The purpose of this study was to correlate biomarkers of metabolic syndrome (MetS), with markers of inflammation and macronutrient intake in 89 women (25-72 years) with MetS. We hypothesized that waist circumference (WC) would have the stronger correlations with inflammatory parameters and would correlate with carbohydrate intake. Values for WC (108.7 ± 11.1 cm) and plasma triglycerides (202.7 ± 52.1 mg/dL) were elevated, whereas plasma glucose levels varied from 66 to 179 mg/dL, with 42% of women having insulin resistance. Plasma levels of interleukin 6 (0.2-15.9 mg/L), tumor necrosis factor α (1.47-12.3 mg/L), and high-sensitivity C-reactive protein (0.06-3.08 mg/dL) varied widely, with most women being above values considered normal. Subjects had high intake of total sugar (92.3 ± 56.4 g/d), high glycemic index (59.8 ± 6.5), and glycemic load (127.2 ± 56.1), whereas dietary fiber (17.1 ± 9.1 g/d) was below recommended intake. Waist circumference was positively correlated with insulin (r = 0.275, P < .01) and with the inflammatory markers interleukin 6 (r = 0.307, P < .01) and tumor necrosis factor α (r = 0.228, P < .05) and negatively correlated with plasma adiponectin (r = -0.309, P < .0001). In addition, WC was positively correlated with total carbohydrate, added sugar, and glycemic load (P < .05) but not with fat or protein. These results are consistent with central obesity being a key marker of the inflammatory state, and they also suggest that carbohydrates, particularly those that are digested rapidly, contribute to increased risk of central obesity and development of MetS.
"The strongest correlations were found between IL-6 and WHR as well as between CRP and WC. It also provided the evidence that abdominal fat was strongly correlated to plasmatic levels of adipocytokines as was previously reported in non-disabled obese women (Ackermann et al. 2011). Similarly, in a previous study, Hayase et al. (2002) concluded plasma TNF-a levels correlated well with visceral fat mass in premenopausal but not in postmenopausal women. "
[Show abstract][Hide abstract] ABSTRACT: Background:
Obesity is a major health problem in people with intellectual disabilities. It is also widely accepted that low-grade systemic inflammation associated to obesity plays a key role in the pathogenic mechanism of several disorders. Fortunately, physical activity has shown to improve inflammation in people with metabolic syndrome and type 2 diabetes. Accordingly, we assessed the influence of aerobic training on pro-inflammatory cytokines and acute phase proteins in women with Down syndrome.
To achieve this outcome, 20 premenopausal obese young women with Down syndrome volunteered for this study. Eleven were randomly assigned to the intervention group and performed a 10-week aerobic training programme, three sessions per week, consisting of a warm-up then a 30- to 40-min treadmill exercise at a work intensity of 55-65% of peak heart rate followed by a cooling-down period. The control group included nine age-, sex- and body mass index-matched women with Down syndrome. Fat mass percentage and fat distribution were measured. Plasmatic levels of tumour necrosis factor (TNF)-α, interleukin (IL)-6 and fibrinogen were assessed by commercial enzyme-linked immunosorbent assay kits. C-reactive protein (CRP) was assessed by nephelometry.
Plasmatic levels of TNF-α (11.7 ± 1.6 vs. 9.2 ± 1.3 pg/ml; P = 0.022), IL-6 (8.2 ± 1.1 vs. 6.1 ± 0.9 pg/ml; P = 0.014) and high sensitive CRP (0.62 ± 0.11 vs. 0.53 ± 0.09 mg/dl; P = 0.009) were significantly reduced in the intervention group. Further, significant correlations between plasmatic and anthropometric parameters were found.
A 10-week training programme reduced pro-inflammatory cytokines and acute phase proteins in obese young women with Down syndrome. Long-term, well-conducted studies are still required to determine whether correction of this low-grade inflammation improves clinical outcomes of women with trisomy 21.
Journal of Intellectual Disability Research 06/2013; 58(6). DOI:10.1111/jir.12056 · 2.41 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Obese individuals are characterized by a chronic, low-grade inflammatory state. Increased levels of C-reactive protein (CRP), a marker of inflammation, have been observed in subjects with the metabolic syndrome. We have previously reported that genes encoding proteins involved in the anti-inflammatory and immune response are differentially expressed in visceral adipose tissue of obese men with or without the metabolic syndrome. Among these genes, the interferon-gamma-inducible protein 30 (IFI30), CD163 molecule (CD163), chemokine (C-X-C motif) ligand 9 (CXCL9) and thymic stromal lymphopoietin (TSLP), were selected for further genetic analyses. The aim of the study was to verify whether IFI30, CD163, CXCL9 and TSLP gene polymorphisms contribute to explain the inter-individual variability of the inflammatory profile of obesity assessed by plasma high-sensitivity CRP concentrations. A total of 1185 severely obese individuals were genotyped for single nucleotide polymorphisms (SNPs) covering most of the sequence-derived genetic variability at the IFI30, CD163, CXCL9 and TSLP gene loci (total of 27 SNPs). Following measurement of plasma CRP levels, subjects were divided into two groups, low vs. high using the median value of plasma CRP levels (8.31 mg/L) as a cutoff point. Genotype frequencies were compared between groups. Associations between genotypes and plasma CRP levels (continuous variable) were also tested after adjustments for age, sex, smoking and BMI. The rs11554159 and rs7125 IFI30 SNPs showed a significant difference in genotype frequencies (p<0.05) between subgroups of low vs. high plasma CRP levels (wild type homozygotes: rs11554159=47% vs. 55%, rs7125=31% vs. 24%, for low vs. high CRP groups, respectively). The association between rs11554159 and CRP levels as a continuous variable remained significant (p=0.004). Both carriers of the GA and AA genotypes demonstrated, on average, a 13% lower CRP levels in comparison with GG homozygotes. No association was observed between SNPs in the CD163, CXCL9 and TSLP genes and CRP levels. The IFI30 rs11554159 polymorphism could partially explain the inter-individual variability observed in the inflammatory profile associated with obesity.
[Show abstract][Hide abstract] ABSTRACT: Patients do not just wake up one morning with cardiac disease. Instead there is an extended preclinical phase during which lifestyle choices determine outcome. Recent advances in our understanding of oxidative stress, endocrine signaling, immune/inflammatory balance, and energy production illuminate opportunities for efficacious intervention. A thorough exploration of these pathophysiologies will allow physicians the opportunity to offer their patients a journey away from illness and disease to optimal wellness.
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