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cck1r  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology cck1r
    (A) Schematic of METH CPP procedure. (B) The expression of <t>CCK1R</t> mRNA. n = 5 mice. (C) The expression of CCK2R mRNA. BLA: Unpaired t test, t = 4.180, P = 0.0031, n = 5 mice. (D) The expression of CCKR mRNA in BLA after METH training. n = 5 mice. (E) Top: Representative immunoblots of CCK1R. Bottom: Relative amounts of CCK1R quantified by densitometry, in BLA. Unpaired t test, t = 0.317, P = 0.759, n = 5 mice. (F) Top: Representative immunoblots of CCK2R. Bottom: Relative amounts of CCK2R quantified by densitometry, in BLA. Unpaired t test, t = 2.620, P = 0.031, n = 5 mice. (G) Schematic of METH CPP procedure. (H) Schematic diagram of virus injection in BLA. Scale bar=200μm . (I, J) Heat map and score bar chart of METH CPP. Two-way RM ANOVA, F treatment (3,44) = 21.94, P <0.001; Tukey’s post hoc comparison, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 mice. (K, L) In vitro electrophysiology: AP spiking patterns evoked by 400 pA current injections and spike numbers and thresholds for AP firing. Two-way RM ANOVA ANOVA, F treatment (3,44) = 31.20, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 4 mice. (M, N) In vivo electrophysiology: AP spiking patterns and bar chart of AP frequency. Ordinary one-way ANOVA, F treatment (3,44) = 12.32, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 3 mice. All data are means ± SEM, * P < 0.05; ** P < 0.01; *** P < 0.001.
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    Images

    1) Product Images from "CCK2R regulates METH-induced CPP acquisition within VTA-BLA-BNST circuit in male mice"

    Article Title: CCK2R regulates METH-induced CPP acquisition within VTA-BLA-BNST circuit in male mice

    Journal: Translational Psychiatry

    doi: 10.1038/s41398-026-03982-y

    (A) Schematic of METH CPP procedure. (B) The expression of CCK1R mRNA. n = 5 mice. (C) The expression of CCK2R mRNA. BLA: Unpaired t test, t = 4.180, P = 0.0031, n = 5 mice. (D) The expression of CCKR mRNA in BLA after METH training. n = 5 mice. (E) Top: Representative immunoblots of CCK1R. Bottom: Relative amounts of CCK1R quantified by densitometry, in BLA. Unpaired t test, t = 0.317, P = 0.759, n = 5 mice. (F) Top: Representative immunoblots of CCK2R. Bottom: Relative amounts of CCK2R quantified by densitometry, in BLA. Unpaired t test, t = 2.620, P = 0.031, n = 5 mice. (G) Schematic of METH CPP procedure. (H) Schematic diagram of virus injection in BLA. Scale bar=200μm . (I, J) Heat map and score bar chart of METH CPP. Two-way RM ANOVA, F treatment (3,44) = 21.94, P <0.001; Tukey’s post hoc comparison, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 mice. (K, L) In vitro electrophysiology: AP spiking patterns evoked by 400 pA current injections and spike numbers and thresholds for AP firing. Two-way RM ANOVA ANOVA, F treatment (3,44) = 31.20, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 4 mice. (M, N) In vivo electrophysiology: AP spiking patterns and bar chart of AP frequency. Ordinary one-way ANOVA, F treatment (3,44) = 12.32, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 3 mice. All data are means ± SEM, * P < 0.05; ** P < 0.01; *** P < 0.001.
    Figure Legend Snippet: (A) Schematic of METH CPP procedure. (B) The expression of CCK1R mRNA. n = 5 mice. (C) The expression of CCK2R mRNA. BLA: Unpaired t test, t = 4.180, P = 0.0031, n = 5 mice. (D) The expression of CCKR mRNA in BLA after METH training. n = 5 mice. (E) Top: Representative immunoblots of CCK1R. Bottom: Relative amounts of CCK1R quantified by densitometry, in BLA. Unpaired t test, t = 0.317, P = 0.759, n = 5 mice. (F) Top: Representative immunoblots of CCK2R. Bottom: Relative amounts of CCK2R quantified by densitometry, in BLA. Unpaired t test, t = 2.620, P = 0.031, n = 5 mice. (G) Schematic of METH CPP procedure. (H) Schematic diagram of virus injection in BLA. Scale bar=200μm . (I, J) Heat map and score bar chart of METH CPP. Two-way RM ANOVA, F treatment (3,44) = 21.94, P <0.001; Tukey’s post hoc comparison, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 mice. (K, L) In vitro electrophysiology: AP spiking patterns evoked by 400 pA current injections and spike numbers and thresholds for AP firing. Two-way RM ANOVA ANOVA, F treatment (3,44) = 31.20, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 4 mice. (M, N) In vivo electrophysiology: AP spiking patterns and bar chart of AP frequency. Ordinary one-way ANOVA, F treatment (3,44) = 12.32, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 3 mice. All data are means ± SEM, * P < 0.05; ** P < 0.01; *** P < 0.001.

    Techniques Used: Expressing, Western Blot, Virus, Injection, Comparison, Plasmid Preparation, In Vitro, Saline, In Vivo

    Related Articles

    Western Blot:

    Article Title: Heterodimerization of cholecystokinin 1 and cholecystokinin 2 receptors in gallbladder cancer: a new mechanism for carcinogenesis.
    Article Snippet: Purpose Cholecystokinin is present in abundance in gallbladder tissue and mediates function through two structurally related receptors, CCK1R and CCK2R.. Heterodimerization of these receptors is known to impact cell growth in vitro.. However, the significance of these heterodimers in gallbladder carcinogenesis is relatively unknown.

    Incubation:

    Article Title: CCK2R regulates METH-induced CPP acquisition within VTA-BLA-BNST circuit in male mice
    Article Snippet: .. Membranes were then blocked for 1 h using 5% skim milk in TBS before overnight incubation at 4 °C with primary antibodies: mouse GAPDH (1:10,000 dilution, ABclonal, AC033), CCK1R (1:150, Santa Cruz, sc-514303) or CCK2R (1:150, Santa Cruz, sc-166690). .. After thorough washing with TBS, membranes were probed with fluorophore-conjugated goat anti-mouse secondary antibody (1:10,000, Rockland, 926-32210) for 1 h at room temperature.

    Article Title: Heterodimerization of cholecystokinin 1 and cholecystokinin 2 receptors in gallbladder cancer: a new mechanism for carcinogenesis.
    Article Snippet: Purpose Cholecystokinin is present in abundance in gallbladder tissue and mediates function through two structurally related receptors, CCK1R and CCK2R.. Heterodimerization of these receptors is known to impact cell growth in vitro.. However, the significance of these heterodimers in gallbladder carcinogenesis is relatively unknown.

    Article Title: CCK2R regulates METH-induced CPP acquisition within VTA-BLA-BNST circuit in male mice.
    Article Snippet: .. Membranes were then blocked for 1 h using 5% skim milk in TBS before overnight incubation at 4 °C with primary antibodies: mouse GAPDH (1:10,000 dilution, ABclonal, AC033), CCK1R (1:150, Santa Cruz, sc-514303) or CCK2R (1:150, Santa Cruz, sc-166690). .. After thorough washing with TBS, membranes were probed with fluorophore-conjugated goat anti-mouse secondary antibody (1:10,000, Rockland, 926-32210) for 1 h at room temperature.

    Gentle:

    Article Title: Heterodimerization of cholecystokinin 1 and cholecystokinin 2 receptors in gallbladder cancer: a new mechanism for carcinogenesis.
    Article Snippet: Purpose Cholecystokinin is present in abundance in gallbladder tissue and mediates function through two structurally related receptors, CCK1R and CCK2R.. Heterodimerization of these receptors is known to impact cell growth in vitro.. However, the significance of these heterodimers in gallbladder carcinogenesis is relatively unknown.



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    (A) Schematic of METH CPP procedure. (B) The expression of <t>CCK1R</t> mRNA. n = 5 mice. (C) The expression of CCK2R mRNA. BLA: Unpaired t test, t = 4.180, P = 0.0031, n = 5 mice. (D) The expression of CCKR mRNA in BLA after METH training. n = 5 mice. (E) Top: Representative immunoblots of CCK1R. Bottom: Relative amounts of CCK1R quantified by densitometry, in BLA. Unpaired t test, t = 0.317, P = 0.759, n = 5 mice. (F) Top: Representative immunoblots of CCK2R. Bottom: Relative amounts of CCK2R quantified by densitometry, in BLA. Unpaired t test, t = 2.620, P = 0.031, n = 5 mice. (G) Schematic of METH CPP procedure. (H) Schematic diagram of virus injection in BLA. Scale bar=200μm . (I, J) Heat map and score bar chart of METH CPP. Two-way RM ANOVA, F treatment (3,44) = 21.94, P <0.001; Tukey’s post hoc comparison, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 mice. (K, L) In vitro electrophysiology: AP spiking patterns evoked by 400 pA current injections and spike numbers and thresholds for AP firing. Two-way RM ANOVA ANOVA, F treatment (3,44) = 31.20, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 4 mice. (M, N) In vivo electrophysiology: AP spiking patterns and bar chart of AP frequency. Ordinary one-way ANOVA, F treatment (3,44) = 12.32, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 3 mice. All data are means ± SEM, * P < 0.05; ** P < 0.01; *** P < 0.001.
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    (A) Schematic of METH CPP procedure. (B) The expression of <t>CCK1R</t> mRNA. n = 5 mice. (C) The expression of CCK2R mRNA. BLA: Unpaired t test, t = 4.180, P = 0.0031, n = 5 mice. (D) The expression of CCKR mRNA in BLA after METH training. n = 5 mice. (E) Top: Representative immunoblots of CCK1R. Bottom: Relative amounts of CCK1R quantified by densitometry, in BLA. Unpaired t test, t = 0.317, P = 0.759, n = 5 mice. (F) Top: Representative immunoblots of CCK2R. Bottom: Relative amounts of CCK2R quantified by densitometry, in BLA. Unpaired t test, t = 2.620, P = 0.031, n = 5 mice. (G) Schematic of METH CPP procedure. (H) Schematic diagram of virus injection in BLA. Scale bar=200μm . (I, J) Heat map and score bar chart of METH CPP. Two-way RM ANOVA, F treatment (3,44) = 21.94, P <0.001; Tukey’s post hoc comparison, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 mice. (K, L) In vitro electrophysiology: AP spiking patterns evoked by 400 pA current injections and spike numbers and thresholds for AP firing. Two-way RM ANOVA ANOVA, F treatment (3,44) = 31.20, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 4 mice. (M, N) In vivo electrophysiology: AP spiking patterns and bar chart of AP frequency. Ordinary one-way ANOVA, F treatment (3,44) = 12.32, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 3 mice. All data are means ± SEM, * P < 0.05; ** P < 0.01; *** P < 0.001.
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    (A) Schematic of METH CPP procedure. (B) The expression of <t>CCK1R</t> mRNA. n = 5 mice. (C) The expression of CCK2R mRNA. BLA: Unpaired t test, t = 4.180, P = 0.0031, n = 5 mice. (D) The expression of CCKR mRNA in BLA after METH training. n = 5 mice. (E) Top: Representative immunoblots of CCK1R. Bottom: Relative amounts of CCK1R quantified by densitometry, in BLA. Unpaired t test, t = 0.317, P = 0.759, n = 5 mice. (F) Top: Representative immunoblots of CCK2R. Bottom: Relative amounts of CCK2R quantified by densitometry, in BLA. Unpaired t test, t = 2.620, P = 0.031, n = 5 mice. (G) Schematic of METH CPP procedure. (H) Schematic diagram of virus injection in BLA. Scale bar=200μm . (I, J) Heat map and score bar chart of METH CPP. Two-way RM ANOVA, F treatment (3,44) = 21.94, P <0.001; Tukey’s post hoc comparison, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 mice. (K, L) In vitro electrophysiology: AP spiking patterns evoked by 400 pA current injections and spike numbers and thresholds for AP firing. Two-way RM ANOVA ANOVA, F treatment (3,44) = 31.20, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 4 mice. (M, N) In vivo electrophysiology: AP spiking patterns and bar chart of AP frequency. Ordinary one-way ANOVA, F treatment (3,44) = 12.32, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 3 mice. All data are means ± SEM, * P < 0.05; ** P < 0.01; *** P < 0.001.
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    Image Search Results


    (A) Schematic of METH CPP procedure. (B) The expression of CCK1R mRNA. n = 5 mice. (C) The expression of CCK2R mRNA. BLA: Unpaired t test, t = 4.180, P = 0.0031, n = 5 mice. (D) The expression of CCKR mRNA in BLA after METH training. n = 5 mice. (E) Top: Representative immunoblots of CCK1R. Bottom: Relative amounts of CCK1R quantified by densitometry, in BLA. Unpaired t test, t = 0.317, P = 0.759, n = 5 mice. (F) Top: Representative immunoblots of CCK2R. Bottom: Relative amounts of CCK2R quantified by densitometry, in BLA. Unpaired t test, t = 2.620, P = 0.031, n = 5 mice. (G) Schematic of METH CPP procedure. (H) Schematic diagram of virus injection in BLA. Scale bar=200μm . (I, J) Heat map and score bar chart of METH CPP. Two-way RM ANOVA, F treatment (3,44) = 21.94, P <0.001; Tukey’s post hoc comparison, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 mice. (K, L) In vitro electrophysiology: AP spiking patterns evoked by 400 pA current injections and spike numbers and thresholds for AP firing. Two-way RM ANOVA ANOVA, F treatment (3,44) = 31.20, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 4 mice. (M, N) In vivo electrophysiology: AP spiking patterns and bar chart of AP frequency. Ordinary one-way ANOVA, F treatment (3,44) = 12.32, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 3 mice. All data are means ± SEM, * P < 0.05; ** P < 0.01; *** P < 0.001.

    Journal: Translational Psychiatry

    Article Title: CCK2R regulates METH-induced CPP acquisition within VTA-BLA-BNST circuit in male mice

    doi: 10.1038/s41398-026-03982-y

    Figure Lengend Snippet: (A) Schematic of METH CPP procedure. (B) The expression of CCK1R mRNA. n = 5 mice. (C) The expression of CCK2R mRNA. BLA: Unpaired t test, t = 4.180, P = 0.0031, n = 5 mice. (D) The expression of CCKR mRNA in BLA after METH training. n = 5 mice. (E) Top: Representative immunoblots of CCK1R. Bottom: Relative amounts of CCK1R quantified by densitometry, in BLA. Unpaired t test, t = 0.317, P = 0.759, n = 5 mice. (F) Top: Representative immunoblots of CCK2R. Bottom: Relative amounts of CCK2R quantified by densitometry, in BLA. Unpaired t test, t = 2.620, P = 0.031, n = 5 mice. (G) Schematic of METH CPP procedure. (H) Schematic diagram of virus injection in BLA. Scale bar=200μm . (I, J) Heat map and score bar chart of METH CPP. Two-way RM ANOVA, F treatment (3,44) = 21.94, P <0.001; Tukey’s post hoc comparison, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 mice. (K, L) In vitro electrophysiology: AP spiking patterns evoked by 400 pA current injections and spike numbers and thresholds for AP firing. Two-way RM ANOVA ANOVA, F treatment (3,44) = 31.20, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 4 mice. (M, N) In vivo electrophysiology: AP spiking patterns and bar chart of AP frequency. Ordinary one-way ANOVA, F treatment (3,44) = 12.32, P <0.001; Tukey’s post hoc comparison, Vector+Saline vs Vector+METH: P <0.001, CCK2R-KO + METH vs Vector+METH: P <0.001, n = 12 cells from 3 mice. All data are means ± SEM, * P < 0.05; ** P < 0.01; *** P < 0.001.

    Article Snippet: Membranes were then blocked for 1 h using 5% skim milk in TBS before overnight incubation at 4 °C with primary antibodies: mouse GAPDH (1:10,000 dilution, ABclonal, AC033), CCK1R (1:150, Santa Cruz, sc-514303) or CCK2R (1:150, Santa Cruz, sc-166690).

    Techniques: Expressing, Western Blot, Virus, Injection, Comparison, Plasmid Preparation, In Vitro, Saline, In Vivo

    (A) Gallbladder weights 15 minutes after oral vehicle (cyan bars) or FOY-251 (green bars) administration to fasted WT control (closed circles) and CCK1R KO (open circles) mice. (B) Effect of increasing doses of oral loxiglumide (beige bars) on gallbladder weight in fasted C57BL/6 mice. (C) Effect of FOY-251 (green bar), loxiglumide (beige bar), or both (green and beige cross-hatched bar) on gallbladder weight in fasted C57BL/6 mice. Animals were first treated with oral vehicle or loxiglumide (t = 0 min), followed by oral vehicle or FOY-251 (t = 30 min); gallbladder weight was measured at t = 45 min. Gallbladders from four fasted naïve mice (grey bar) were included to demonstrate an absence of effect of vehicle treatment. Values are expressed as mean ± SEM; *p < 0.05 for the indicated comparisons.

    Journal: PLOS One

    Article Title: Role of CCK1 receptor in metabolic benefits of intestinal enteropeptidase inhibition in mice

    doi: 10.1371/journal.pone.0312927

    Figure Lengend Snippet: (A) Gallbladder weights 15 minutes after oral vehicle (cyan bars) or FOY-251 (green bars) administration to fasted WT control (closed circles) and CCK1R KO (open circles) mice. (B) Effect of increasing doses of oral loxiglumide (beige bars) on gallbladder weight in fasted C57BL/6 mice. (C) Effect of FOY-251 (green bar), loxiglumide (beige bar), or both (green and beige cross-hatched bar) on gallbladder weight in fasted C57BL/6 mice. Animals were first treated with oral vehicle or loxiglumide (t = 0 min), followed by oral vehicle or FOY-251 (t = 30 min); gallbladder weight was measured at t = 45 min. Gallbladders from four fasted naïve mice (grey bar) were included to demonstrate an absence of effect of vehicle treatment. Values are expressed as mean ± SEM; *p < 0.05 for the indicated comparisons.

    Article Snippet: The CCK1R antagonist loxiglumide was purchased from Tocris Biotechne (Minneapolis, MN).

    Techniques: Control

    (A) Daily FOY-251 compound dose calculated using diet consumption and body weight. FOY-251 was formulated at 1.59 mg/gm of 60% HFD. (B) Daily food intake WT and CCK1R KO mice provided with non-medicated diet (Control), HFD with FOY-251, and animals pair-fed (PF) non-medicated diet at the same amount as that consumed by respective FOY-251 treated groups. ^ p < 0.05 WT-Control vs WT-FOY-251; $ p < 0.05 WT-Control vs WT-PF; *p < 0.05 CCK1R KO-Control vs CCK1R KO-FOY-251; # p < 0.05 CCK1R KO-Control vs CCK1R KO-PF. Weekly cumulative food intake over 4 weeks in wild type mice (C) or CCK1R KO mice (D) treated with FOY-251 (green bars), or non-medicated HFD Control (cyan bars) or animals pair fed to the same level as FOY-251 treated mice (black bars). *p < 0.05 Control vs FOY-251 for each genotype. Percent change in body weight in WT (E) and CCK1R KO (F) mice treated with FOY-251, non-medicated HFD Control or pair-fed (PF) non-medicated HFD at the same level as FOY-251-treated group. *p < 0.05 vs Control. Data represent Mean±SEM of 9-10 animals per group.

    Journal: PLOS One

    Article Title: Role of CCK1 receptor in metabolic benefits of intestinal enteropeptidase inhibition in mice

    doi: 10.1371/journal.pone.0312927

    Figure Lengend Snippet: (A) Daily FOY-251 compound dose calculated using diet consumption and body weight. FOY-251 was formulated at 1.59 mg/gm of 60% HFD. (B) Daily food intake WT and CCK1R KO mice provided with non-medicated diet (Control), HFD with FOY-251, and animals pair-fed (PF) non-medicated diet at the same amount as that consumed by respective FOY-251 treated groups. ^ p < 0.05 WT-Control vs WT-FOY-251; $ p < 0.05 WT-Control vs WT-PF; *p < 0.05 CCK1R KO-Control vs CCK1R KO-FOY-251; # p < 0.05 CCK1R KO-Control vs CCK1R KO-PF. Weekly cumulative food intake over 4 weeks in wild type mice (C) or CCK1R KO mice (D) treated with FOY-251 (green bars), or non-medicated HFD Control (cyan bars) or animals pair fed to the same level as FOY-251 treated mice (black bars). *p < 0.05 Control vs FOY-251 for each genotype. Percent change in body weight in WT (E) and CCK1R KO (F) mice treated with FOY-251, non-medicated HFD Control or pair-fed (PF) non-medicated HFD at the same level as FOY-251-treated group. *p < 0.05 vs Control. Data represent Mean±SEM of 9-10 animals per group.

    Article Snippet: The CCK1R antagonist loxiglumide was purchased from Tocris Biotechne (Minneapolis, MN).

    Techniques: Control

    Body composition of WT and CCK1R KO mice fed control HFD, FOY-251 HFD admixture, and animals pair-fed to the FOY-251 group was measured by whole body MRI to measure fat mass (A) and lean mass (B). Data represent change in body composition from baseline for each individual animal. Cumulative protein in excreted feces over the 4 weeks of treatment was normalized to total fecal output (C) or presented as absolute total protein excreted (D) in WT and CCK1R KO mice receiving non-medicated high fat diet, FOY-251 HFD admixture or pair fed non-medicated HFD. (E) Weekly cumulative total fecal protein excretion over the 4-week study period in CCK1R KO mice and WT controls. Data represent the mean±SEM of 8-10 animals per group; *p < 0.05 for the indicated comparisons.

    Journal: PLOS One

    Article Title: Role of CCK1 receptor in metabolic benefits of intestinal enteropeptidase inhibition in mice

    doi: 10.1371/journal.pone.0312927

    Figure Lengend Snippet: Body composition of WT and CCK1R KO mice fed control HFD, FOY-251 HFD admixture, and animals pair-fed to the FOY-251 group was measured by whole body MRI to measure fat mass (A) and lean mass (B). Data represent change in body composition from baseline for each individual animal. Cumulative protein in excreted feces over the 4 weeks of treatment was normalized to total fecal output (C) or presented as absolute total protein excreted (D) in WT and CCK1R KO mice receiving non-medicated high fat diet, FOY-251 HFD admixture or pair fed non-medicated HFD. (E) Weekly cumulative total fecal protein excretion over the 4-week study period in CCK1R KO mice and WT controls. Data represent the mean±SEM of 8-10 animals per group; *p < 0.05 for the indicated comparisons.

    Article Snippet: The CCK1R antagonist loxiglumide was purchased from Tocris Biotechne (Minneapolis, MN).

    Techniques: Control

    (A) Post-mortem organ fat content measured using MRI in WT and KO mice fed control HFD, FOY-251 HFD admixture, and animals pair-fed to the FOY-251 group. (B) Representative hematoxylin & eosin stained liver tissue sections from WT and CCK1R KO mice; blue sections indicate the software analysis algorithm determined tissue area for representative CCK1R KO samples. Black scale bars represent 500μm. (C) Quantitative image analysis for steatosis measuring vacuolar burden (%vacuole area/liver area) using Visiopharm software. (D) Semiquantitative blinded histopathology grading of liver vacuolation (distinct clear vacuoles of variable size, with displacement of nucleus) consistent with lipidosis (steatosis) severity: [minimal (grade 1), mild (grade 2), moderate (grade 3), marked (grade 4) and severe (grade 5)]. *p < 0.05 for indicated comparisons.

    Journal: PLOS One

    Article Title: Role of CCK1 receptor in metabolic benefits of intestinal enteropeptidase inhibition in mice

    doi: 10.1371/journal.pone.0312927

    Figure Lengend Snippet: (A) Post-mortem organ fat content measured using MRI in WT and KO mice fed control HFD, FOY-251 HFD admixture, and animals pair-fed to the FOY-251 group. (B) Representative hematoxylin & eosin stained liver tissue sections from WT and CCK1R KO mice; blue sections indicate the software analysis algorithm determined tissue area for representative CCK1R KO samples. Black scale bars represent 500μm. (C) Quantitative image analysis for steatosis measuring vacuolar burden (%vacuole area/liver area) using Visiopharm software. (D) Semiquantitative blinded histopathology grading of liver vacuolation (distinct clear vacuoles of variable size, with displacement of nucleus) consistent with lipidosis (steatosis) severity: [minimal (grade 1), mild (grade 2), moderate (grade 3), marked (grade 4) and severe (grade 5)]. *p < 0.05 for indicated comparisons.

    Article Snippet: The CCK1R antagonist loxiglumide was purchased from Tocris Biotechne (Minneapolis, MN).

    Techniques: Control, Staining, Software, Histopathology

    Fasted blood glucose (A) and plasma insulin levels (B) were obtained on day 27 of treatment following a 5-hour fast in WT mice (filled symbols) and CCK1R KO mice (open symbols) given non-medicated high fat diet (circles), HFD formulated with FOY-251 (squares), or animals pair-fed non-medicated diet (triangles) at the same amount consumed by FOY-251 treated mice. *p < 0.05 for indicated comparisons. (C) Plasma FGF-21 was measured in terminal fed plasma samples taken during sacrifice after 4-weeks of treatment. Data represent mean±SEM of 9-10 animals per group.

    Journal: PLOS One

    Article Title: Role of CCK1 receptor in metabolic benefits of intestinal enteropeptidase inhibition in mice

    doi: 10.1371/journal.pone.0312927

    Figure Lengend Snippet: Fasted blood glucose (A) and plasma insulin levels (B) were obtained on day 27 of treatment following a 5-hour fast in WT mice (filled symbols) and CCK1R KO mice (open symbols) given non-medicated high fat diet (circles), HFD formulated with FOY-251 (squares), or animals pair-fed non-medicated diet (triangles) at the same amount consumed by FOY-251 treated mice. *p < 0.05 for indicated comparisons. (C) Plasma FGF-21 was measured in terminal fed plasma samples taken during sacrifice after 4-weeks of treatment. Data represent mean±SEM of 9-10 animals per group.

    Article Snippet: The CCK1R antagonist loxiglumide was purchased from Tocris Biotechne (Minneapolis, MN).

    Techniques: Clinical Proteomics

    Inhibition of EP/T causes weight loss by caloric excretion via protein in feces, and also partially via CCK release from the small intestine. CCK acts centrally to reduce food intake, as well as on CCK1R receptors to reduce gastric emptying and increase bile acid secretion. Results from the current study indicated CCK1R-dependent and -independent effects of EP/T inhibition on weight loss in mice, with concomitant improvement of steatosis.

    Journal: PLOS One

    Article Title: Role of CCK1 receptor in metabolic benefits of intestinal enteropeptidase inhibition in mice

    doi: 10.1371/journal.pone.0312927

    Figure Lengend Snippet: Inhibition of EP/T causes weight loss by caloric excretion via protein in feces, and also partially via CCK release from the small intestine. CCK acts centrally to reduce food intake, as well as on CCK1R receptors to reduce gastric emptying and increase bile acid secretion. Results from the current study indicated CCK1R-dependent and -independent effects of EP/T inhibition on weight loss in mice, with concomitant improvement of steatosis.

    Article Snippet: The CCK1R antagonist loxiglumide was purchased from Tocris Biotechne (Minneapolis, MN).

    Techniques: Inhibition