2016
DOI: 10.1016/j.ijcard.2016.04.089
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Obesity can predict and promote systemic inflammation in healthy adults

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Cited by 59 publications
(47 citation statements)
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“…The observed correlations with H9N2 and MM can represent differing apolipoprotein B levels or glycosylation thereof, and may be indicative of an unhealthy glycosylation profile with regard to lipid transport and metabolism. The association of MM with inflammatory marker hsCRP is likely a consequence of the connection between inflammation and obesity (84), as a model corrected for BMI no longer shows significant association between high mannose size and inflammation (data not shown). The effect size being less pronounced with hsCRP than with BMI is explainable by the aforementioned increase in IgM, which contains the smaller high-mannose compositions H5N2 and H6N2 at its Asn 279 site (80).…”
Section: Discussionmentioning
confidence: 96%
“…The observed correlations with H9N2 and MM can represent differing apolipoprotein B levels or glycosylation thereof, and may be indicative of an unhealthy glycosylation profile with regard to lipid transport and metabolism. The association of MM with inflammatory marker hsCRP is likely a consequence of the connection between inflammation and obesity (84), as a model corrected for BMI no longer shows significant association between high mannose size and inflammation (data not shown). The effect size being less pronounced with hsCRP than with BMI is explainable by the aforementioned increase in IgM, which contains the smaller high-mannose compositions H5N2 and H6N2 at its Asn 279 site (80).…”
Section: Discussionmentioning
confidence: 96%
“…In the state of obesity, the pro-inflammatory adipokines, derived from adipose tissue, are overexpressed, increased production, and secretion of inflammatory mediators: interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) [8,9]. The increased circulatory levels of inflammatory mediators particularly IL-6 have been associated with hepatocyte stimulation to synthesize and produce a low-grade systemic inflammation marker C-reactive protein (CRP) [8]. This protein was discovered in 1930 by Tillet and Francis, being insulated in the serum of patients with acute inflammatory processes.…”
Section: Introductionmentioning
confidence: 99%
“…The development of these conditions is likely related to increased production of pro-inflammatory adipokines (e.g., interleukin 6 and tumor necrosis factor alpha) and decreased production of (or decreased tissue sensitivity to) anti-inflammatory adipokines (e.g., adiponectin). The final result is that those individuals are in an inflammatory state and show increased levels of acute phase reagents such as C-reactive protein (8) .…”
mentioning
confidence: 99%