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Abstract Background Non-alcoholic fatty liver disease (NAFLD) accounts as a crucial health concern with a huge burden on health and economic systems. The aim of this study is to evaluate the effect of soy isoflavones supplementation on metabolic status in patients with NAFLD. Methods In this randomized clinical trial, 50 patients with NAFLD were randomly allocated to either soy isoflavone or placebo groups for 12 weeks. The soy isoflavone group took 100 mg/d soy isoflavone and the placebo group took the similar tablets containing starch. Anthropometric indices, blood lipids, glycemic parameters and blood pressure were measured at the beginning and at the end of the study. Results At the end of week 12 the level of serum triglyceride (TG), low density lipoprotein (LDL) and total cholesterol (TC) was significantly decreased only in soy isoflavone group compared to baseline (P 0.05). Conclusions This study revealed that soy isoflavones could significantly reduce TG, LDL TC, WC and HC in NAFLD patients. Trial registration The Ethics committee of Ahvaz Jundishapur University of Medical Sciences approved the protocol of the present clinical research (IR.AJUMS.REC.1401.155). The study was in accordance with the Declaration of Helsinki. This study’s registered number and date are IRCT20220801055597N1 and 20.09.2022, respectively at https://fa.irct.ir .

Abstract Background Dilated cardiomyopathy (DCMP) is characterized by the enlargement and weakening of the heart and is a major cause of heart failure in children. Infection and nutritional deficiencies are culprits for DCMP. Zinc is an important nutrient for human health due to its anti-oxidant effect that protects cell against oxidative damage. This case-control study aimed to investigate the relationship between dietary intake of zinc and selenium and the risk of DCMP in pediatric patients. Methods A total of 36 DCMP patients and 72 matched controls were recruited, and their dietary intakes were assessed via a validated food frequency questionnaire. We used chi-square and sample T-test for qualitative and quantitative variables, respectively. Logistic regression analysis was applied to assess the relationship between selenium and zinc intake with the risk of DCMP. Results After fully adjusting for confounding factors, analyses showed that selenium (OR = 0.19, CI = 0.057–0.069, P trend

Abstract Background Dietary advanced glycation end products (AGEs) can play an important role in increasing inflammatory factors and oxidative stress as risk factors for cancers. In the present study, we aimed to assess the relationship between dietary AGEs and the risk of breast cancer (BC) in Iranian adult women. Methods This hospital-based case-control study includes 401 participants aged ≥ 30 years old. The cases group consisted of 134 women diagnosed with histologically confirmed BC. The control group included 267 women enrolled randomly from patients admitted to the same hospitals. Dietary intake information was determined using a validated food frequency questionnaire, and dietary AGEs intake was computed for all participants. Logistic regression models, adjusted for potential confounders, were used to determine the odds ratios (OR) and 95% confidence interval (CI) of BC across tertiles of dietary AGEs. Results The mean ± SD age and body mass index of the study population were 47.92 ± 10.33 years and 29.43 ± 5.51 kg/m2, respectively. The median (interquartile) of dietary AGEs in all individuals was 9251(7450, 11,818) kU/day. After adjusting for age, first pregnancy age, and energy intake, participants in the highest tertile of dietary AGEs intakes had higher odds of BC compared to those in the lowest tertile of dietary AGEs (OR:2.29;95%CI:1.19–4.39, Ptrend:0.012). Additionally, in the multivariable model, after adjusting for age, age at first pregnancy, energy, menopausal status, family history of cancer, anti-inflammatory drug use, Vitamin D supplementation, physical activity, body mass index, number of childbirths, and history of abortion, breastfeeding, and oral contraceptive pills use, the odds of BC were increased across tertiles of dietary AGEs intake (OR: 2.33; 95%CI: 1.18–4.60, Ptrend: 0.017). Conclusion The present findings suggest that a diet with high AGEs is associated with a higher likelihood of BC in adult women.

Abstract Background Liver cirrhosis is a worldwide burden and is associated with poor clinical outcomes, including increased mortality. The beneficial effects of dietary modifications in reducing morbidity and mortality are inevitable. Aim The current study aimed to evaluate the potential association of dietary protein intake with the cirrhosis-related mortality. Methods In this cohort study, 121 ambulatory cirrhotic patients with at least 6 months of cirrhosis diagnosis were followed-up for 48 months. A 168-item validated food frequency questionnaire was used for dietary intake assessment. Total dietary protein was classified as dairy, vegetable and animal protein. We estimated crude and multivariable-adjusted hazard ratios (HRs) with 95% confidence intervals (CIs), applying Cox proportional hazard analyses. Results After full adjustment for confounders, analyses showed that total (HR = 0.38, 95% CI = 0.2–1.1, p trend = 0.045) and dairy (HR = 0.38, 95% CI = 0.13–1.1, p trend = 0.046) protein intake was associated with a 62% lower risk of cirrhosis-related mortality. While a higher intake of animal protein was associated with a 3.8-fold increase in the risk of mortality in patients (HR = 3.8, 95% CI = 1.7–8.2, p trend = 0.035). Higher intake of vegetable protein was inversely but not significantly associated with mortality risk. Conclusion A comprehensive evaluation of the associations of dietary protein intake with cirrhosis-related mortality indicated that a higher intakes of total and dairy protein and a lower intakes of animal protein are associated with a reduced risk of mortality in cirrhotic patients.

Abstract Background The combined role of important environmental factors as a single lifestyle index in predicting non-alcoholic fatty liver disease (NAFLD) risk is not fully assessed. Therefore, we aimed to investigate the association of healthy lifestyle factor score (HLS) with the odds of NAFLD in Iranian adults. Methods This case-control study was conducted on 675 participants, aged ≥ 20–60 years, including 225 new NAFLD cases and 450 controls. We measured dietary intake information using a validated food frequency questionnaire and determined diet quality based on the alternate healthy eating index-2010(AHEI-2010). The score of HLS was calculated based on four lifestyle factors, including a healthy diet, normal body weight, non-smoking, and high physical activity. An ultrasound scan of the liver was used to detect NAFLD in participants of the case group. Logistic regression models were used to determine the odds ratios(ORs) and 95% confidence interval(CI) of NAFLD across tertiles of HLS and AHEI. Results Mean ± SD age of the participants were 38.13 ± 8.85 years. The Mean ± SD HLS in the case and control groups was 1.55 ± 0.67 and 2.53 ± 0.87, respectively. Also, the Mean ± SD AHEI in the case and control groups was 48.8 ± 7.7 and 54.1 ± 8.1, respectively. Based on the age and sex-adjusted model, the odds of NAFLD were decreased across tertiles of AHEI (OR:0.18;95%CI:0.16–0.29,Ptrend

Abstract Background Dietary advanced glycation end products(AGEs) may contribute to increased inflammation and oxidative stress as risk factors for chronic diseases such as liver disease. In the current study, we aimed to examine the possible association of dietary AGEs with the odds of non-alcoholic fatty liver disease (NAFLD) in Iranian adults. Methods A total of 675 participants (225 newly diagnosed NAFLD cases and 450 controls), aged 20–60 years, were recruited for this case-control study. Nutritional data were measured using a validated food frequency questionnaire, and dietary AGEs were determined for all participants. An ultrasound scan of the liver performed the detection of NAFLD in participants of the case group without alcohol consumption and other causes of hepatic disorders. We used logistic regression models, adjusted for potential confounders, to estimate the odds ratios(ORs) and 95% confidence interval(CI) of NAFLD across tertiles of dietary AGEs. Results Mean ± SD age and body mass index of the participants were 38.13 ± 8.85 years and 26.85 ± 4.31 kg/m2, respectively. The median(IQR) of dietary AGEs in participants was 3262(2472–4301). In the sex and age-adjusted model, the odds of NAFLD were increased across tertiles of dietary AGEs intake(OR:16.48;95%CI:9.57–28.40, Ptrend

Abstract Background Gallstone disease (GSD) and its complications are major public health issues globally. Although many community-based studies had addressed the risk factors for GSD, little is known about the associations between dietary factors and risk of disease. The present study aimed to investigate the potential associations between dietary fibers with the risk of gallstone disease. Methods In this case–control study, 189 GSD patients with less than one month of diagnosis and 342 age‑matched controls were enrolled. Dietary intakes were assessed using a 168-item semi-quantitative validated food frequency questionnaire. Crude and multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated through cox proportional hazards regression models. Results Comparing the highest versus the lowest tertile, significant reverse associations were observed between odds of GSD and each category of dietary fiber intake including total (OR T3 vs. T1 = 0.44, 95% CI: 0.37–0.7, P for trend = 0.015), soluble (OR T3 vs. T1 = 0.51, 95% CI: 0.3–0.8, P for trend = 0.048) and insoluble (OR T3 vs. T1 = 0.56, 95% CI: 0.3–0.9, P for trend

Abstract Background A dietary pattern with a high glycemic index (GI) and glycemic load (GL) can be a precursor to sleep disorders that link to many chronic diseases. We aimed to assess the association of dietary GI and GL with the risk of insomnia in Iranian adults. Methods A total of 111 newly diagnosed insomnia cases and 333 controls aged 18–60 years were included in this case–control study. The participants’ dietary intakes were collected using a valid and reliable food frequency questionnaire. The diagnosis of insomnia in subjects was performed by a neurologist using the Insomnia Severity Index (ISI) questionnaire. Multivariable logistic regression models, adjusted for the potential confounders, were used to determine the risk of insomnia according to tertiles of dietary glycemic indices. Results The mean (SD) age and BMI of the study population (78.6% female) were 31.8 (10.0) years and 24.70 (3.62) kg/m2, respectively. The median (IQR) of dietary GI and GL in subjects was 62.7 (57.0–68.6) and 213.5(167.4–268.5), respectively. Based on the multivariable-adjusted model, after controlling for age, sex, physical activity, obesity, smoking, socioeconomic score, general health questionnaire (GHQ) score, and dietary energy intake, the odds of insomnia were increased across tertiles of dietary GL[(OR:2.72,95%CI:1.10–6.70),(Ptrend = 0.017)], however, no significant association was observed between high GI diet and insomnia risk [(OR:1.38,95%CI:0.77–2.47),(Ptrend = 0.298)]. Conclusions Our results revealed that greater adherence to dietary pattern with high GL could be increased the odds of insomnia in Iranian adults.

Abstract Background Potential dietary inflammation can precursor chronic diseases such as hepatic disorders. We aimed to examine the association of empirical dietary inflammatory patterns (EDIP) and dietary inflammation scores (DIS) with the risk of nonalcoholic fatty liver diseases (NAFLD) in Iranian adults. Methods This case–control study was conducted on 225 newly diagnosed NAFLD cases and 450 controls aged 20–60 years. The individuals’ dietary data were collected using a validated food frequency questionnaire. The detection of NAFLD in subjects was done using the ultrasonography scan of the liver and confirmation of gastroenterologists. To calculate of EDIP score, the average daily intakes of each item (15 food items) were multiplied by the proposed weights, and then all the weighted values were summed. Also, to calculate the DIS score, each food item (18 food items) is multiplied by its specific weight to obtain the weighted values of each item. The weighted values were then standardized using the Z-score. Finally, the standardized weighted values of all the items were summed to get the overall DIS score for the individuals. Logistic regression models, adjusted for potential confounders, were used to estimate the odds ratios and 95% confidence interval (CI) of NAFLD across tertiles of EDIP and DIS. Results The mean (SD) age and BMI of the study population (53% male) were 38.1 (8.8) years and 26.8 (4.3) kg/m2, respectively. The median (IQR) of EDIP and DIS scores in individuals were 0.52 (0.34, 0.73), and 0.04 (− 0.55, 0.59), respectively. Based on the multivariable-adjusted model, after controlling for age, sex, physical activity, smoking, marital status, waist-to-hip ratio, and dietary energy intake, individuals in the second (OR 2.01, 95% CI 1.07–3.76) and third tertiles of DIS (OR 2.54, 95% CI 1.39–4.63) had a higher odds of NAFLD compared to the lowest tertile of DIS (Ptrend = 0.003). Also, in the final model, there is a significant direct association between EDIP score and odds of NAFLD [(OR T2 vs. T1 = 0.88, 95% CI 0.50–1.57) and (OR T3 vs. T1 = 1.82, 95% CI 1.02–3.23)], (Ptrend = 0.031). Conclusion Our results suggested that higher scores of EDIP and DIS, indicating the high inflammatory potential of dietary pattern, are associated with increased odds of NAFLD in Iranian adults.

Abstract Background Obesity is considered a major health concern and mounting evidence suggests that the exposure to environmental endocrine disruptors, including Bisphenol-A (BPA), may enhance the risk to develop the disease. Moreover, growing documents propose that the vitamin D may contribute to adipogenic signaling and lipid accumulation during adipocyte differentiation. We focused on the molecular mechanism of vitamin D and BPA in human adipose-derived mesenchymal stem cells (hADMSCs) which vitamin D and BPA may influence adipose tissue development and function. Methods Human adipose-derived mesenchymal stem cells were cultured for 14 days in lipogenic differentiation media containing continuous concentrations of vitamin D plus BPA (0.1 nM or 10 nM). The expression of adipogenic markers including the peroxisome proliferator-activated receptor γ (PPARγ), CCAAT-enhancer-binding protein α (C/EBP α) CCAAT-enhancer-binding protein β (C/EBP β), fatty acid synthase (FASN), lipoprotein lipase (LPL), sterol regulatory element-binding protein-1c (SREBP1c), insulin-induced gene-2 (INSIG2), vitamin D receptor (VDR), estrogen receptor-beta (ER-β), fatty acid-binding protein-4 (FABP4), and glucose transporter-4 (GLUT4) was measured using Quantitative polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay (ELISA). Lipid accumulation was visualized with staining with Oil Red O. Results In the morphological assessment of mesenchymal stem cells treated with a concentration of 10 nM vitamin D plus BPA, more lipid accumulations were observed in comparison with the group with 0.1 nM concentration. Treatment of hADMSCs with vitamin D plus BPA (0.1 nM) significantly inhibited the induction of PPARγ, C/EBP β, C/EBP α, and FASN related to adipocyte differentiation and development. However, the exposure of cells to the concentration of 10 nM vitamin D plus BPA induced the expression of these genes associated to the adipogenesis. The remarkable increase in the level of SREBP1c was associated to the suppression of INSIG2 in treated preadipocytes with 10 nM vitamin D plus BPA. Our findings showed that the expression of VDR, ERβ, GLUT4, and FABP4 were upregulated through differentiation with the highest concentrations in 0.1 nM vitamin D plus BPA group for VDR, ERβ, and GLUT4. Conclusions Vitamin D plus BPA at concentration of 10 nM boosted the adipogenesis during the critical stages of adipocytes development, whereas it seems to inhibit this process at concentration of 0.1 nM.

Abstract Purpose 1,25-dihydroxyvitamin D3 may regulate adipogenesis in adipocytes in-vitro, but little is known about possible molecular mechanisms related to the inhibitory effect of 1,25-dihydroxyvitamin D3 on adipogenesis in humans҆ adipose tissue. Methodology In this study, human adipose-derived mesenchymal stem cells (hASCs) were cultured for 14 days in adipogenic differentiation media containing concentrations of 1,25-dihydroxyvitamin D3 (10−10–10−8 M). The extent of adipogenic differentiation in ASCs was assessed by Oil Red O staining and quantitative polymerase chain reaction (PCR) to determine expression levels of key adipogenic markers. Results Our results showed that vitamin D receptor (VDR), as a mediator of most actions of 1,25-dihydroxyvitamin D3, glucose trasporter-4 (GLUT4),and fatty acid binding protein-4 (FABP4) was expressed in vitamin D-treated hASCs. However, the protein level of these markers was lower than the control group. Treatment of human preadipocytes with 1,25-dihydroxyvitamin D3 significantly altered expression of adipogenic markers and triglyceride accumulation in a dose-dependent manner. 1,25-dihydroxyvitamin D3 at concentration of 10−8 M enhanced expression of sterol regulatory element-binding protein-1c (SREBP1c), CCAAT-enhancer-binding protein-β (C/EBPβ), a mitotic clonal expansion, peroxisome proliferator-activated receptor-gamma (PPARγ), fatty acid synthase (FASN), a marker of de novo lipogenesis,and lipoprotein lipase (LPL). Conclusion Our findings revealed that 1,25-dihydroxyvitamin D3 may provoke adipocyte development in critical periods of adipogenesis at concentration of 10−8 M, thereby leading to a greater risk of obesity in adulthood and an augmented risk of obesity-related diseases including diabetes, cardiovascular diseases, and some cancers.

Abstract Background The endocrine disruptor Bisphenol-A (BPA), has been involved in dysregulating adipose tissue development and increasing the risk of obesity. The objective of this experiment was to investigate whether treatment of human mesenchymal stem cells with BPA could modulate adipogenesis and adipocyte differentiation. Methods In this experimental study, the human adipose-derived mesenchymal stem cells (hASCs) were cultured for 2 weeks with continuous exposure to 10− 10 M or 10− 8 M concentrations of BPA. The extent of triglyceride accumulation was visualized by Oil Red O staining. To evaluate BPA effect on the expression levels of key adipogenic trascripotion factors and proteins, we used Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) and ELISA. Results The results presented a dose-dependent triglyceride accumulation in treated cells with BPA. Additionally, we observed that BPA induced transcription of the Peroxisome proliferator-activated receptor-gamma (PPARγ), CCAAT-enhancer-binding protein-alpha (C/EBPα), CCAAT-enhancer-binding protein-beta (C/EBPβ), sterol regulatory element-binding protein-1c (SREBP1c), Fatty acid synthase (FASN), and lipoprotein lipase (LPL); BPA suppressed the expression of Fatty acid binding protein-4 (FABP4) and Estrogen receptor-beta (ERβ). Conclusions Our findings supported the hypothesis that BPA enhances adipogenic differentiation thereby may play a role in development of obesity and dysregulation of metabolic homoeostasis.

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