The Prevalence of Non-Alcoholic Fatty Liver Disease in Iranian Children and Adult Population: A Systematic Review and Meta-Analysis.

Background: Non-alcoholic fatty liver disease (NAFLD) is the world's most common etiology of chronic liver disease. In this systematic review and meta-analysis, we estimated the prevalence of NAFLD in the Iranian children and adult population. Methods: A comprehensive search of five international databases, including PubMed, ISI/WOS, ProQuest, Scopus, and Google Scholar, was done from inception to Nov 2022. Studies on NAFLD patients and their risk factors were selected for meta-analysis. The quality of the included studies was assessed by The Joanna Briggs Institute (JBI) Critical Appraisal Checklist for cross-sectional, and cohort studies. The heterogeneity between studies was investigated using Cochran test and I2 statistics. Random and fixed effect models were used for heterogenic and non-heterogenic studies, respectively. We used Comprehensive Meta-Analysis version 3 for conducting meta-analysis. Results: Twenty studies were finally included. The total prevalence of NAFLD in children, boys, and girls was 6.7% (95% CI: 0.02-0.18), 12.5% (95% CI: 0.04-0.29) and, 10.1% (95% CI: 0.04-0.21), respectively. The total prevalence of NAFLD in obese children, obese boys, and obese girls was 42% (95% CI: 0.18-0.69), 44% (95% CI: 0.13-0.80), and 33 % (95% CI: 0.13-0.62), respectively. The total prevalence of NAFLD in adults was 36.9% (95% CI: 0.31-0.42). The prevalence of NAFLD in men and women was 33.8% (95% CI: 0.27-0.41) and 29.9% (95% CI: 0.21-0.40), respectively. Conclusion: NAFLD prevalence in Iranian adults and obese children is considerable; however, data about the children population was insufficient.

The association of 25 (OH) D3 serum level with ischemic cerebrovascular accident risk, severity and outcome in Iranian population.

OBJECTIVES: The role of combined presence of vitamin D deficiency and other risk factors of stroke in ischemic cerebrovascular accident (CVA) development in Iranian adults has been unclear, so far. The association of vitamin D status at admission with ischemic CVA severity and outcome in this community is not yet well elucidated. This study aimed to clarify these ambiguities. METHODS: In a cross-sectional study 104 hospitalized ischemic CVA patients and 104 healthy controls participated. The serum level of 25 (OH) D3 and baseline biochemical parameters were measured in ischemic patients within the first 24 h of admission, as well as healthy controls. The severity of CVA and clinical outcome were assessed using National Institutes Health Stroke Scale and Modified Rankin Scale, respectively. Data were analyzed using the Chi-square test, independent t-test, and multiple logistic regression. RESULTS: There was a significant difference between patients and controls regarding the presence of vitamin D3 deficiency, hypertension, smoking, and baseline level of LDL and FBS. Vitamin D3 deficiency boosted the risk of ischemic in males and those having family history of CVA. A low serum level of 25 (OH) D3 was associated with more severity and poor outcome of CVA. The CVA severity, vitamin D3 deficiency, and hypertension were predictors of poor outcome. CONCLUSIONS: The study highlights the increased risk of ischemia in Iranians by cooccurrence of vitamin D3 deficiency and other risk factors of CVA. Clinical significance of vitamin D3 deficiency control may be suggested in those at risk of CVA and functional poor outcomes.

Improvement of pyridoxine-induced peripheral neuropathy by Cichorium intybus hydroalcoholic extract through GABAergic system.

Pyridoxine (vitamin B6) toxicity is a well-known model for peripheral neuropathy. GABA and glutamate are two neurotransmitters in neural pathways involved in the peripheral neuropathy. Cichorium intybus (Chicory) contains glycosides and triterpenoids, which inhibit glutamatergic transmission and enhance GABAergic transmission. The present study was aimed at studying the effect of chicory extract (CE) on the pyridoxine-induced peripheral neuropathy with a particular focus on glutamatergic and GABAergic systems. In this experimental study, a high dose of pyridoxine (800 mg/kg, i.p.) was injected for 14 days to induce neuropathy in male rats. To evaluate the behavioral symptoms, three tests including rotarod, hot plate, and foot fault were used. After the induction of neuropathy, CE (50 mg/kg i.p.) was injected intraperitoneally for 10 consecutive days. Morphologically, the sciatic nerve and the DRG neurons were evaluated in the control, neuropathy, and chicory groups by H&E staining. For evaluating the mechanism, picrotoxin (1 mg/kg) and MK-801 (0.1 mg/kg) were also individually injected 15 min before the extract administration. The concentration of TNF-α in rat sciatic nerve and DRG neurons were also measured by enzyme-linked-immunoassay (ELISA). Morphological and physiological changes occurred in the DRG and sciatic nerve following pyridoxine intoxication. The CE exerted an anti-neuropathic effect on the sciatic nerve and DRG neurons and also decreased reaction time in hot plate test (p < 0.05), increased balance time in rotarod test (p < 0.001), and improved foot fault performance (p < 0.01). Moreover, CE administration reduced TNF-α level in DRG (p < 0.001) and sciatica nerve (p < 0.001). Picrotoxin, unlike MK-801, showed a significant difference in all three behavioral tests and reduced TNF-α content in comparison with group received extraction alone (with p < 0.001 for all three tests). Our results showed beneficial effects of CE on pyridoxine-induced peripheral neuropathy. Modulating of the GABAergic system mediated by TNF-α may be involved in the anti-neurotoxic effect of CE.

Cholesterol suppresses antimicrobial effect of statins.

OBJECTIVES: Isoprenoid biosynthesis is a key metabolic pathway to produce a wide variety of biomolecules such as cholesterol and carotenoids, which target cell membranes. On the other hand, it has been reported that statins known as inhibitors of isoprenoid biosynthesis and cholesterol lowering agents, may have a direct antimicrobial effect on the some bacteria. The exact action of statins in microbial metabolism is not clearly understood. It is possible that statins inhibit synthesis or utilization of some sterol precursor necessary for bacterial membrane integrity. Accordingly, this study was designed in order to examine if statins inhibit the production of a compound, which can be used in the membrane, and whether cholesterol would replace it and rescue bacteria from toxic effects of statins. MATERIALS AND METHODS: To examine the possibility we assessed antibacterial effect of statins with different classes; lovastatin, simvastatin, and atorvastatin, alone and in combination with cholesterol on two Gram-positive (Staphylococcus aureus and Enterococcus faecalis) and two Gram-negative (Pseudomonas aeruginosa and Escherichia coli) bacteria using gel diffusion assay. RESULTS: Our results showed that all of the statins except for lovastatin had significant antibacterial property in S. aureus, E. coli, and Enter. faecalis. Surprisingly, cholesterol nullified the antimicrobial action of effective statins in statin-sensitive bacteria. CONCLUSION: It is concluded that statins may deprive bacteria from a metabolite responsible for membrane stability, which is effectively substituted by cholesterol.

Effects of ovariectomy and estrogen replacement therapy on visceral adipose tissue and serum adiponectin levels in rats.

BACKGROUND: Excess visceral adipose tissue accumulation after menopause is closely associated with decreased insulin sensitivity and adiponectin levels. OBJECTIVE: The purpose of this study was to determine the effect of ovariectomy and estrogen replacement on visceral fat and serum adiponectin levels in ovariectomized (OVX) rats. METHOD: Forty 11-week-old female Wistar rats were divided into the four following groups (n = 10 rats per group): sham-operated control (SHAM); sedentary OVX (OVX-SED); OVX with estrogen replacement (OVX-ER); and OVX with sesame oil treatment (OVX-C). Rats in OVX-ER and OVX-C groups received 17ß-estradiol valerate (30 µg/kg, subcutaneously) and sesame oil as vehicle, five days a week, respectively. All animals were sacrificed after eight weeks of intervention. RESULTS: Ovariectomy after eight weeks increased body weight and visceral fat (P < 0.05) in OVX-SED and OVX-C groups compared with SHAM rats with no change in plasma adiponectin levels. Estrogen replacement in OVX animals decreased body weight (13.4%, P < 0.05) and visceral fat (10.4%). Although they were not statistically significant, adiponectin, insulin sensitivity and lipid profile of OVX rats were ameliorated with estrogen treatment. CONCLUSION: We conclude that ovarian hormone withdrawal leads to higher body weight and visceral adipose tissue in rats, but surprisingly does not change adiponectin levels. Although a substantial decrease in body weight was achieved by estrogen replacement therapy in OVX animals, the beneficial metabolic effects of weight loss seems to be only mechanical, having a tendency to improve insulin sensitivity without elevating adiponectin production.