A particular subgroup of obese adults, considered as metabolically healthy obese (MHO), has a reduced risk of metabolic complications. However, the molecular basis contributing to this healthy phenotype remains unclear. The objective of this work was to identify obesity-related metabolite patterns differed between MHO and metabolically unhealthy obese (MUHO) groups and examine whether these patterns are associated with the development of cardiometabolic disorders in a sample of Iranian adult population aged 18-50 years. Valid metabolites were defined as metabolites that passed the quality control analysis of the study. In this case-control study, 104 valid metabolites of 107 MHO and 100 MUHO patients were separately compared to those of 78 normal-weight metabolically healthy (NWMH) adults. Multivariable linear regression was used to investigate all potential relations in the study. A targeted metabolomic approach using liquid chromatography coupled to triple quadrupole mass spectrometry was employed to profile plasma metabolites. The study revealed that, after Bonferroni correction, branched-chain amino-acids, tyrosine, glutamic acid, diacyl-phosphatidylcholines C32:1 and C38:3 were directly and acyl-carnitine C18:2, acyl-lysophosphatidylcholines C18:1 and C18:2, and alkyl-lysophosphatidylcholines C18.0 were inversely associated with MHO phenotype. The same patterns were observed in MUHO patients except for the acyl-carnitine and lysophosphatidylcholine profiles where acyl-carnitine C3:0 and acyl-lysophosphatidylcholine C16:1 were higher and acyl-lysophosphatidylcholines C18:1, C18:2 were lower in this phenotype. Furthermore, proline, and diacyl-phosphatidylcholines C32:2 and C34:2 were directly and serine, asparagines, and acyl-alkyl-phosphatidylcholine C34:3 were negatively linked to MUHO group. Factors composed of amino acids were directly and those containing lysophosphatidylcholines were inversely related to cardiometabolic biomarkers in both phenotypes. Interestingly, the diacyl-phosphatidylcholines-containing factor was directly associated with cardiometabolic disorders in the MUHO group. A particular pattern of amino acids and choline-containing phospholipids may aid in the identification of metabolic health among obese patients.
Background Type 2 diabetes mellitus (T2DM) is a multidimensional consequence of environmental and genetic factors. Cholesteryl ester transfer protein (CETP) Taq1B polymorphism has been reported as a main predictor of dyslipidaemia, comprising an important complication in persons with T2DM. However, diet could affect T2DM patients metabolic health. Methods We investigated the combination of gene–diet effects on some metabolic biomarkers. In our cross‐sectional study, blood samples of 220 patients were collected. Dietary indices (healthy eating index, dietary quality index and dietary phytochemical index) were obtained from a validated semi‐quantitative food frequency questionnaire. CETP Taq1B polymorphism was genotyped by a polymerase chain reaction‐restriction fragment polymorphism method. Data were analysed by analysis of covariance. Results The interaction between the CETP Taq1B polymorphism and dietary indices on low density lipoprotein/high density lipoprotein was significant (p < 0.001 both crude and adjusted models). In addition, the interaction between polymorphism and dietary quality index on total antioxidant capacity (p = 0.004 crude model, p = 0.005 after adjusting) and pentraxin 3 (p = 0.01 both crude and adjusted models) was significant. Also, the interaction between polymorphism and healthy eating index on waist circumference (p = 0.005 both crude and adjusted models) and dietary phytochemical index on interleukin‐18 (p = 0.03 crude model) was significant. Conclusions Our results indicated the effect of CETP Taq1B polymorphism on some inflammatory and anthropometrics markers (total antioxidant capacity, pentraxin 3, interleukin‐18, low density lipoprotein/high density lipoprotein and waist circumference) with high and low adherence to dietary incides.
Clinical trial studies revealed conflicting results on the effect of Ashwagandha extract on anxiety and stress. Therefore, we aimed to evaluate the effect of Ashwagandha supplementation on anxiety as well as stress. A systematic search was performed in PubMed/Medline, Scopus, and Google Scholar from inception until December 2021.We included randomized clinical trials (RCTs) that investigate the effect of Ashwagandha extract on anxiety and stress. The overall effect size was pooled by randomeffects model and the standardized mean difference (SMD) and 95% confidence interval (CIs) for outcomes were applied. Overall, 12 eligible papers with a total sample size of 1,002 participants and age range between 25 and 48 years were included in the current systematic review and meta-analysis. We found that Ashwagandha supplementation significantly reduced anxiety (SMD: À1.55, 95% CI: À2.37, À0.74; p = .005; I 2 = 93.8%) and stress level (SMD: À1.75; 95% CI: À2.29, À1.22; p = .005; I 2 = 83.1%) compared to the placebo. Additionally, the non-linear dose-response analysis indicated a favorable effect of Ashwagandha supplementation on anxiety until 12,000 mg/d and stress at dose of 300-600 mg/d. Finally, we identified that the certainty of the evidence was low for both outcomes. The current systematic review and dose-response meta-analysis of RCTs revealed a beneficial effect in both stress and anxiety following Ashwagandha supplementation. However, further highquality studies are needed to firmly establish the clinical efficacy of the plant.
Abstract. Background: Peroxisome proliferator-activated receptor γ (PPARγ) Pro12Ala polymorphism (rs1801282) has been associated with metabolic syndrome components in some studies. Moreover, the PPARγ gene may mediate the physiological response to dietary fat intake in a ligand-dependent manner. Methods: Metabolic syndrome components (body mass index, waist circumference, and lipid profile) were determined in 290 type 2 diabetes mellitus patients in a cross-sectional study. DNA genotyping for determining PPARγ Pro12Ala polymorphism was conducted using the polymerase chain reaction-restriction length polymorphism method. A semi-quantitative food frequency questionnaire was used to assess the participants’ dietary intakes in the previous year. Results: There were significant differences between the two genotype groups of PPARγ Pro12Ala polymorphism, Ala carriers (Pro/Ala + Ala/Ala) versus non-Ala carriers (Pro/Pro), in terms of mean body mass index (p = 0.04) and waist circumference (p = 0.02). Below the median percentage of energy from monounsaturated and polyunsaturated fatty acids, Ala carriers had a higher body mass index (p = 0.01) compared to non-Ala carriers. Furthermore, a significant interaction between this single-nucleotide polymorphism and polyunsaturated fatty acids intake on serum triglyceride levels (p = 0.01) was seen, and in higher polyunsaturated fatty acids intake (≥ median) Ala carriers had lower triglyceride levels than non-Ala carriers (p = 0.007). Conclusions: The findings of the current study support a significant association between PPARγ Pro12Ala polymorphism and metabolic syndrome components, and they suggest that this polymorphism can modulate the biological response of dietary fat intake on body mass index and triglyceride levels.
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