The inverse relation of HDL anti-oxidative functionality with serum amyloid a is lost in metabolic syndrome subjects

Introduction Although high-density lipoprotein (HDL) is inversely correlated with cardiovascular risk, HDL loses its protective role in pathologic inflammatory states like type 2 diabetes (T2DM). HDL dysfunction contributes to accelerated atherosclerosis in T2DM, but the mechanism is incompletely defined. The acute phase reactant serum amyloid A (SAA) displaces apolipoprotein A-I and may impair HDL-mediated reverse cholesterol efflux. We hypothesized that SAA alters the inverse association between HDL and coronary artery calcium (CAC) in the Penn Diabetes Heart Study, a cross-sectional study of T2DM patients free of overt cardiovascular or renal disease. Methods We measured SAA in serum samples by immunonephelometry (N=975; mean age 58 ± 9 years; 63% male, 57% Caucasian; mean BMI 33 ± 6 kg/m 2 ). HDL was measured enzymatically in lipoprotein fractions after ultracentrifugation. Agatston CAC scores were quantified from electron beam tomography at the same visit. Spearman correlation and logistic regression were used to test associations of SAA with clinical factors and metabolic syndrome. We used Tobit regression to analyze associations between CAC and HDL, both overall and stratified by 3 categories of SAA: undetectable, lower half detectable, and upper half detectable. Results Spearman correlations revealed moderate association of SAA with C-reactive protein (r=0.52) and weak associations of SAA with BMI (r=0.25) and HDL (r=0.17; all p<0.001). In logistic regression, the group with highest SAA levels had increased odds of metabolic syndrome compared to those with undetectable levels (OR 1.56, 95% CI 1.03 to 2.38, p=0.036). In adjusted Tobit regression, HDL was inversely associated with CAC (Tobit coefficient for 1-SD increase in HDL: -0.30; 95% CI -0.54 to -0.06; p=0.013). Across the categories of SAA, however, there was no difference in the association of HDL with CAC (Tobit coefficient for 1-SD increase in HDL: -0.17 [95% CI -0.49 to 0.16] for undetectable vs. -0.31 [95% CI -0.79 to 0.17] for lower half detectable vs. -0.49 [95% CI -1.01 to 0.03] for upper half detectable). Conclusions Despite the association of SAA with metabolic syndrome, these data suggest that elevated SAA may not change the inverse relationship of HDL with CAC in T2DM.

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Serum concentrations and expressions of serum amyloid A and leptin in adipose tissue are interrelated: the Genobin Study

Acta Endocrinologica ◽

10.1530/eje-07-0598 ◽

2008 ◽

Vol 158 (3) ◽

pp. 333-341 ◽

Cited By ~ 19

Author(s):

T Lappalainen ◽

M Kolehmainen ◽

U Schwab ◽

L Pulkkinen ◽

D E Laaksonen ◽

...

Keyword(s):

Gene Expression ◽

Metabolic Syndrome ◽

Adipose Tissue ◽

Weight Reduction ◽

Serum Amyloid A ◽

Normal Weight ◽

Serum Amyloid ◽

Serum Concentrations ◽

Amyloid A ◽

Obese Subjects

ObjectiveSerum amyloid A (SAA) is a novel link between increased adipose tissue mass and low-grade inflammation in obesity. Little is known about the factors regulating its serum concentration and mRNA levels. We investigated the association between SAA and leptin in obese and normal weight subjects and analyzed the effect of weight reduction on serum SAA concentration and gene expression in adipose tissue of the obese subjects.MethodsSeventy-five obese subjects (60±7 years, body mass index (BMI) 32.9±2.8 kg/m2, mean±s.d.) with impaired fasting plasma glucose or impaired glucose tolerance and other features of metabolic syndrome, and 11 normal weight control subjects (48±9 years, BMI 23.7±1.9 kg/m2) were studied at the baseline. Twenty-eight obese subjects underwent a 12-week intensive weight reduction program followed by 5 months of weight maintenance. Blood samples and abdominal s.c. adipose tissue biopsies were taken at the baseline and after the follow-up. Gene expression was studied using real-time quantitative PCR.ResultsThe gene expressions in women and serum concentrations of leptin and SAA were interrelated independently of body fat mass in the obese subjects (r=0.54, P=0.001; r=0.24, P=0.039 respectively). In multiple linear regression analyses, leptin mRNA explained 38% of the variance in SAA mRNA (P=0.002) in the obese women. Weight loss of at least 5% increased SAA mRNA expression by 48 and 36% in men and women, but serum SAA concentrations did not change.ConclusionsThe association between SAA and leptin suggests an interaction between these two adipokines, which may have implications in inflammatory processes related to obesity and the metabolic syndrome.

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229 CORRELATION BETWEEN SERUM AMYLOID A AND FATTY ACIDS COMPOSITION OF HIGH-DENSITY LIPOPROTEIN IN METABOLIC SYNDROME PATIENTS

Journal of Hypertension ◽

10.1097/01.hjh.0000420054.57510.b1 ◽

2012 ◽

Vol 30 ◽

pp. e69-e70

Author(s):

Viktoria G. Lizogub ◽

O.O. Voloshyna ◽

V.M. Turkevych ◽

T.S. Bruzgina

Keyword(s):

Metabolic Syndrome ◽

Fatty Acids ◽

High Density Lipoprotein ◽

Serum Amyloid A ◽

Density Lipoprotein ◽

High Density ◽

Serum Amyloid ◽

Fatty Acids Composition ◽

Amyloid A

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Homocysteine but not Serum Amyloid A, Vitamin A and E Related to Increased Risk of Metabolic Syndrome in Post-Menopausal Thai Women

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000191 ◽

2014 ◽

Vol 84 (1-2) ◽

pp. 35-44 ◽

Cited By ~ 2

Author(s):

Kanjana Suriyaprom ◽

Benjaluck Phonrat ◽

Pratana Satitvipawee ◽

Anchalee Tungtrongchitr ◽

Rungsunn Tungtrongchitr

Keyword(s):

Metabolic Syndrome ◽

Vitamin A ◽

Serum Amyloid A ◽

Anthropometric Measurements ◽

Serum Amyloid ◽

Thai Women ◽

Amyloid A ◽

Increased Risk ◽

Menopausal Women ◽

Post Menopausal

This study aims to investigate serum amyloid A, homocysteine, and biochemical-anthropometric measurements in post-menopausal women with and without metabolic syndrome (MS), and determine whether serum amyloid A and homocysteine are linked to MS among this group. This study was performed with 405 post-menopausal Thai volunteers with a mean age of 57.95 ± 5.90 years (135 subjects with MS and 270 subjects without MS). The levels of serum amyloid A, homocysteine, vitamins, glucose, and lipids were measured. Homocysteine levels were significantly higher in the group with MS than in that without MS (p < 0.001), whereas for serum amyloid A, vitamin A, vitamin E and vitamin B12, there were no significant differences. There were significant differences between the groups in folate, HDL-C, and anthropometric measurements (p < 0.001). Thirty seven percent of the group with MS and 14.1 % of the group without MS were classified as having hyperhomocysteinemia (p < 0.001). Furthermore, logistic regression analysis revealed that hyperhomocysteinemia (odds ratio (OR): 2.67, 95 % confidence interval (95 %CI): 1.57 - 4.58), low folate (OR: 1.79, 95 %CI: 1.11 - 2.89), and BMI (OR: 1.25, 95 %CI: 1.16 - 1.33) were significantly related to MS. These findings suggest that increased homocysteine levels and decreased folate concentrations may influence susceptibility to MS and this effect may be an early event in the development of cardiovascular diseases among post-menopausal women. Therefore, there is a need to evaluate homocysteine levels, especially among post-menopausal Thai women.

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