The Bulletin, Annual Catalogue, Academic Year 1952-1953, Series 48, Number 1, August (1952)

https://red.mnstate.edu/bulletins/1032/thumbnail.jp

Data_Sheet_1_The mediatory role of inflammatory markers on the relationship between the NOVA classification system and obesity phenotypes among obese and overweight adult women: a cross-sectional study.docx

BackgroundDiet and inflammation both play important roles in the occurrence of obesity. We aimed to investigate the role of inflammation in the development of both metabolically healthy obese (MHO) and metabolically unhealthy obese (MUHO) individuals.MethodsThis cross-sectional study included 221 overweight and obese women aged 18–56 years. The study assessed the metabolic health phenotypes of the participants using the Karelis criterion score. Additionally, dietary intakes were evaluated using a 147-item semi-quantitative questionnaire and the NOVA classification system (comprising 37 food groups and beverages). The study also collected and analyzed the blood parameters, as well as biochemical and anthropometric indices, for all participants.ResultsAmong the women included in the study, 22.9% had MHO phenotypes but 77.1% had MUHO phenotypes. A significant association between the third quartile of the NOVA classification system and the increased likelihood of having the MUHO phenotype was observed (OR = 1.40, 95% CI = 1.09–4.92, p = 0.04). Regarding the potential role of inflammatory markers, high-sensitivity C-reactive protein (hs-CRP) (p = 0.84), transforming growth factor-β (TGF-β) (p = 0.50), monocyte chemoattractant protein-1 (MCP-1) (p = 0.49), plasminogen activator inhibitor-1 (PAI-1) (p = 0.97), and homeostatic model assessment for insulin resistance (HOMA-IR) (p = 0.92) were found to be mediators.ConclusionWe observed a significant positive association between ultra-processed food (UPF) consumption and the MUHO phenotype in overweight and obese women. This association appeared to be mediated by some inflammatory markers, such as hs-CRP, TGF-β, MCP-1, PAI-1, and HOMA-IR. Additional studies are needed to validate these findings.</p

Schematic diagram of the proposed mechanism for the pathogenesis of MS.

<p>The elevation of circulating adipocytokines and pro-inflammatory mediators on one hand, and the reduction of FoxP3 expression on the other hand have provided strong evidences into understanding the pathogenesis of MS. Additionally, it is plausible that high level of resistin, visfatin and leptin could enhance pro-inflammatory cytokine secretion in a positive feedback loop, which in turn lead to the loss of Foxp3 expression.</p

Comparison of Foxp3 mRNA expression and circulating adipocytokines and inflammatory mediators in MS patients in term of the clinical course of disease.

<div><p>In parallel with disease progression in patients with MS, the level of inflammatory markers as well as adipocytokines including resistin and leptin decreased and the expression of FoxP3 and circulating level of visfatin increased.</p> <p>TNF-α: tumor necrosis factor-alpha; IL-1β: interleukin-1 beta; hs-CRP: high sensitivity C-reactive protein; Foxp3: forkhead box P3.</p></div