Circulating Inflammatory Markers May Mediate the Relationship between Healthy Plant-Based Diet and Metabolic Phenotype Obesity in Women: A Cross-Sectional Study.

Background: It has been posited that both metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUHO) could be emergent from diet and inflammatory markers. Thus, we sought to investigate the influence of plant-based diet on MHO and MUHO phenotypes mediated by inflammatory markers in overweight and obese women. Methods: This cross-sectional study was conducted on 289 women aged ≥18 years, with a body mass index (BMI) ≥25 kg/m2. Dietary intake was measured using 147 item food frequency questionnaire, as well as anthropometrics and biochemistry panel, in all participants. Metabolic health phenotypes were considered using Karelis score, while plant-based diet indices (PDI) were evaluated based on 18 food groups, where healthy and unhealthy PDI were identified. Results: Accordingly, 26.9% of women had MHO and 73.1% had MUHO phenotypes. After adjusting for potential confounders, TGF-ß1 had a significant inverse association with hPDI (ß: -0.28; 95% CI: 452.99, -85.25; P: 0.004). Moreover, we found that women with higher hPDI had lower odds of MUHO (OR: 0.95; 95% CI: 0.39, 2.30; P: 0.03). Regarding the mediatory effect of the inflammatory markers, TGF-ß1 (P: 0.73), IL-ß1 (P: 0.14), and MCP1 (P: 0.51) played a role in decreasing the odds of MUHO among hPDI tertiles. Conclusion: There was a significant inverse relationship between adherence to hPDI and MUHO phenotype in overweight and obese Iranian women. This association appeared to be mediated by TGF-ß1, IL-ß1, and MCP1.

Inflammatory markers may mediate the relationship between processed meat consumption and metabolic unhealthy obesity in women: a cross sectional study.

Metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUHO) are known to be affected by diet and inflammatory factors (such as TGF-ß1, IL-ß1, MCP1). We sought to survey that consume of processed meat could effect on MHO and MUHO phenotypes, mediated through inflammatory markers, in overweight and obese Iranian women. The current cross-sectional study was done on 224 women 18-48 years, with a body mass index (BMI) ≥ 25 kg/m2. A 147- item food frequency questionnaire (FFQ) was used to evaluate dietary intake. In all participants, anthropometric indices and biochemical factors, as well as metabolic health phenotypes based on Karelis score, were evaluated. According to results, 22.6% of participants had MHO and 75.7% had MUHO phenotypes. There was an association between higher adherence to processed meats and increasing odds of MUHO phenotype in Iranian women (OR:2.54; 95% CI 0.009, 7.51; P = 0.05). Moreover, we found that the relation can be affected by agents such as TGF-ß1, IL-ß1, and MCP1; however, more research is needed to confirm these results and finding.

The association between adherence to diet quality index and cardiometabolic risk factors in overweight and obese women: a cross-sectional study.

Background: Obesity and overweight status increase the risk of cardiovascular disease. Diet quality can also predict the risk of cardiovascular diseases in obese and overweight patients. Therefore, in this study, we sought to examine the relationship between diet quality index (DQI) and cardiometabolic risk factors in obese and overweight women. Method: A cross-sectional study was conducted on 197 Iranian women with a Body Mass Index (BMI) > 25, 18-48 years, and recruited from 20 Tehran Health Centers. Nutrition intake and DQI were assessed using a 147-item semi-quantitative food frequency questionnaire (FFQ). Additionally, anthropometric measurements, body composition, biochemical evaluations, and cardiometabolic risk factors were evaluated. Results: There was an association between DQI and waist-to-hip ratio (WHR), atherogenic index of plasma (AIP), and CHOLINDEX in obese women, after adjusting for potential confounders. Whereas, there were no significant associations of the tertiles of DQI compared with the first tertile in other cardiometabolic risk factors, before and after adjustment. Conclusion: This study provides evidence that dietary intake and DQI are associated with cardiometabolic risk factors and that dietary modification may be a predictor for reducing WHR, AIP, and CHOLINDEX. However, more research is needed to develop a DQI that reflects changes in cardiometabolic risk factors by considering women's eating habits and patterns.

Estrogen stimulates adenosine receptor expression subtypes in human breast cancer MCF-7 cell line.

Estrogen is a steroid hormone that plays a key role in the development and regulation of reproductive system. It has been shown that estrogen is related to breast cancer development through binding to its receptors. In order to uncover the estrogen effects on adenosine receptor expression, estrogen-positive MCF-7 cells were used to treat with agonist and antagonist of estrogen and then the mRNA expression of adenosine receptor subtypes were evaluated. Estrogen-positive MCF-7 cells were treated with various concentrations of 17ß estradiol (E2) as an estrogen agonist, and ICI 182,780 as an estrogen antagonist. The gene expression of adenosine receptor subtypes were detected by real time RT-PCR. The results of MTT assay showed that E2 increased cell viability in a dose dependent manner. The expression pattern of all adenosine receptor subtypes are as follow; A2b > A1 > A2a > A3 in untreated MCF-7 cells. Obtained results showed that E2 incubation at 0.001-0.01 µM led to up-regulation of A1ARs, A2aARs and A3ARs dose dependently. E2 at 0.001 µM also had no significant effect on A2bARs expression but, at higher doses induced a considerable decrease in mRNA A2bARs expression. Treatment with antagonist confirmed that up-regulation of these receptors is mediated by estrogen receptor. Taken together, our results indicate that treatment of MCF-7 cells with E2 led to up-regulation of adenosine receptors. However, these effects were partially restored by treatment with antagonist suggesting that such effects are mediated by estrogen receptors.