Publications by authors named "Reyhane Basirat"

3 Publications

  • Page 1 of 1

Serum irisin levels in metabolically healthy versus metabolically unhealthy obesity: A case-control study.

Med J Islam Repub Iran 2020 11;34:46. Epub 2020 May 11.

Department of Clinical Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran.

Metabolically healthy obese (MHO) individuals appear to be protected or more resistant to the progression of obesity-related metabolic disorders. Hormonal regulation associated with adipose or muscular tissues such as irisin and leptin may facilitate the healthy metabolic profile of MHO cases. In this case-control study, the differences between serum level of irisin was investigated in metabolically unhealthy obese (MUO) and metabolically healthy obese (MHO) individuals. The study participants included obese individuals with metabolic syndrome (MetS) (n=51) and 2 control groups that included weight matched cases without MetS (n=51) and normal weight cases without MetS (n=51). Diagnosis of MetS was made based on the Adult Treatment Panel III (ATPIII) criteria. Serum levels of leptin and irisin were determined by enzyme-linked immune-sorbent assay (ELISA) kit. Receiver Operator Characteristic (ROC) curve, multiple linear regression, and one-way ANOVA analysis were used in SPSS 16 software. Significant level was set at 0.05. Based on the statistical analysis, serum levels of irisin were 2.91±1.6, 3.14±1.4, and 4.47±3.23 (ng/mL) in MUO, MHO, and nonobese metabolically healthy participants, respectively (P = 0.001). Also, serum levels of leptin were 14.06±12.4, 11.2±9.3, and 7.09±7.1 (ng/mL) in MUO, MHO, and nonobese metabolically healthy cases, respectively (p=0.002). After adjusting for demographic variables, a significant association was found between irisin and study groups (β = 0.77, P = 0.001), weight (β=-0.03, p=0.014), BMI (β=-0.11, p=0.006), TG (β=-0.003, p=0.025), fat mass (β=-0.04, p=0.046), and fat free mass (β=0.08, p=0.014). Obese patients with/without MetS had lower level of irisin than normal weight participants.
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http://dx.doi.org/10.34171/mjiri.34.46DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7456437PMC
May 2020

Household socioeconomic status in relation to childhood general and central obesity in Farrokhshahr, Iran.

ARYA Atheroscler 2019 Sep;15(5):211-217

Professor, Obesity and Eating Habits Research Center, Endocrinology and Metabolism Molecular-Cellular Sciences Institute AND Department of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran AND Food Security Research Center AND Department of Community Nutrition, School of Nutrition and Food Sciences, Isfahan University of Medical Sciences, Isfahan, Iran.

Background: Although the association between socioeconomic status (SES) and general/central obesity has extensively been examined, limited data are available in this regard among children. The aim of this study was to examine the association between household SES and obesity among children.

Methods: This cross-sectional study was done in Farrokhshahr, Iran, among primary school children aged 6-12 years in 2009. SES was examined using participants' and their parents' oral responses to a pretested questionnaire. In the current study, participants were classified based on tertiles of SES score to low, medium, and high SES categories. General as well as central obesity was defined based on age- and sex-specific national cut-off points.

Results: Comparing individuals in the highest versus lowest tertile of SES, there was no significant difference in mean waist circumference (WC), but those in the middle tertile of SES had greater means of body mass index (BMI) than those in the lowest tertile after controlling for potential confounders (16.19 ± 0.27 vs. 15.27 ± 0.27 kg/m2, P = 0.002). We observed a greater chance of general obesity for those in the highest tertile of SES compared with those in the lowest tertile [odds ratio (OR): 4.00, 95% confidence interval (CI): 1.53-10.59, Ptrend = 0.004]. No significant association was seen between SES and central obesity, either before or after controlling for potential confounders.

Conclusion: We found that children in the highest SES class had a greater chance of general obesity than those in the lowest SES class. There was no significant association between SES and central obesity.
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http://dx.doi.org/10.22122/arya.v15i5.1640DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6954359PMC
September 2019

Molecular aspects of pancreatic β-cell dysfunction: Oxidative stress, microRNA, and long noncoding RNA.

J Cell Physiol 2019 06 22;234(6):8411-8425. Epub 2018 Nov 22.

School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Metabolic syndrome is known as a frequent precursor of type 2 diabetes mellitus (T2D). This disease could affect 8% of the people worldwide. Given that pancreatic β-cell dysfunction and loss have central roles in the initiation and progression of the disease, the understanding of cellular and molecular pathways associated with pancreatic β-cell dysfunction can provide more information about the underlying pathways involved in T2D. Multiple lines evidence indicated that oxidative stress, microRNA, and long noncoding RNA play significant roles in various steps of diseases. Oxidative stress is one of the important factors involved in T2D pathogenesis. This could affect the function and survival of the β cell via activation or inhibition of several processes and targets, such as receptor-signal transduction, enzyme activity, gene expression, ion channel transport, and apoptosis. Besides oxidative stress, microRNAs and noncoding RNAs have emerged as epigenetic regulators that could affect pancreatic β-cell dysfunction. These molecules exert their effects via targeting a variety of cellular and molecular pathways involved in T2D pathogenesis. Here, we summarized the molecular aspects of pancreatic β-cell dysfunction. Moreover, we highlighted the roles of oxidative stress, microRNAs, and noncoding RNAs in pancreatic β-cell dysfunction.
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http://dx.doi.org/10.1002/jcp.27755DOI Listing
June 2019