Curcumin effects on glycaemic indices, lipid profile, blood pressure, inflammatory markers and anthropometric measurements of non-alcoholic fatty liver disease patients: A systematic review and meta-analysis of randomized clinical trials.

OBJECTIVES: Curcumin has antioxidant properties and has been proposed as a potential treatment for NAFLD. The aim of current systematic review and meta-analysis was to evaluate previous findings for the effect of curcumin supplementation on glycaemic indices, lipid profile, blood pressure, inflammatory markers, and anthropometric measurements of NAFLD patients. METHODS: Relevant studies published up to January 2024 were searched systematically using the following databases: PubMed, SCOPUS, WOS, Science Direct, Ovid and Cochrane. The systematic review and meta-analysis were conducted according to the 2020 PRISMA guidelines. The quality of the papers was assessed the using the Joanna Briggs Institute (JBI) Critical Appraisal Checklist. Pooled effect sizes were calculated using a random-effects model and reported as the WMD and 95% CI. Also, subgroup analyses were done to find probable sources of heterogeneity among studies. RESULTS: Out of 21010 records initially identified, 21 eligible RCTs were selected for inclusion in a meta-analysis. Overall, 1191 participants of both genders, 600 in the intervention and 591 in the control group with NAFLD were included. There are several limitations in the studies that were included, for instance, the results are weakened substantially by potential bias or failure to account for potential adulteration (with pharmaceuticals) or contamination (with other herbs) of the curcumin supplements that were tested. However, previous studies have reported curcumin to be a safe complementary therapy for several conditions. Our study indicated that curcumin supplementation in doses of 50-3000 mg/day was associated with significant change in FBG [WMD: -2.83; 95% CI: -4.61, -1.06), I2 = 51.3%], HOMA-IR [WMD: -0.52; 95% CI: -0.84, -0.20), I2= 82.8%], TG [WMD: -10.31; 95% CI: -20.00, -0.61), I2 = 84.5%], TC [WMD: -11.81; 95% CI: -19.65, -3.96), I2 = 94.6%], LDL [WMD: -8.01; 95% CI: -15.79, -0.24), I2 = 96.1%], weight [WMD: -0.81; 95% CI: -1.28, -0.35), I2= 0.0%] and BMI [WMD: -0.35; 95% CI: -0.57, -0.13), I2= 0.0%] in adults with NAFLD. There was no significant change in HbA1C, plasma insulin, QUICKI, HDL, SBP, DBP, CRP, TNF-α and WC after curcumin therapy. Subgroup analysis suggested a significant changes in serum FBG, TG, SBP, WC in RCTs for intervention durations of ≥ 8 weeks, and SBP, TG, LDL, HDL, BMI, WC in RCTs with sample size > 55 participants. CONCLUSION: Curcumin supplementation in doses of 50-3000 mg/day over 8-12 weeks was associated with significant reductions in levels of FBG, HOMA-IR, TG, TC, LDL, weight and BMI in patients with NAFLD. Previous studies have reported curcumin as a safe complementary therapy for several diseases. We would suggest that should curcumin supplements be used clinically in specific conditions, it should be used with caution. Also, difference in grades of NAFLD may effect the evaluated outcomes, so it is suggested that future studies be conducted with an analyses on subgroups according to their NAFLD grade. Furthermore, because of the failure to conduct independent biochemical assessment of the turmeric/curcumin product used in most studies as well as potential sources of bias, results should be interpreted with caution.

Are Women with Normal-Weight Obesity at Higher Risk for Cardiometabolic Disorders?

OBJECTIVES: This study aimed to evaluate the cardiometabolic abnormalities in women with normal-weight obesity (NWO) in comparison with lean, overweight, and obese women. METHODS: This cross-sectional study evaluated the assessment of cardiometabolic abnormalities of women with NWO compared to lean, overweight, and obese women. NWO was defined as a BMI < 25 kg.m-2 and a BFP higher than 30%. Anthropometric variables, cardiometabolic abnormality markers (fasting blood glucose (FBG), blood pressure (BP), lipid profile, insulin resistance, and high-sensitivity C-reactive protein (hs-CRP)), and liver enzymes were also examined. RESULTS: Significant differences were observed in HDL concentrations between NWO, lean, and obese participants (p < 0.05). There were no significant differences in FBG, insulin resistance, liver enzymes, or cholesterol between groups (p > 0.05). The prevalence of the abnormal metabolic phenotype was higher in NWO compared to the lean group (4.0% and 24.1%, respectively; p < 0.05). Women with type 2 and 3 obesity had abnormal metabolic profiles (60.9% and 73.9%, respectively) compared to NWO participants (p < 0.01). The NWO group had a significantly higher incidence of cardiometabolic abnormalities compared to the lean participants (p < 0.05), while the type 2 and 3 obese individuals had significantly higher incidences compared to the NWO group (p < 0.001 and p < 0.001, respectively). CONCLUSIONS: Individuals with NWO had a significantly higher incidence of cardiometabolic abnormalities when compared to lean participants. These abnormalities strongly relate to BFP and waist circumferences.

Toxico-clinical study of patients poisoned with household products; a two-year cross-sectional study.

BACKGROUND: Several studies worldwide have investigated household product poisoning. We conducted a toxico-clinical study on the two-year prevalence of poisoning with household products. METHODS: This cross-sectional study was performed in Khorshid Hospital, the main referral center for poisoning cases in Isfahan, affiliated to Isfahan University of Medical Sciences, Isfahan, central Iran. All patients with intentional or unintentional household substance poisoning, referring to the poisoning emergency center of the hospital, were evaluated with respect to epidemiological and toxico-clinical features and outcomes. RESULTS: During the study period, 5946 patients were hospitalized, of which 83 (1.39%) had been poisoned with household products including 48 (57.8%) men and 35 (42.2%) women with a mean ± SD age of 34.40 ± 17.71 years. Most patients (54.2%) were in the 20-40-year-old age group. Accidental poisoning (63.9%) was the most common type of exposure (P = 0.02) predominantly in men (57.8%, P = 0.51). The most common household products were sodium hypochlorite (32.53%) followed by petroleum hydrocarbon (21.68%). Most of the accidental poisonings (77.8%) were due to petroleum hydrocarbon. 59% of cases were poisoned at home (P < 0.0001). No patient died. CONCLUSION: Household products were not common means of poisoning in our referral center. Sodium hypochlorite and petroleum hydrocarbon were the most common substances. Most of the patients were men with accidental exposure at home. Because of the availability of the household product, the frequency and outcomes may be varied in different societies.

The effect of adiponectin on osteonectin gene expression by oxidized low density lipoprotein-treated vascular smooth muscle cells.

Osteonectin is a bone- associated protein involved in vascular calcification. Adiponectin may protect against cardiovascular disease but possible effects on vascular calcification have been poorly studied. The aim of this study was to investigate the modulatory effect of adiponectin on oxidized low density lipoprotein (oxLDL)- induced expression of osteonectin in human aorta vascular smooth muscle cells (HA/VSMCs). HA/VSMCs were cultured in F12K media and then treated with oxLDL (100 µg/mL) in the presence or absence of adoponectin (5 µg/mL) for 24 and 48 hours. mRNA expression and protein level of osteonectin were determined by quantitative real-time PCR and western blot analysis, respectively. After exposure to oxLDL, osteonectin expression increased 1.62 ± 0.23- and 6.62 ± 0.48-fold after 24 and 48 hours respectively compared to the control. Adiponectin increased oxLDL- induced osteonectin expression in a time-dependent manner after 24 and 48 hours (3.24 ± 0.39- and 24.93 ± 2.15-fold, respectively). Western blotting confirmed that osteonectin protein was upregulated by adiponectin.Our data suggest that OxLDL might cause the increase of osteonectin expression both at mRNA and protein level. This upregulation is intensified by adiponectin.