat

doi:10.1007/s00011-010-0163-y

Cited by 94 publications

(82 citation statements)

References 90 publications

(148 reference statements)

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“…Increased SAA expression in subcutaneous white adipose tissue can result in increased circulatory levels of SAA (29). The epidemic of obesity is accompanied by an increase in atherosclerotic diseases and may have a close association with SAA levels (30). The increase in adiposederived SAA in obesity may be a mechanistic link between obesity and accelerated atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Serum Amyloid A Directly Accelerates the Progression of Atherosclerosis in Apolipoprotein E-Deficient Mice

Dong

Qin

et al. 2011

Mol Med

111

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Although serum amyloid A (SAA) is an excellent marker for coronary artery disease, its direct effect on atherogenesis in vivo is obscure. In this study we investigated the direct effect of SAA on promoting the formation of atherosclerosis in apolipoprotein E-deficient (ApoE -/-) mice. Murine SAA lentivirus was constructed and injected into ApoE -/-mice intravenously. Then, experimental mice were fed a chow diet (5% fat and no added cholesterol) for 14 wks. The aortic atherosclerotic lesion area was larger with than without SAA treatment. With increased SAA levels, the plasma levels of interleukin-6 and tumor necrosis factor-α were significantly increased. Macrophage infiltration in atherosclerotic regions was enhanced with SAA treatment. A migration assay revealed prominent dose-dependent chemotaxis of SAA to macrophages. Furthermore, the expression of monocyte chemotactic protein-1 and vascular cell adhesion molecule-1 (VCAM-1) was upregulated significantly with SAA treatment. SAA-induced VCAM-1 production was detected in human aortic endothelial cells in vitro. Thus, an increase in plasma SAA directly accelerates the progression of atherosclerosis in ApoE -/-mice. SAA is not only a risk marker for atherosclerosis but also an active participant in atherogenesis.

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Section: Discussionmentioning

confidence: 99%

Serum Amyloid A Directly Accelerates the Progression of Atherosclerosis in Apolipoprotein E-Deficient Mice

Dong

Qin

et al. 2011

Mol Med

111

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“…SAA is an acute-phase protein and primarily synthesized in the liver in response to proinflammatory stimuli. Interleukin 1(IL-1), IL-6, and tumor necrosis factor (TNF)-α could induce SAA production [8]. HSP is a systematic inflammatory disease and nonspecific proinflammatory cytokines, such as TNF-α, IL-6, IL-1, and IL-8, were reported to be higher in acute HSP than in convalescent stage and healthy controls [18][19][20][21].…”

Section: Discussionmentioning

confidence: 99%

“…Serum amyloid A (SAA) is an acute-phase reactant whose level in the blood markedly increases in response to various stimuli [8]. Expression studies showed local production of SAA proteins in atherosclerotic lesions, Alzheimer brain tissues, inflammatory tissues, tumor tissues, and rheumatoid arthritis [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Serum Amyloid A Levels Associated with Gastrointestinal Manifestations in Henoch-Schönlein Purpura

Zhao

et al. 2012

Inflammation

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Henoch-Schönlein purpura (HSP) is considered as an immune-mediated inflammatory disease. Serum amyloid A (SAA) is an acute-phase protein with proinflammatory effects. We investigated the levels of SAA in HSP patients and examined whether SAA levels are associated with organ involvement and disease severity. Seventy patients with HSP, including 35 with nephritis (HSPN) and 35 without HSPN, and 20 controls were recruited in our study. SAA levels were measured and other clinical laboratory parameters, including C-reactive protein, erythrocyte sedimentation rate, complement 3 (C3), C4, and immunoglobulin (Ig) A, were recorded. SAA levels were not found to be independently associated with renal, joint involvement, and disease severity. However, higher SAA levels were observed in HSP patients with gastrointestinal (GI) manifestations (p=0.006, p (c)=0.048). Moreover, the levels of SAA were significantly associated with duration of disease (p<0.005, p(c)<0.04). Our findings suggested that SAA was significantly associated with disease duration and GI manifestations in HSP patients.

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“…This is important because obesity is characterized by adiposopathy and increased inflammation (8). One molecule that is released from hypertrophic adipocytes and that has been shown to predict CVD, is serum amyloid-A (SAA) (9,10). Furthermore, SAA has been suggested as a candidate molecule linking increased fat load and its comorbidities (11).…”

mentioning

confidence: 99%

High-density lipoprotein subfractions display proatherogenic properties in overweight and obese children

et al. 2013

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Background:In adults, obesity-driven inflammation can lead to increased cardiovascular disease (CVD). However, information regarding childhood obesity and its inflammatory sequelae is less well defined. Serum amyloid-A (SAA) is an inflammatory molecule that rapidly associates with highdensity lipoproteins (HDLs) and renders them dysfunctional. Therefore, SAA may be a useful biomarker to identify increased CVD potential in overweight and obese children. Methods: Young Hearts 2000 is a cross-sectional cohort study in which 92 children who were obese were matched for age and sex with 92 overweight and 92 lean children. HDL 2 and HDL 3 (HDL 2&3 ) were isolated from plasma by a three-step rapid-ultracentrifugation procedure. SAA was measured in serum and HDL 2&3 by an enzyme-linked immunosorbent assay procedure, and the activities of cholesterol ester transfer protein (CETP) and lecithin cholesteryl acyltransferase (LCAT) were measured by fluorimetric assays. results: Trends across the groups indicated that SAA increased in serum and HDL 2&3 as BMI increased, as did HDL 2 -CETP and HDL 2 -LCAT activities. conclusion: These results have provided evidence that overweight and obese children are exposed to an inflammatory milieu that impacts the antiatherogenic properties of HDL and that could increase CVD risk. This supports the concept that it is important to target childhood obesity to help minimize future cardiovascular events.

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Association between serum amyloid A and obesity: a meta-analysis and systematic review

Cited by 94 publications

References 90 publications

Serum Amyloid A Directly Accelerates the Progression of Atherosclerosis in Apolipoprotein E-Deficient Mice

Serum Amyloid A Directly Accelerates the Progression of Atherosclerosis in Apolipoprotein E-Deficient Mice

Serum Amyloid A Levels Associated with Gastrointestinal Manifestations in Henoch-Schönlein Purpura

High-density lipoprotein subfractions display proatherogenic properties in overweight and obese children

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