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  1. Article ; Online: Inhibition of both NOX and TNF-α exerts substantial renoprotective effects in renal ischemia reperfusion injury rat model.

    Bayoumi, Amina A / Ahmad, Enssaf Ahmad / Ibrahim, Islam A A E-H / Mahmoud, Mona F / Elbatreek, Mahmoud H

    European journal of pharmacology

    2024  Volume 970, Page(s) 176507

    Abstract: Background and aims: Acute kidney injury (AKI) due to renal ischemia-reperfusion injury (RIRI) is associated with high morbidity and mortality, with no renoprotective drug available. Previous research focused on single drug targets, yet this approach ... ...

    Abstract Background and aims: Acute kidney injury (AKI) due to renal ischemia-reperfusion injury (RIRI) is associated with high morbidity and mortality, with no renoprotective drug available. Previous research focused on single drug targets, yet this approach has not reached translational success. Given the complexity of this condition, we aimed to identify a disease module and apply a multitarget network pharmacology approach.
    Methods: Identification of a disease module with potential drug targets was performed utilizing Disease Module Detection algorithm using NADPH oxidases (NOXs) as seeds. We then assessed the protective effect of a multitarget network pharmacology targeting the identified module in a rat model of RIRI. Rats were divided into five groups; sham, RIRI, and RIRI treated with setanaxib (NOX inhibitor, 10 mg/kg), etanercept (TNF-α inhibitor, 10 mg/kg), and setanaxib and etanercept (5 mg/kg each). Kidney functions, histopathological changes and oxidative stress markers (MDA and reduced GSH) were assessed. Immunohistochemistry of inflammatory (TNF-α, NF-κB) apoptotic (cCasp-3, Bax/Bcl 2), fibrotic (α-SMA) and proteolysis (MMP-9) markers was performed.
    Results: Our in-silico analysis yielded a disease module with TNF receptor 1 (TNFR1A) as the closest target to both NOX1 and NOX2. Targeting this module by a low-dose combination of setanaxib, and etanercept, resulted in a synergistic effect and ameliorated ischemic AKI in rats. This was evidenced by improved kidney function and reduced expression of inflammatory, apoptotic, proteolytic and fibrotic markers.
    Conclusions: Our findings show that applying a multitarget network pharmacology approach allows synergistic renoprotective effect in ischemic AKI and might pave the way towards translational success.
    MeSH term(s) Rats ; Animals ; Tumor Necrosis Factor-alpha/pharmacology ; Etanercept/pharmacology ; Kidney ; Reperfusion Injury/complications ; Reperfusion Injury/drug therapy ; Reperfusion Injury/prevention & control ; Ischemia/pathology ; Acute Kidney Injury/drug therapy ; Acute Kidney Injury/prevention & control
    Chemical Substances Tumor Necrosis Factor-alpha ; Etanercept (OP401G7OJC)
    Language English
    Publishing date 2024-03-15
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 80121-5
    ISSN 1879-0712 ; 0014-2999
    ISSN (online) 1879-0712
    ISSN 0014-2999
    DOI 10.1016/j.ejphar.2024.176507
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    Zs.A 522: Show issues Location:
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  2. Article ; Online: Hepatic β-arrestins: potential roles in liver health and disease.

    Eissa, Alzahraa Muhammad / Hassanin, Mohamed H / Ibrahim, Islam A A E H

    Molecular biology reports

    2023  Volume 50, Issue 12, Page(s) 10399–10407

    Abstract: Β-arrestins are intracellular scaffolding proteins that have multifaceted roles in different types of disorders. In this review article, we gave a summary about the discovery, characterization and classification of these proteins and their intracellular ... ...

    Abstract Β-arrestins are intracellular scaffolding proteins that have multifaceted roles in different types of disorders. In this review article, we gave a summary about the discovery, characterization and classification of these proteins and their intracellular functions. Moreover, this review article focused on the hepatic expression of β-arrestins and their hepatocellular distribution and function in each liver cell type. Also, we showed that β-arrestins are key regulators of distinct types of hepatic disorders. On the other hand, we addressed some important points that have never been studied before regarding the role of β-arrestins in certain types of hepatic disorders which needs more research efforts to cover.
    MeSH term(s) Humans ; beta-Arrestins/metabolism ; Arrestins/metabolism ; Signal Transduction ; Liver Diseases ; Proteins/metabolism
    Chemical Substances beta-Arrestins ; Arrestins ; Proteins
    Language English
    Publishing date 2023-10-16
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 186544-4
    ISSN 1573-4978 ; 0301-4851
    ISSN (online) 1573-4978
    ISSN 0301-4851
    DOI 10.1007/s11033-023-08898-0
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  3. Article: Editorial: Natural products as potential therapies for non-alcoholic fatty liver disease.

    Ibrahim, Islam A A E H / Amen, Yhiya / Mostafa, Islam / Cádiz-Gurrea, María De La Luz

    Frontiers in pharmacology

    2023  Volume 14, Page(s) 1180263

    Language English
    Publishing date 2023-04-11
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2023.1180263
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  4. Article ; Online: Adrenergic receptors blockade alleviates dexamethasone-induced neurotoxicity in adult male Wistar rats: Distinct effects on β-arrestin2 expression and molecular markers of neural injury.

    Mohamed, Rasha M S M / Ahmad Ahmad, Enssaf / Amin, Dalia M / Abdo, Samar Ahmed / Ibrahim, Islam A A E-H / Mahmoud, Mona F / Abdelaal, Shimaa

    Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences

    2023  

    Abstract: Background: Dexamethasone-induced neurotoxicity has been previously reported. However, the molecular mechanisms are still not completely understood.: Objectives: The current work aimed to investigate the modulatory effects of α- and β-adrenergic ... ...

    Abstract Background: Dexamethasone-induced neurotoxicity has been previously reported. However, the molecular mechanisms are still not completely understood.
    Objectives: The current work aimed to investigate the modulatory effects of α- and β-adrenergic receptors on dexamethasone-induced neurotoxicity in rats focused on changes in β-arrestin2 and molecular markers of neural injury in cerebral cortex.
    Methods: Male Wistar rats were subcutaneously injected with dexamethasone (10 mg/kg/day) for 7 days to induce neural injury in the cerebral cortex. The experiment involved 5 groups: control, dexamethasone, carvedilol, propranolol, and doxazosin. In the last 3 groups, drugs were given 2 hours before dexamethasone injection. At the end of experiment, brain samples were collected for measurement of brain derived neurotrophic factor (BDNF), glial fibrillary acidic protein (GFAP), kinase activity of protein kinase B (Akt), diacylglycerol (DAG), α-smooth muscle actin (α-SMA), Smad3, β-amyloid and phospho-tau protein levels in addition to histopathological examination of brain tissue using hematoxylin-eosin, Nissl, and Sirius red stains. Moreover, β-arrestin2 levels in the cerebral cortex were measured using immunohistochemical examination.
    Results: Dexamethasone slightly reduced brain weight and significantly decreased BDNF, Akt kinase activity and β-arrestin2 but markedly induced degeneration of cortical neurons and significantly increased GFAP, DAG, α-SMA, Smad3, β-amyloid and phospho-tau protein levels compared to controls. Carvedilol, propranolol, and doxazosin reversed all dexamethasone-induced molecular changes and slightly ameliorated the histopathological changes. Carvedilol significantly increased brain weight and β-arrestin2 levels compared to dexamethasone, propranolol, and doxazosin groups.
    Conclusion: blocking α- and/or β-adrenergic receptors alleviate dexamethasone-induced neurotoxicity despite their distinct effects on β-arrestin2 levels in the cerebral cortex.
    Language English
    Publishing date 2023-11-15
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2129183-4
    ISSN 2008-2231 ; 1560-8115
    ISSN (online) 2008-2231
    ISSN 1560-8115
    DOI 10.1007/s40199-023-00490-y
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  5. Article ; Online: Effect of imidazoline-1 receptor agonists on renal dysfunction in rats associated with chronic, sequential fructose and ethanol administration.

    Elkomy, Nesreen M I M / Ibrahim, Islam A A E-H / El-Fayoumi, Hassan M / Elshazly, Shimaa M

    Clinical and experimental pharmacology & physiology

    2020  Volume 47, Issue 4, Page(s) 609–619

    Abstract: Insulin resistance and chronic alcoholism are risk factors for renal dysfunction. This study investigated the therapeutic effects of two imidazoline-1 receptor (I1R) agonists on renal dysfunction in rats after chronic, sequential fructose and ethanol ... ...

    Abstract Insulin resistance and chronic alcoholism are risk factors for renal dysfunction. This study investigated the therapeutic effects of two imidazoline-1 receptor (I1R) agonists on renal dysfunction in rats after chronic, sequential fructose and ethanol administration. Daily drinking water was supplemented with fructose (10%, w/v) for 12 weeks and then with ethanol (20%, v/v) for another 8 weeks. Rats were treated with rilmenidine and clonidine in the last two weeks of the study. Blood glucose and serum insulin (sIns) levels, lipid profiles, kidney function and renal histopathology were evaluated at the end of the experiment. Additionally, renal gene expression of nischarin, phosphatidylcholine-specific phospholipase C (PC-PLC) and prostaglandin E2 (PGE2) were measured. Renal levels of superoxide dismutase (SOD), malondialdehyde (MDA), myeloperoxidase (MPO), inducible nitric oxide synthase (iNOS) and total NO (tNO) were detected, and we determined the relative renal gene expression levels of alpha smooth muscle actin (α-SMA), hydroxyproline, interleukin 10 (IL-10), tumour necrosis factor alpha (TNF-α) and caspase-3. The results showed significant deterioration of blood glucose, sIns, lipid profiles, kidney function and renal histopathology in fructose/ethanol-fed rats. Additionally, markers of inflammation, fibrosis, apoptosis and oxidative stress were upregulated. The administration of rilmenidine or clonidine significantly improved blood glucose and sIns levels and reduced renal dysfunction. Our work showed that chronic, sequential fructose and ethanol administration induced fasting hyperglycaemia and renal impairment, and these effects were ameliorated by I1R agonists.
    Language English
    Publishing date 2020-01-22
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 189277-0
    ISSN 1440-1681 ; 0305-1870 ; 0143-9294
    ISSN (online) 1440-1681
    ISSN 0305-1870 ; 0143-9294
    DOI 10.1111/1440-1681.13232
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    Zs.A 990: Show issues Location:
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  6. Article ; Online: Effect of omega-3 fatty acids on glucose homeostasis: role of free fatty acid receptor 1.

    El-Fayoumi, Shaimaa H / Mahmoud, Amr A A / Fahmy, Ahmed / Ibrahim, Islam A A E-H

    Naunyn-Schmiedeberg's archives of pharmacology

    2020  Volume 393, Issue 10, Page(s) 1797–1808

    Abstract: Insulin resistance is a worldwide health problem. This study investigated the acute effects of eicosapentanoic acid (EPA) on glucose homeostasis focusing on the role of free fatty acid receptor 1 (FFAR1) and the chronic effects of fish oil omega-3 fatty ... ...

    Abstract Insulin resistance is a worldwide health problem. This study investigated the acute effects of eicosapentanoic acid (EPA) on glucose homeostasis focusing on the role of free fatty acid receptor 1 (FFAR1) and the chronic effects of fish oil omega-3 fatty acids on insulin resistance. Insulin resistance was induced by feeding mice high-fructose, high-fat diet (HFrHFD) for 16 weeks. In the first part, the acute effects of EPA alone and in combination with GW1100 and DC260126 (FFAR1 blockers) on glucose homeostasis and hepatic phosphatidyl-inositol 4,5-bisphosphate (PIP2) and diacylglycerol (DAG) were investigated in standard chow diet (SCD)- and HFrHFD-fed mice. In the second part, mice were treated with fish oil omega-3 fatty acids for 4 weeks starting at the week 13 of feeding HFrHFD. Changes in the blood- and liver tissue-insulin resistance markers and FFAR1 downstream signals were recorded at the end of experiment. Results showed that EPA increased 0 and 30 min blood glucose levels after glucose load in SCD-fed mice but improved glucose tolerance in HFrHFD-fed mice. Moreover, FFAR1 blockers reduced EPA effects on glucose tolerance and hepatic PIP2 and DAG levels. On the other hand, chronic use of fish oil omega-3 fatty acids increased FBG levels and decreased serum insulin and triglycerides levels without improving the index of insulin resistance. Also, they increased hepatic β-arrestin-2, PIP2, and pS473 Akt levels but decreased DAG levels. In conclusion, EPA acutely improved glucose homeostasis in HFrHFD-fed mice by modulating the activity of FFAR1. However, the chronic use of fish oil omega-3 fatty acids did not improve the insulin resistance.
    MeSH term(s) Animals ; Benzoates/pharmacology ; Blood Glucose/drug effects ; Blood Glucose/metabolism ; Diet, High-Fat/adverse effects ; Eicosapentaenoic Acid/pharmacology ; Fatty Acids, Omega-3/pharmacology ; Fructose/administration & dosage ; Fructose/toxicity ; Insulin Resistance/physiology ; Male ; Mice ; Pyrimidines/pharmacology ; Receptors, G-Protein-Coupled/antagonists & inhibitors ; Receptors, G-Protein-Coupled/metabolism
    Chemical Substances Benzoates ; Blood Glucose ; Fatty Acids, Omega-3 ; Ffar1 protein, mouse ; GW1100 ; Pyrimidines ; Receptors, G-Protein-Coupled ; Fructose (30237-26-4) ; Eicosapentaenoic Acid (AAN7QOV9EA)
    Language English
    Publishing date 2020-05-09
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 121471-8
    ISSN 1432-1912 ; 0028-1298
    ISSN (online) 1432-1912
    ISSN 0028-1298
    DOI 10.1007/s00210-020-01883-5
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  7. Article ; Online: Carvedilol Diminishes Cardiac Remodeling Induced by High-Fructose/High-Fat Diet in Mice via Enhancing Cardiac β-Arrestin2 Signaling.

    Ibrahim, Wael S / Ibrahim, Islam A A E-H / Mahmoud, Mona F / Mahmoud, Amr A A

    Journal of cardiovascular pharmacology and therapeutics

    2020  Volume 25, Issue 4, Page(s) 354–363

    Abstract: Background: Insulin resistance (IR) is a well-known risk factor for cardiovascular complications. This study aimed to investigate the effect of a dietary model of IR in mice on cardiac remodeling, cardiac β-arrestin2 signaling, and the protective ... ...

    Abstract Background: Insulin resistance (IR) is a well-known risk factor for cardiovascular complications. This study aimed to investigate the effect of a dietary model of IR in mice on cardiac remodeling, cardiac β-arrestin2 signaling, and the protective effects of carvedilol as a β-arrestin-biased agonist.
    Methods and results: Insulin resistance was induced by feeding mice high-fructose/high-fat diet (HFrHFD) for 16 weeks. Carvedilol was adiministered for 4 weeks starting at week 13. At the end of the experiment, body weight, heart weight, left and right ventricular thickness, visceral fat weight, fasting blood glucose (FBG), serum insulin, IR index, and serum endothelin-1 were measured. In addition, cardiac tissue samples were histopathologically examined. Also, cardiac levels of cardiotrophin-1, β-arrestin2, phosphatidylinositol 4,5 bisphosphate (PIP2), diacylglycerol (DAG), and phosphoserine 473 Akt (pS473 Akt) were measured. Results showed significant increases in the FBG, serum insulin, IR index, serum endothelin-1, cardiac DAG, cardiac fibrosis, and degenerated cardiac myofibrils in HFrHFD-fed mice associated with a significant reduction in cardiac levels of cardiotrophin-1, β-arrestin2, PIP2, and pS473 Akt. On the other hand, carvedilol significantly reduced the heart weight, FBG, serum insulin, IR index, serum endothelin-1, cardiac DAG, left ventricular thickness, right ventricular fibrosis, and degeneration of cardiac myofibrils. In addition, carvedilol significantly increased cardiac levels of cardiotrophin-1, β-arrestin2, PIP2, and pS473 Akt.
    Conclusion: Carvedilol enhances cardiac β-arrestin2 signaling and reduces cardiac remodeling in HFrHFD-fed mice.
    MeSH term(s) Animals ; Cardiomegaly/etiology ; Cardiomegaly/metabolism ; Cardiomegaly/physiopathology ; Cardiomegaly/prevention & control ; Carvedilol/pharmacology ; Cytokines/metabolism ; Diet, High-Fat ; Dietary Sugars ; Disease Models, Animal ; Fibrosis ; Fructose ; Insulin Resistance ; Male ; Mice ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Phosphatidylinositol 4,5-Diphosphate/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Ventricular Function, Left/drug effects ; Ventricular Function, Right/drug effects ; Ventricular Remodeling/drug effects ; beta-Arrestin 2/agonists ; beta-Arrestin 2/metabolism
    Chemical Substances Arrb2 protein, mouse ; Cytokines ; Dietary Sugars ; Phosphatidylinositol 4,5-Diphosphate ; beta-Arrestin 2 ; Carvedilol (0K47UL67F2) ; Fructose (30237-26-4) ; cardiotrophin 1 (AJ7U77BR8I) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2020-02-13
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1329372-2
    ISSN 1940-4034 ; 1074-2484
    ISSN (online) 1940-4034
    ISSN 1074-2484
    DOI 10.1177/1074248420905683
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    Zs.A 4895: Show issues Location:
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  8. Article ; Online: Quercetin and lithium chloride potentiate the protective effects of carvedilol against renal ischemia-reperfusion injury in high-fructose, high-fat diet-fed Swiss albino mice independent of renal lipid signaling.

    Rezk, Asmaa M / Ibrahim, Islam A A E-H / Mahmoud, Mona F / Mahmoud, Amr A A

    Chemico-biological interactions

    2020  Volume 333, Page(s) 109307

    Abstract: Renal ischemia-reperfusion injury (R-IRI) is the main cause of acute renal failure. Carvedilol has been shown to protect against R-IRI. However, the underlying mechanisms are still not completely clarified. This study aimed to investigate the role of ... ...

    Abstract Renal ischemia-reperfusion injury (R-IRI) is the main cause of acute renal failure. Carvedilol has been shown to protect against R-IRI. However, the underlying mechanisms are still not completely clarified. This study aimed to investigate the role of lipid signaling in mediating carvedilol protective effects against R-IRI in insulin-resistant mice by using two different lipid signaling modulators, quercetin and lithium chloride (LiCl). Mice were fed high-fructose, high-fat diet (HFrHFD) for 16 weeks to induce insulin resistance. At the end of feeding period, mice were randomly distributed into five groups; Sham, R-IRI, Carvedilol (20 mg/kg, i.p.), Carvedilol + Quercetin (10 mg/kg, i.p.), Carvedilol + LiCl (200 mg/kg, i.p.). R-IRI was performed by applying 30 min of unilateral renal ischemia followed by one hour of reperfusion. Quercetin and LiCl were administered 30 min before carvedilol administration and carvedilol was administered 30 min before ischemia. Changes in kidney function tests, histopathology, fibrosis area, lipid signaling, inflammatory, apoptosis and oxidative stress markers in the kidney were measured. Results showed that R-IRI decreased kidney function, impaired renal tissue integrity, modulated lipid signaling and increased renal inflammation, apoptosis and oxidative stress. Carvedilol treatment decreased the detrimental effects induced by R-IRI. In addition, pre-injection of both quercetin and LiCl potentiated the reno-protective effects of carvedilol against R-IRI independent of changes in lipid mediators like phosphatidyl inositol 4,5 bisphosphate (PIP2) and diacylglycerol (DAG). In conclusion, quercetin and LiCl potentiate the protective effects of carvedilol against R-IRI in HFrHFD-fed mice by reducing inflammation and oxidative stress independent of lipid signaling.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Carvedilol/pharmacology ; Cytoprotection/drug effects ; Diet, High-Fat/adverse effects ; Drug Synergism ; Fructose/administration & dosage ; Kidney/blood supply ; Kidney/drug effects ; Kidney/metabolism ; Kidney/pathology ; Lithium Chloride/pharmacology ; Male ; Malondialdehyde/metabolism ; Mice ; Oxidative Stress/drug effects ; Quercetin/pharmacology ; Reperfusion Injury/chemically induced ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; Reperfusion Injury/prevention & control ; Signal Transduction/drug effects
    Chemical Substances Carvedilol (0K47UL67F2) ; Fructose (30237-26-4) ; Malondialdehyde (4Y8F71G49Q) ; Quercetin (9IKM0I5T1E) ; Lithium Chloride (G4962QA067)
    Language English
    Publishing date 2020-11-04
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 218799-1
    ISSN 1872-7786 ; 0009-2797
    ISSN (online) 1872-7786
    ISSN 0009-2797
    DOI 10.1016/j.cbi.2020.109307
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  9. Article ; Online: Propranolol and low-dose isoproterenol ameliorate insulin resistance, enhance β-arrestin2 signaling, and reduce cardiac remodeling in high-fructose, high-fat diet-fed mice: Comparative study with metformin.

    Ibrahim, Wael S / Ahmed, Hoda M S / Mahmoud, Amr A A / Mahmoud, Mona F / Ibrahim, Islam A A E-H

    Life sciences

    2021  Volume 286, Page(s) 120055

    Abstract: Aims: β-Arrestin2 signaling has emerged as a promising therapeutic target for the management of insulin resistance and related complications. Moreover, recent studies have shown that certain G protein-coupled receptor (GPCR) ligands can modulate β- ... ...

    Abstract Aims: β-Arrestin2 signaling has emerged as a promising therapeutic target for the management of insulin resistance and related complications. Moreover, recent studies have shown that certain G protein-coupled receptor (GPCR) ligands can modulate β-arrestin2 signaling. The current study examined the effects of the β-blocker propranolol and a low dose of the agonist isoproterenol (L-D-ISOPROT) on β-arrestin2 signaling, insulin resistance, and cardiac remodeling in high-fructose, high-fat diet (HFrHFD)-fed mice. In addition, the effects of these agents were compared to those of the clinical antidiabetic agent, metformin.
    Materials and methods: Insulin resistance was induced by HFrHFD feeding for 16 weeks. Mice were then randomly allocated to groups receiving propranolol, L-D-ISOPROT, metformin, or vehicle (control) for 4 weeks starting on week 13 of HFrHFD feeding. Survival rate, body weight, visceral fat weight, blood glucose, serum insulin, insulin resistance index, hepatic β-arrestin2 signaling, heart weight, left and right ventricular thicknesses, cardiac fibrosis severity, serum endothelin-1, cardiac cardiotrophin-1, and cardiac β-arrestin2 signaling were then compared among groups.
    Key findings: HFrHFD for 16 weeks significantly increased insulin resistance index, cardiac fibrosis area, and serum endothelin-1, and reduced hepatic β-arrestin2 signaling, cardiac cardiotrophin-1, and cardiac β-arrestin2 signaling without significant changes in survival rate, body weight, visceral fat weight, heart weight, or left and right ventricular thicknesses. All three drugs reduced insulin resistance and cardiac remodeling parameters and enhanced β-arrestin2 signaling with variable efficacies.
    Significance: Propranolol and L-D-ISOPROT, like metformin, can reduce insulin-resistance and cardiac remodeling in HFrHFD-fed mice, possibly by upregulating β-arrestin2 signaling activity. Therefore, β-arrestin2-signaling modulation might be a promising strategy for insulin-resistance treatment.
    MeSH term(s) Animals ; Blood Glucose/drug effects ; Diet, High-Fat/adverse effects ; Fructose/pharmacology ; Glucose/metabolism ; Heart/drug effects ; Insulin/pharmacology ; Insulin Resistance/physiology ; Isoproterenol/metabolism ; Isoproterenol/pharmacology ; Male ; Metformin/metabolism ; Metformin/pharmacology ; Mice ; Propranolol/metabolism ; Propranolol/pharmacology ; Signal Transduction/drug effects ; Ventricular Remodeling/physiology ; beta-Arrestin 2/drug effects ; beta-Arrestin 2/metabolism
    Chemical Substances Blood Glucose ; Insulin ; beta-Arrestin 2 ; Fructose (30237-26-4) ; Metformin (9100L32L2N) ; Propranolol (9Y8NXQ24VQ) ; Glucose (IY9XDZ35W2) ; Isoproterenol (L628TT009W)
    Language English
    Publishing date 2021-10-15
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2021.120055
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  10. Article ; Online: Acute and chronic metabolic effects of carvedilol in high-fructose, high-fat diet-fed mice: implication of β-arrestin2 pathway.

    Ahmed, Hoda M S / Mohamed, Samar G / Ibrahim, Wael S / Rezk, Asmaa M / Mahmoud, Amr A A / Mahmoud, Mona F / Ibrahim, Islam A A E-H

    Canadian journal of physiology and pharmacology

    2021  Volume 100, Issue 1, Page(s) 68–77

    Abstract: We aimed to investigate the acute and chronic effects of carvedilol on insulin resistance in high-fructose, high-fat diet (HFrHFD) - fed mice and the implication of the β-arrestin2 pathway. The acute effect of carvedilol (10 mg/kg, i.p.) on glucose ... ...

    Abstract We aimed to investigate the acute and chronic effects of carvedilol on insulin resistance in high-fructose, high-fat diet (HFrHFD) - fed mice and the implication of the β-arrestin2 pathway. The acute effect of carvedilol (10 mg/kg, i.p.) on glucose tolerance and hepatic lipid signaling in normal and insulin resistant mice was investigated. Then, the chronic effect of carvedilol on insulin resistance and dyslipidemia in HFrHFD-fed mice was examined. Changes in β-arrestin2 and its downstream signals in liver, skeletal muscle, and adipose tissue were measured. This involved measuring phosphatidylinositol 4,5-bisphosphate (PIP2) and diacylglycerol (DAG) levels and protein kinase B (AKT) activity. Carvedilol acutely reduced fasting blood glucose levels in both normal and insulin resistant mice without significantly affecting the glucose tolerance. These acute effects were associated with increased hepatic PIP2 but decreased hepatic DAG levels. Chronic administration of carvedilol significantly ameliorated insulin resistance and dyslipidemia in HFrHFD-fed mice. These chronic effects were associated with increased β-arrestin2, PIP2, and AKT activity levels but decreased DAG levels in the classical insulin target tissues. In conclusion, carvedilol acutely maintains glucose homeostasis and chronically ameliorates insulin resistance and dyslipidemia in HFrHFD-fed mice. The insulin sensitizing effects of carvedilol are highly correlated with the upregulation of β-arrestin2 pathway.
    MeSH term(s) Animals ; Carvedilol/administration & dosage ; Carvedilol/pharmacology ; Diet, High-Fat/adverse effects ; Dietary Carbohydrates/administration & dosage ; Dietary Carbohydrates/adverse effects ; Diglycerides/metabolism ; Dyslipidemias/drug therapy ; Dyslipidemias/etiology ; Dyslipidemias/metabolism ; Fructose/administration & dosage ; Fructose/adverse effects ; Glucose/metabolism ; Homeostasis/drug effects ; Insulin Resistance/physiology ; Lipid Metabolism/drug effects ; Liver/metabolism ; Male ; Mice ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Signal Transduction/physiology ; Up-Regulation/drug effects ; beta-Arrestin 2/metabolism
    Chemical Substances Arrb2 protein, mouse ; Dietary Carbohydrates ; Diglycerides ; beta-Arrestin 2 ; Carvedilol (0K47UL67F2) ; Fructose (30237-26-4) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2021-09-27
    Publishing country Canada
    Document type Journal Article
    ZDB-ID 127527-6
    ISSN 1205-7541 ; 0008-4212
    ISSN (online) 1205-7541
    ISSN 0008-4212
    DOI 10.1139/cjpp-2021-0299
    Database MEDical Literature Analysis and Retrieval System OnLINE

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