The implication of obesity and central fat on markers of chronic inflammation: The ATTICA study

Panagiotakos, Demosthenes B.; Pitsavos, Christos; Yannakoulia, Mary; Chrysοhoou, Christina; Stefanadis, Christodoulos

doi:10.1016/j.atherosclerosis.2005.03.010

Cited by 288 publications

(234 citation statements)

References 31 publications

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“…It is possible that the simple assessment of obesity, that is, by prepregnancy BMI without attention to visceral as opposed to subcutaneous fat may not have been sufficiently sensitive. 17 The nonsignificant difference found in plasma TNFα by BMI during pregnancy and preeclampsia in our study may be a result of the generalized inflammatory response in pregnancy, characterized by innate immune system (Type 1) activation and adaptive immune system (Type 2) suppression. 25 Type 1 cytokines, such as TNFα, IFN-γ, and IL-2 that are augmented in preeclampsia may overcome any additional effect of obesity.…”

Section: Commentcontrasting

confidence: 48%

“…[10][11][12]17 Reproductive age, nonpregnant obese women were found to have higher TNFα concentrations compared to nonpregnant lean subjects of similar age. 18,19,24 In these studies, TNFα concentrations correlated directly with waist to hip ratio (WHR) and glucose tolerance test insulin levels, but not with BMI, and was higher in obese women with a WHR greater than 0.90.…”

Section: Commentmentioning

confidence: 97%

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A Comparison of Circulating TNF-α in Obese and Lean Women with and without Preeclampsia

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Powers

Patrick

et al. 2008

Hypertension in Pregnancy

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Objectives: We hypothesized that TNFα would be higher in obese versus lean preeclamptic subjects. Methods:Total plasma TNFα was measured in a nested case-control study of 123 nulliparous lean and obese control and preeclamptic subjects.Results: Adjusted mean TNFα concentrations were 0.97±0.11 (pg/ml ± SEM) in lean controls, 1.01 ±0.10 in obese controls, 1.43±0.11 in lean preeclamptics and 1.16±0.11 in obese preeclamptics. Pregnancy outcome was the single predictor of TNFα concentration in the general linear regression model (p=0.04). Conclusion:TNFα concentration was higher in preeclamptic compared to control subjects. Obesity was not associated with higher TNFα concentrations in preeclamptic or control subjects.

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Section: Commentcontrasting

confidence: 48%

Section: Commentmentioning

confidence: 97%

A Comparison of Circulating TNF-α in Obese and Lean Women with and without Preeclampsia

Founds

Powers

Patrick

et al. 2008

Hypertension in Pregnancy

View full text Add to dashboard Cite

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“…The relation of CRP to abdominal adiposity has been reported to be due to the production of cytokines in adipose tissue, tumor necrosis factor (TNF)-α ,and interleukin (IL)-6. Indeed, the serum concentrations of TNF-α [47][48][49][50] and soluble serum TNFreceptor-2 [49] are higher in obesity; and TNF-α induces hepatic CRP production [51]. Likewise, IL-6 also induces hepatic production of CRP [52]; and serum IL-6 concentrations are higher in obesity [50].…”

Section: Discussionmentioning

confidence: 99%

Fat redistribution preferentially reflects the anti-inflammatory benefits of pioglitazone treatment

Moon

Kim

et al. 2011

Metabolism

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“…In humans, although acute inflammatory events can lead to 100-to 1000-fold elevations of SAA, insulin resistance, obesity, or cholesterol feeding are all associated with modest but chronic elevations of SAA. 62,63 Modest elevations of SAA are associated with increased cardiovascular risk 64,65 ; thus, the concentrations used in this study are physiologically relevant.…”

Section: Discussionmentioning

confidence: 99%

Serum Amyloid A, but Not C-Reactive Protein, Stimulates Vascular Proteoglycan Synthesis in a Pro-Atherogenic Manner

Wilson

Thompson

Webb

et al. 2008

The American Journal of Pathology

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Inflammatory markers serum amyloid A (SAA) and C-reactive protein (CRP) are predictive of cardiac disease and are proposed to play causal roles in the development of atherosclerosis, in which the retention of lipoproteins by vascular wall proteoglycans is critical. The purpose of this study was to determine whether SAA and/or CRP alters vascular proteoglycan synthesis and lipoprotein retention in a pro-atherogenic manner. Vascular smooth muscle cells were stimulated with either SAA or CRP (1 to 100 mg/L) and proteoglycans were then isolated and characterized. SAA, but not CRP, increased proteoglycan sulfate incorporation by 50 to 100% in a dose-dependent manner (P < 0.0001), increased glycosaminoglycan chain length, and increased low-density lipoprotein (LDL) binding affinity (K d , 29 g/ml LDL versus 90 g/ml LDL for SAA versus control proteoglycans; P < 0.005). Furthermore, SAA up-regulated biglycan via the induction of endogenous transforming growth factor (TGF)-␤. To determine whether SAA stimulated proteoglycan synthesis in vivo, ApoE ؊/؊ mice were injected with an adenovirus expressing human SAA-1, a null virus, or saline. Mice that received adenovirus expressing SAA had increased TGF-␤ concentrations in plasma and increased aortic biglycan content compared with mice that received either null virus or saline. Thus, SAA alters vascular proteoglycans in a pro-atherogenic manner via the stimulation of TGF-␤ and may play a causal role in the development of atherosclerosis.

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The implication of obesity and central fat on markers of chronic inflammation: The ATTICA study

Cited by 288 publications

References 31 publications

A Comparison of Circulating TNF-α in Obese and Lean Women with and without Preeclampsia

A Comparison of Circulating TNF-α in Obese and Lean Women with and without Preeclampsia

Fat redistribution preferentially reflects the anti-inflammatory benefits of pioglitazone treatment

Serum Amyloid A, but Not C-Reactive Protein, Stimulates Vascular Proteoglycan Synthesis in a Pro-Atherogenic Manner

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