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Träfflista för sökning "WFRF:(Ardalani Hamidreza) "

Sökning: WFRF:(Ardalani Hamidreza)

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1.
  • Ardalani, Hamidreza, et al. (författare)
  • Dietary quercetin impacts the concentration of pesticides in honey bees
  • 2021
  • Ingår i: Chemosphere. - : Elsevier BV. - 0045-6535 .- 1879-1298. ; 262
  • Tidskriftsartikel (refereegranskat)abstract
    • Honey bees are important pollinators and are subject to numerous stressors, such as changing floral resources, parasites, and agrochemical exposure. Pesticide exposure has been linked to the decline in the global honey bee population. We have limited knowledge of the metabolic pathways and synergistic effects of xenobiotics in bees. Quercetin is one of the most abundant phytochemicals in plants and is therefore abundant in the honey bee diet. Quercetin can upregulate the detoxification system in honey bees; however, it is still unknown to what extent quercetin ingestion can reduce the content of absorbed pesticides. In this study, we investigated the effect of dietary quercetin on the contents of three pesticides in honey bees: imidacloprid (insecticide), tebuconazole (fungicide), and tau-fluvalinate (insecticide and acaricide). Bees were divided into two main groups and fed either quercetin-sucrose paste or only sucrose for 72 h. Thereafter, they were orally exposed to ∼10 ng/bee imidacloprid or contact-exposed to ∼0.9 μg/bee tau-fluvalinate or ∼5.2 μg/bee tebuconazole. After 1 h of oral exposure or 24 h of contact exposure, the bees were anaesthetised with CO2, sacrificed by freezing, and extracted with a validated QuEChERS method. Subsequently, the concentrations of the three pesticides and quercetin in the bees were determined with a triple quadrupole tandem mass spectrometer coupled to an HPLC system. No significant effect on the concentration of tebuconazole or tau-fluvalinate was observed in bees fed quercetin. Intake of quercetin led to a reduction in the concentration of imidacloprid in honey bees. Quercetin-rich plants may be exploited in future beekeeping.
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2.
  • Ardalani, Hamidreza, et al. (författare)
  • Potential antidiabetic phytochemicals in plant roots : a review of in vivo studies
  • 2021
  • Ingår i: Journal of Diabetes and Metabolic Disorders. - : Springer Science and Business Media LLC. - 2251-6581. ; 20:2, s. 1837-1854
  • Forskningsöversikt (refereegranskat)abstract
    • Background: Medicinal plants are used to treat various disorders, including diabetes, globally in a range of formulations. While attention has mainly been on the aerial plant parts, there are only a few review studies to date that are focused on the natural constituents present in the plant roots with health benefits. Thus, the present study was performed to review in vivo studies investigating the antidiabetic potential of the natural compounds in plant roots. Methods: We sorted relevant data in 2001–2019 from scientific databases and search engines, including Web of Knowledge, PubMed, ScienceDirect, Medline, Reaxys, and Google Scholar. The class of phytochemicals, plant families, major compounds, active constituents, effective dosages, type of extracts, time of experiments, and type of diabetic induction were described. Results: In our literature review, we found 104 plants with determined antidiabetic activity in their root extracts. The biosynthesis pathways and mechanism of actions of the most frequent class of compounds were also proposed. The results of this review indicated that flavonoids, phenolic compounds, alkaloids, and phytosteroids are the most abundant natural compounds in plant roots with antidiabetic activity. Phytochemicals in plant roots possess different mechanisms of action to control diabetes, including inhibition of α-amylase and α-glucosidase enzymes, oxidative stress reduction, secretion of insulin, improvement of diabetic retinopathy/nephropathy, slow the starch digestion, and contribution against hyperglycemia. Conclusion: This review concludes that plant roots are a promising source of bioactive compounds which can be explored to develop against diabetes and diabetes-related complications. Graphical abstract: [Figure not available: see fulltext.]
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3.
  • Huang, Mi, et al. (författare)
  • Identification of a weight loss-associated causal eQTL in MTIF3 and the effects of MTIF3 deficiency on human adipocyte function
  • 2023
  • Ingår i: eLife. - 2050-084X.
  • Tidskriftsartikel (refereegranskat)abstract
    • Genetic variation at the MTIF3 (Mitochondrial Translational Initiation Factor 3) locus has been robustly associated with obesity in humans, but the functional basis behind this association is not known. Here, we applied luciferase reporter assay to map potential functional variants in the haplotype block tagged by rs1885988 and used CRISPR-Cas9 to edit the potential functional variants to confirm the regulatory effects on MTIF3 expression. We further conducted functional studies on MTIF3-deficient differentiated human white adipocyte cell line (hWAs-iCas9), generated through inducible expression of CRISPR-Cas9 combined with delivery of synthetic MTIF3-targeting guide RNA. We demonstrate that rs67785913-centered DNA fragment (in LD with rs1885988, r2 > 0.8) enhances transcription in a luciferase reporter assay, and CRISPR-Cas9-edited rs67785913 CTCT cells show significantly higher MTIF3 expression than rs67785913 CT cells. Perturbed MTIF3 expression led to reduced mitochondrial respiration and endogenous fatty acid oxidation, as well as altered expression of mitochondrial DNA-encoded genes and proteins, and disturbed mitochondrial OXPHOS complex assembly. Furthermore, after glucose restriction, the MTIF3 knockout cells retained more triglycerides than control cells. This study demonstrates an adipocyte function-specific role of MTIF3, which originates in the maintenance of mitochondrial function, providing potential explanations for why MTIF3 genetic variation at rs67785913 is associated with body corpulence and response to weight loss interventions.
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4.
  • Huang, Peng, et al. (författare)
  • Cryo-EM structure supports a role of AQP7 as a junction protein
  • 2023
  • Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 14, s. 1-12
  • Tidskriftsartikel (refereegranskat)abstract
    • Aquaglyceroporin 7 (AQP7) facilitates glycerol flux across the plasma membrane with a critical physiological role linked to metabolism, obesity, and associated diseases. Here, we present the single-particle cryo-EM structure of AQP7 determined at 2.55 Å resolution adopting two adhering tetramers, stabilized by extracellularly exposed loops, in a configuration like that of the well-characterized interaction of AQP0 tetramers. The central pore, in-between the four monomers, displays well-defined densities restricted by two leucine filters. Gas chromatography mass spectrometry (GC/MS) results show that the AQP7 sample contains glycerol 3-phosphate (Gro3P), which is compatible with the identified features in the central pore. AQP7 is shown to be highly expressed in human pancreatic α- and β- cells suggesting that the identified AQP7 octamer assembly, in addition to its function as glycerol channel, may serve as junction proteins within the endocrine pancreas.
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5.
  • Neuhaus, Mathis, et al. (författare)
  • EHD2 regulates plasma membrane integrity and downstream insulin receptor signalling events
  • 2023
  • Ingår i: Molecular Biology of the Cell. - 1939-4586. ; 34:12
  • Tidskriftsartikel (refereegranskat)abstract
    • Adipocyte dysfunction is a crucial driver of insulin resistance and type 2 diabetes. We identified EH domain-containing protein 2 (EHD2) as one of the most highly upregulated genes at the early stage of adipose tissue expansion. EHD2 is a dynamin-related ATPase influencing several cellular processes, including membrane recycling, caveolae dynamics and lipid metabolism. Here, we investigated the role of EHD2 in adipocyte insulin signalling and glucose transport. Using C57BL6/N EHD2 knockout mice under short-term high-fat diet conditions and 3T3-L1 adipocytes we demonstrate that EHD2 deficiency is associated with deterioration of insulin signal transduction and impaired insulin-stimulated GLUT4 translocation. Furthermore, we show that lack of EHD2 is linked with altered plasma membrane lipid and protein composition, reduced insulin receptor expression, and diminished insulin-dependent SNARE protein complex formation. In conclusion, these data highlight the importance of EHD2 for the integrity of the plasma membrane milieu, insulin receptor stability, and downstream insulin receptor signalling events, involved in glucose uptake and ultimately underscore its role in insulin resistance and obesity.
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