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glp1 mimetics semaglutide  (Mimetics)

 
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    Mimetics glp1 mimetics semaglutide
    Exogenous activation of peripheral CB 1 Rs blocks fat-induced GIP and aGLP1 secretion. Compared to the control (0.5 mL saline by oral gavage and vehicle by IP injection), corn oil (CO; 0.5 mL by oral gavage) increased levels of the incretins GIP [treatment effect F (3,17) = 10.53, P = .0004] (A) and active <t>GLP1</t> [treatment effect F (3,17) = 18.06, P < .0001] (B) but did not significantly increase levels of plasma insulin (C) in plasma of fasted mice. This effect was blocked by pretreatment with CB 1 R agonist, WIN 55,212-2 (WIN, IP 3 mg per kg 30 minutes before CO). The inhibitory effects of WIN on incretins were inhibited by coadministration with the peripherally-restricted CB 1 R antagonist, AM6545 (AM; IP 10 mg per kg 30 minutes before CO). Data expressed as means ± S.E.M. and analyzed by one-way ANOVA with post hoc Holm-Sidak multiple comparison tests. n = 4–6 per condition, ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.
    Glp1 Mimetics Semaglutide, supplied by Mimetics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/glp1 mimetics semaglutide/product/Mimetics
    Average 90 stars, based on 1 article reviews
    glp1 mimetics semaglutide - by Bioz Stars, 2026-02
    90/100 stars

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    1) Product Images from "Cannabinoids Block Fat-induced Incretin Release via CB 1 -dependent and CB 1 -independent Pathways in Intestinal Epithelium"

    Article Title: Cannabinoids Block Fat-induced Incretin Release via CB 1 -dependent and CB 1 -independent Pathways in Intestinal Epithelium

    Journal: Gastro Hep Advances

    doi: 10.1016/j.gastha.2024.07.006

    Exogenous activation of peripheral CB 1 Rs blocks fat-induced GIP and aGLP1 secretion. Compared to the control (0.5 mL saline by oral gavage and vehicle by IP injection), corn oil (CO; 0.5 mL by oral gavage) increased levels of the incretins GIP [treatment effect F (3,17) = 10.53, P = .0004] (A) and active GLP1 [treatment effect F (3,17) = 18.06, P < .0001] (B) but did not significantly increase levels of plasma insulin (C) in plasma of fasted mice. This effect was blocked by pretreatment with CB 1 R agonist, WIN 55,212-2 (WIN, IP 3 mg per kg 30 minutes before CO). The inhibitory effects of WIN on incretins were inhibited by coadministration with the peripherally-restricted CB 1 R antagonist, AM6545 (AM; IP 10 mg per kg 30 minutes before CO). Data expressed as means ± S.E.M. and analyzed by one-way ANOVA with post hoc Holm-Sidak multiple comparison tests. n = 4–6 per condition, ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.
    Figure Legend Snippet: Exogenous activation of peripheral CB 1 Rs blocks fat-induced GIP and aGLP1 secretion. Compared to the control (0.5 mL saline by oral gavage and vehicle by IP injection), corn oil (CO; 0.5 mL by oral gavage) increased levels of the incretins GIP [treatment effect F (3,17) = 10.53, P = .0004] (A) and active GLP1 [treatment effect F (3,17) = 18.06, P < .0001] (B) but did not significantly increase levels of plasma insulin (C) in plasma of fasted mice. This effect was blocked by pretreatment with CB 1 R agonist, WIN 55,212-2 (WIN, IP 3 mg per kg 30 minutes before CO). The inhibitory effects of WIN on incretins were inhibited by coadministration with the peripherally-restricted CB 1 R antagonist, AM6545 (AM; IP 10 mg per kg 30 minutes before CO). Data expressed as means ± S.E.M. and analyzed by one-way ANOVA with post hoc Holm-Sidak multiple comparison tests. n = 4–6 per condition, ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

    Techniques Used: Activation Assay, Control, Saline, Injection, Clinical Proteomics, Comparison



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    glp1 mimetics semaglutide  (Mimetics)
    90
    Mimetics glp1 mimetics semaglutide
    Exogenous activation of peripheral CB 1 Rs blocks fat-induced GIP and aGLP1 secretion. Compared to the control (0.5 mL saline by oral gavage and vehicle by IP injection), corn oil (CO; 0.5 mL by oral gavage) increased levels of the incretins GIP [treatment effect F (3,17) = 10.53, P = .0004] (A) and active <t>GLP1</t> [treatment effect F (3,17) = 18.06, P < .0001] (B) but did not significantly increase levels of plasma insulin (C) in plasma of fasted mice. This effect was blocked by pretreatment with CB 1 R agonist, WIN 55,212-2 (WIN, IP 3 mg per kg 30 minutes before CO). The inhibitory effects of WIN on incretins were inhibited by coadministration with the peripherally-restricted CB 1 R antagonist, AM6545 (AM; IP 10 mg per kg 30 minutes before CO). Data expressed as means ± S.E.M. and analyzed by one-way ANOVA with post hoc Holm-Sidak multiple comparison tests. n = 4–6 per condition, ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.
    Glp1 Mimetics Semaglutide, supplied by Mimetics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/glp1 mimetics semaglutide/product/Mimetics
    Average 90 stars, based on 1 article reviews
    glp1 mimetics semaglutide - by Bioz Stars, 2026-02
    90/100 stars
    		  Buy from Supplier

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    Exogenous activation of peripheral CB 1 Rs blocks fat-induced GIP and aGLP1 secretion. Compared to the control (0.5 mL saline by oral gavage and vehicle by IP injection), corn oil (CO; 0.5 mL by oral gavage) increased levels of the incretins GIP [treatment effect F (3,17) = 10.53, P = .0004] (A) and active GLP1 [treatment effect F (3,17) = 18.06, P < .0001] (B) but did not significantly increase levels of plasma insulin (C) in plasma of fasted mice. This effect was blocked by pretreatment with CB 1 R agonist, WIN 55,212-2 (WIN, IP 3 mg per kg 30 minutes before CO). The inhibitory effects of WIN on incretins were inhibited by coadministration with the peripherally-restricted CB 1 R antagonist, AM6545 (AM; IP 10 mg per kg 30 minutes before CO). Data expressed as means ± S.E.M. and analyzed by one-way ANOVA with post hoc Holm-Sidak multiple comparison tests. n = 4–6 per condition, ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

    Journal: Gastro Hep Advances

    Article Title: Cannabinoids Block Fat-induced Incretin Release via CB 1 -dependent and CB 1 -independent Pathways in Intestinal Epithelium

    doi: 10.1016/j.gastha.2024.07.006

    Figure Lengend Snippet: Exogenous activation of peripheral CB 1 Rs blocks fat-induced GIP and aGLP1 secretion. Compared to the control (0.5 mL saline by oral gavage and vehicle by IP injection), corn oil (CO; 0.5 mL by oral gavage) increased levels of the incretins GIP [treatment effect F (3,17) = 10.53, P = .0004] (A) and active GLP1 [treatment effect F (3,17) = 18.06, P < .0001] (B) but did not significantly increase levels of plasma insulin (C) in plasma of fasted mice. This effect was blocked by pretreatment with CB 1 R agonist, WIN 55,212-2 (WIN, IP 3 mg per kg 30 minutes before CO). The inhibitory effects of WIN on incretins were inhibited by coadministration with the peripherally-restricted CB 1 R antagonist, AM6545 (AM; IP 10 mg per kg 30 minutes before CO). Data expressed as means ± S.E.M. and analyzed by one-way ANOVA with post hoc Holm-Sidak multiple comparison tests. n = 4–6 per condition, ∗ P < .05, ∗∗ P < .01, ∗∗∗ P < .001.

    Article Snippet: Indeed, GLP1 mimetics (eg, semaglutide, liraglutide) reduce body mass in obese and diabetic patients, partly due to the hypophagic effects of activating GLP1 receptors.

    Techniques: Activation Assay, Control, Saline, Injection, Clinical Proteomics, Comparison