Publications by authors named "Gheibi S"

Article Synopsis
  • The study explores the genetic factors influencing β-cell function (BCF) and their relationship to type 2 diabetes (T2D), expanding on previous genetic research using large-scale data.
  • By analyzing GWAS data from around 26,000 individuals, the researchers identified 55 unique genetic associations related to BCF traits derived from oral glucose tolerance tests.
  • The findings reveal key genes that regulate insulin secretion and illustrate how different genetic mechanisms can affect T2D risk, offering a deeper understanding of the complex biology behind the disease.
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Background: The objective is to determine the prevalence of household food insecurity (HFI) based on sociodemographic factors and their relationship to obesity in youth.

Methods: The study included a sample of 1,962 youth (aged 6-18) from the National Health and Nutrition Examination Survey (NHANES). The US Household Food Security Survey Module is used to measure food security over the past 12 months.

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  • Ulcerative colitis (UC) is an inflammatory bowel disease that causes inflammation in the rectum and colon, with a rising prevalence especially in developed countries and a potential link to colorectal cancer (CRC).
  • The study analyzed data from 91 UC patients who underwent colectomy to identify risk factors for dysplasia, noting that older age was a significant risk factor but found no other strong associations.
  • The findings highlight the importance of age in assessing dysplasia risk for UC patients, suggesting that older patients may need more careful management and screening for CRC; more research is needed to confirm these results.
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Background: Engaging in physical activity (PA) and reducing sedentary behaviors among youth are linked to improved mental and physical health. This study aimed to examine demographic differences among youth adhering to PA and Screen Time (ST) recommendations.

Methods: The present study utilized data from the 2017-2018 National Health and Nutrition Examination Survey (NHANES).

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Background: Data on the epidemiology of inflammatory bowel disease (IBD) in the Middle East are scarce. We aimed to describe the clinical phenotype, disease course, and medication usage of IBD cases from Iran in the Middle East.

Methods: We conducted a cross-sectional study of registered IBD patients in the Iranian Registry of Crohn's and Colitis (IRCC) from 2017 until 2022.

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Article Synopsis
  • Access to Human Beta Cells
  • : The study presents EndoC-βH5 cells as an advanced model for understanding human pancreatic beta cell functions and potential diabetes treatments, closely mimicking primary adult cells.
  • Cell Generation and Features
  • : These cells were created by integrating specific genes into human fetal pancreas, with successful removal of unwanted transgenes, resulting in cells that are easy to use and assess for insulin secretion and other functions.
  • Findings and Applications
  • : EndoC-βH5 cells demonstrate strong glucose-dependent insulin secretion and are suitable for drug testing and studying beta cell behavior, indicating their utility in diabetes research and therapy.
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Objectives: Nitrite, a nitric oxide (NO) donor, increases insulin secretion from pancreatic islets and has positive metabolic effects in type 2 diabetes (T2D). Here, we test the hypothesis of whether nitrite-induced insulin secretion is due to blunting of diabetes-induced oxidative stress in the islets.

Materials And Methods: T2D was created in male rats using a combination of streptozotocin at 25 mg/kg and a high-fat diet.

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Reversible phosphorylation is an important regulatory mechanism. Regulation of protein phosphorylation in β-cells has been extensively investigated, but less is known about protein dephosphorylation. To understand the role of protein dephosphorylation in β-cells and type 2 diabetes (T2D), we first examined mRNA expression of the type 2C family (PP2C) of protein phosphatases in islets from T2D donors.

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Article Synopsis
  • Type 2 diabetes (T2D) is linked to insufficient insulin secretion from pancreatic β cells, prompting a study of human pancreatic islets from around 300 individuals to find candidate genes involved in T2D.
  • The research identified 395 differentially expressed genes (DEGs) related to T2D, including several novel genes and previous candidates, with a notable fraction possibly predisposing individuals to diabetes.
  • Functional experiments on mouse models indicated that specific DEGs, particularly OPRD1, PAX5, and SLC2A2, are crucial for regulating glucose levels and body composition, with PAX5 potentially acting as a major transcriptional regulator of T2D-related gene expression in pancreatic islets.
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  • EPDR1 is a human batokine that plays a role in regulating mitochondrial respiration and thermogenesis in brown fat, but its effects on pancreatic β-cells and glucose metabolism remain unexplored.
  • Research showed that EPDR1 levels were higher in pancreatic islets from type 2 diabetes (T2D) and obese donors and were linked to insulin secretion (GSIS) and other metabolic metrics.
  • Silencing EPDR1 in β-cell models reduced insulin secretion and disrupted mitochondrial function, suggesting that increasing EPDR1 may help improve β-cell activity and glucose regulation in obese individuals.
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Decreased heart levels of nitric oxide (NO) and hydrogen sulfide (HS) in type 2 diabetes (T2D) are associated with a higher risk of mortality following ischemia-reperfusion (IR) injury. This study aimed to determine the effects of co-administration of sodium nitrite and sodium hydrosulfide (NaSH) on IR injury in the isolated heart from rats with T2D. Two-month-old male rats were divided into 5 groups (n = 7/group): Control, T2D, T2D + nitrite, T2D + NaSH, and T2D + nitrite + NaSH.

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A 78-year-old man with COVID-19 infection was admitted. Initial echocardiography indicated left ventricular ejection fraction (LVEF) of 15%, high pulmonary arterial pressure, severe left ventricular dysfunction, mild diastolic dysfunction, mild regurgitation mitral valve, and normal septal thickness. Considering the probable diagnosis of COVID-19-related myocarditis, the patient was early managed with the antivirals, immunomodulatory agents, a high dose of ascorbic acid, melatonin, and immunoglobulin therapy.

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We previously reported that loss of mitochondrial transcription factor B1 (TFB1M) leads to mitochondrial dysfunction and is involved in the pathogenesis of type 2 diabetes (T2D). Whether defects in ribosomal processing impact mitochondrial function and could play a pathogenetic role in β-cells and T2D is not known. To this end, we explored expression and the functional role of dimethyladenosine transferase 1 homolog (DIMT1), a homolog of TFB1M and a ribosomal RNA (rRNA) methyltransferase implicated in the control of rRNA.

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Background: As a rising epidemic in developing countries, childhood obesity and overweight need particular attention.

Methods: The sample ( = 2432) was randomly selected among children aged 24-59 months living in West Azerbaijan Province whose information was recorded in SIB software. The survey questionnaire is derived from the Demographic and Health Survey and the Multiple Indicator Cluster Survey questionnaires designed by the WHO 2017 and UNICEF 2017, respectively.

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Skeletal muscle is an endocrine organ secreting exercise-induced factors (exerkines), which play a pivotal role in interorgan cross talk. Using mass spectrometry (MS)-based proteomics, we characterized the secretome and identified thymosin β4 (TMSB4X) as the most upregulated secreted protein in the media of contracting C2C12 myotubes. TMSB4X was also acutely increased in the plasma of exercising humans irrespective of the insulin resistance condition or exercise mode.

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Objective: Increased renal and hepatic gluconeogenesis are important sources of fasting hyperglycemia in type 2 diabetes (T2D). The inhibitory effect of co-administration of sodium nitrite and sodium hydrosulfide (NaSH) on hepatic but not renal gluconeogenesis has been reported in rats with T2D. The present study aimed to determine the effects of co-administration of sodium nitrite and NaSH on the expression of genes involved in renal gluconeogenesis in rats with T2D.

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Septic shock, known as the most severe complication of sepsis, is a serious medical condition that can lead to death. Clinical symptoms of sepsis include changes in body temperature in the form of hypothermia or hyperthermia, tachypnea or hyperventilation, tachycardia, leukocytosis or leukopenia, and variations in blood pressure, as well as altered state of consciousness. One of the main problems in septic shock is poor response along with reduced vascular reactivity to vasopressors used to increase blood pressure.

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Objective: A deficiency in hydrogen sulfide (HS) and nitric oxide (NO) contributes to the development of type 2 diabetes (T2D). An inhibitory effect on liver gluconeogenesis has been reported in rats with T2D with co-administration of sodium nitrite and sodium hydrosulfide (NaSH); the underlying mechanisms have however not yet been elucidated. The aim of this study is to determine the long-term effects of co-administering sodium nitrite and NaSH on expression of genes involved in liver gluconeogenesis in rats with T2D.

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Type 2 diabetes, characterized by dysfunction of pancreatic β-cells and insulin resistance in peripheral organs, accounts for more than 90% of all diabetes. Despite current developments of new drugs and strategies to prevent/treat diabetes, there is no ideal therapy targeting all aspects of the disease. Restoration, however, of insulin-producing β-cells, as well as insulin-responsive cells, would be a logical strategy for the treatment of diabetes.

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Nitric oxide (NO) is a gas that serves as a ubiquitous signaling molecule participating in physiological activities of various organ systems. Nitric oxide is produced in the endocrine pancreas and contributes to synthesis and secretion of insulin. The potential role of NO in insulin secretion is disputable - both stimulatory and inhibitory effects have been reported.

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Evidence for potential effects of inorganic nitrate (NO) on body weight is limited to inconsistent findings of animal experiments. In this systematic review and meta-analysis, we aimed to quantify the overall effect of inorganic NO, administered via drinking water, on body weight gain in rats. We searched PubMed, Scopus, and Embase databases, and the reference lists of published papers.

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Alzheimer's disease (AD) is characterized with increased formation of amyloid-β (Aβ) in the brain. Aβ peptide toxicity is associated with disturbances of several intracellular signaling pathways such as mitogen activated protein kinases (MAPKs). The aim of this study was to investigate the role of MAPKs and their interactions in Aβ-induced neurotoxicity using isolated hippocampal neurons from the rat.

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Objective: Subjects with type 2 diabetes (T2D) have lower circulating hydrogen sulfide (HS) levels following myocardial ischemia and a higher risk of mortality. The aim of this study was to determine the dose-dependent favorable effects of sodium hydrosulfide (NaSH) on myocardial ischemia-reperfusion (IR) injury in rats with T2D.

Methods: T2D was induced using a high-fat diet (HFD) and low-dose of streptozotocin.

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Decreased circulating levels of hydrogen sulfide (HS) are associated with higher mortality following myocardial ischemia. This study aimed at determining the long-term dose-dependent effects of sodium hydrosulfide (NaSH) administration on myocardial ischemia-reperfusion (IR) injury. Male rats were divided into control and NaSH groups that were treated for 9 weeks with daily intraperitoneal injections of normal saline or NaSH (0.

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Graphs, an effective form of data presentation, are used for summarizing complex information and making them easier to understand. Extracting numerical data from graphs, which is commonly required in systematic reviews and meta-analyses, is however a challenging issue. Since this kind of results presentation is common, ignorance of such data may result in publication bias when conducting meta-analyses.

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