Discriminative value of serum amyloid A and other acute-phase proteins for coronary heart disease

Delanghe, Joris; Langlois, Michel; Bacquer, Dirk De; Mak, Rudolf; Capel, Paul D.; Renterghem, L Van; Backer, Guy De

doi:10.1016/s0021-9150(01)00607-4

Cited by 51 publications

(38 citation statements)

References 29 publications

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“…After 24 h, the mice were killed by cardiac puncture under anesthesia. Blood was collected without EDTA, and the sera separated by centrifugation were stored at 4 Њ C in the presence of 1 mM PMSF (in ethanol) and anti-bacterial agents (per milliliter of plasma: 0.5 g of gentamycin sulfate, 50 g of NaN 3 , and 1 g of chloramphenicol) and used within 2 weeks. Sera were used because some of the mice used in this study were also used for the study of paraoxonase (10), which is irreversibly inactivated by EDTA.…”

Section: Production Of Saa-hdl In Vivo During the Aprmentioning

confidence: 99%

“…Two proteins of the innate acute inflammatory response are the focus of intensive research, C-reactive protein and serum amyloid A (SAA). These proteins have been shown to exhibit higher risk relationships with cardiovascular disease than serum cholesterol (3,4). Whether these proteins have any causal relationship with cardiovascular diseases or are simply markers of the inflammatory process is not known.…”

mentioning

confidence: 99%

“…Its role in atherogenesis is circumstantial, although evidence is accumulating that it may be more than an innocent bystander and may affect processes and functions related to atherogenesis. For example, SAA circulates in plasma bound to HDL 3 , and when incubated with HDL in vitro, can displace apolipoprotein A-I (apoA-I) (8,9), which may result in decreased HDL levels. We have shown also that SAA can displace the antioxidant enzyme paraoxonase from HDL (10) and that this may contribute to the reduction in the antioxidant properties of HDL after the acute phase (11).…”

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confidence: 99%

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Influence of apoA-I and apoE on the formation of serum amyloid A-containing lipoproteins in vivo and in vitro

Cabana

Feng

Reardon

et al. 2004

Journal of Lipid Research

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Serum amyloid A (SAA) circulates bound to HDL 3 during the acute-phase response (APR), and recent evidence suggests that elevated levels of SAA may be a risk factor for cardiovascular disease. In this study, SAA-HDL was produced in vivo during the APR and without the APR by injection of an adenoviral vector expressing human SAA-1. SAA-HDL was also produced in vitro by incubating mouse HDL with recombinant mouse SAA and by SAA-expressing cultured hepatoma cells. Whether produced in vivo or in vitro, SAA-HDL floated at a density corresponding to that of human HDL 3 (d 1.12 g/ml) separate from other apolipoproteins, including apolipoprotein A-I (apoA-I; d 1.10 g/ml) when either apoA-I or apolipoprotein E (apoE) was present. In the absence of both apoA-I and apoE, SAA was found in VLDL and LDL, with low levels in the HDL and the lipidpoor fractions suggesting that other HDL apolipoproteins are incapable of facilitating the formation of SAA-HDL. We conclude that SAA does not exist in plasma as a lipidfree protein. In the presence of HDL-associated apoA-I or apoE, SAA circulates as SAA-HDL with a density corresponding to that of human HDL 3 . In the absence of both apoA-I and apoE, SAA-HDL is not formed and SAA associates with any available lipoprotein.-Cabana, V.

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Section: Production Of Saa-hdl In Vivo During the Aprmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Influence of apoA-I and apoE on the formation of serum amyloid A-containing lipoproteins in vivo and in vitro

Cabana

Feng

Reardon

et al. 2004

Journal of Lipid Research

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“…The chosen markers have all previously been observed to be affected by obesity and/or weight loss, but have been investigated in a very different manner. 9,10,[25][26][27][28][29][30] Therefore, we also compared the changes in the well-investigated markers, hs-CRP and IL-6, with the mentioned acute phase reactants as an effect of weight loss regimens and maintenance. Furthermore, we attempted to compare hs-CRP and IL-6 with more traditional risk markers of the insulin resistance syndrome (IRS) and CVD.…”

Section: Introductionmentioning

confidence: 99%

Effect of diet-induced energy deficit and body fat reduction on high-sensitive CRP and other inflammatory markers in obese subjects

et al. 2009

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Aims:To dissociate the possible differential effects of negative energy balance and reduction in body fat mass (FM) on inflammatory markers: C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), haptoglobin, transferrin and the adipokines leptin and adiponectin. Methods: Thirty-three obese subjects (BMI: 34.0±3.1 kg/m 2 , age: 43.0±10.5 years, mean±s.d., 16 men) participated in a 20-week controlled dietary intervention divided into four periods. Weight reduction was induced by an 8-week low energy diet (3.4 MJ d À1 ) (LED-1) followed by a 4-week weight maintenance program (M-1). Subsequently participants underwent an additional 4-week LED (4.2 MJ d À1 ) (LED-2) followed by a final 4-week weight maintenance diet (M-2). Blood samples and anthropometrics were assessed at baseline and after LED-1, M-1, LED-2 and M-2. Results: Body weight was significantly reduced by 13% (13.7 ± 4.0 kg, Po0.0001) after LED-1. However, a reduction in highsensitive CRP (hs-CRP) by 35% (À1.1 (95% CI: À2.5:0.2) mg l À1 , P ¼ 0.02) only became apparent after LED-2, which produced an additional weight loss of 2.9 kg compared to baseline, and it was maintained after M-2 (À1.0 (À1.4:0.4) mg l À1 , P ¼ 0.02). Also IL-6 was reduced by 21% (À0.6 (À2.4:0.2) ng l À1 , P ¼ 0.02) after M-2. The reductions in hs-CRP and IL-6 were both associated with reduction in FM but not body weight. Haptoglobin, transferrin and leptin were significantly reduced after both LED-1 and LED-2, but increased during weight maintenance. Adiponectin was not significantly changed during the intervention. Conclusions: The results suggest that, whereas haptoglobin and transferrin respond more rapidly and are more susceptible to the acute change in energy balance, a reduction in hs-CRP and IL-6 seems to be achieved by a reduction in FM when a new steady state has been established.

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“…Associations exist between increased risk of cardiovascular events and elevated levels of inflammatory markers such as C-reactive protein (CRP) [1][2][3][4] and serum amyloid A (SAA). [5][6][7] In addition, both CRP and SAA levels are increased with obesity and with insulin resistance. 8 -14 Although a high intake of dietary cholesterol also is associated with increased cardiovascular risk, 15,16 the effect of dietary cholesterol on plasma lipid levels varies substantially 17 and is influenced by the presence of lipid disorders, 18,19 as well as by obesity and insulin resistance.…”

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confidence: 99%

Cholesterol Feeding Increases C-Reactive Protein and Serum Amyloid A Levels in Lean Insulin-Sensitive Subjects

et al. 2005

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Background— Inflammatory markers associated with elevated cardiovascular risk are increased by cholesterol feeding in animal models. However, whether dietary cholesterol increases inflammatory marker levels in humans is not known. Methods and Results— C-reactive protein (CRP), serum amyloid A (SAA), and lipoprotein levels were compared in 201 healthy subjects on an American Heart Association–National Cholesterol Education Program step 1 diet at baseline and after addition of 4 eggs per day for 4 weeks. Subjects were classified a priori into 3 groups based on their body mass index (BMI) and insulin sensitivity index (S I ): lean insulin sensitive (LIS), mean±SEM BMI, 23.2±0.3 kg/m 2 , and S I , 6.7±0.3×10 −4 min −1 /(μU/mL), n=66; lean insulin resistant (LIR), BMI, 24.5±0.2 kg/m 2 and S I , 2.9±0.1×10 −4 min −1 /(μU/mL), n=76; or obese insulin resistant (OIR), BMI, 31.4±0.5 kg/m 2 and S I , 2.1±0.1×10 −4 min −1 /(μU/mL), n=59. Insulin resistance and obesity each were associated with increased baseline levels of both CRP ( P for trend, <0.001) and SAA ( P for trend=0.015). Egg feeding was associated with significant increases in both CRP and SAA in the LIS group (both P <0.01) but not in the LIR or OIR groups. Egg feeding also was associated with a significant increase in non-HDL cholesterol ( P <0.001) in LIS subjects; however, there was no correlation between the change in non-HDL cholesterol or changes in either CRP or SAA in this group. Conclusions— A high-cholesterol diet leads to significant increases in both inflammatory markers and non-HDL cholesterol levels in insulin-sensitive individuals but not in lean or obese insulin-resistant subjects.

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Discriminative value of serum amyloid A and other acute-phase proteins for coronary heart disease

Cited by 51 publications

References 29 publications

Influence of apoA-I and apoE on the formation of serum amyloid A-containing lipoproteins in vivo and in vitro

Influence of apoA-I and apoE on the formation of serum amyloid A-containing lipoproteins in vivo and in vitro

Effect of diet-induced energy deficit and body fat reduction on high-sensitive CRP and other inflammatory markers in obese subjects

Cholesterol Feeding Increases C-Reactive Protein and Serum Amyloid A Levels in Lean Insulin-Sensitive Subjects

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