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dpp4 inhibitor sitagliptin  (MedChemExpress)


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    MedChemExpress dpp4 inhibitor sitagliptin
    A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and <t>DPP4</t> which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO-1 is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).
    Dpp4 Inhibitor Sitagliptin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 31 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    dpp4 inhibitor sitagliptin - by Bioz Stars, 2026-03
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    Images

    1) Product Images from "Characterizing the SASP-Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types"

    Article Title: Characterizing the SASP-Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types

    Journal: bioRxiv

    doi: 10.64898/2026.02.10.705129

    A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO-1 is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).
    Figure Legend Snippet: A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO-1 is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).

    Techniques Used: Activation Assay, RNA sequencing, Expressing, Standard Deviation



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    A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and <t>DPP4</t> which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO-1 is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).
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    Image Search Results


    Quantification of ACE2 , dACE2 , TMPRSS2, NRP1, CTSL , BSG (CD147), DPP4 (CD26), AXL , KREMEN1 , and ASGR1 gene expression. mRNA levels normalized to GAPDH (2 -ΔCT ) in ( a ) NHDF, NHEKs, RHE, and human skin samples and in ( b ) Caco-2/TC-7, Calu-3, and HaCaT cell lines. Gene expression was quantified by RT-qPCR in triplicate. Data represent the mean ± SEM from ( a ) 3 to 14 independent experiments using biological samples from different individuals and ( b ) 3 or 4 independent experiments from cultured cells. NHDF, normal human dermal fibroblast; NHEK, normal human epidermal keratinocyte; RHE, reconstructed human epidermis.

    Journal: JID Innovations

    Article Title: Human keratinocytes exhibit limited potential for SARS-CoV-2 infection despite ACE2 and mature cathepsin L expression

    doi: 10.1016/j.xjidi.2025.100447

    Figure Lengend Snippet: Quantification of ACE2 , dACE2 , TMPRSS2, NRP1, CTSL , BSG (CD147), DPP4 (CD26), AXL , KREMEN1 , and ASGR1 gene expression. mRNA levels normalized to GAPDH (2 -ΔCT ) in ( a ) NHDF, NHEKs, RHE, and human skin samples and in ( b ) Caco-2/TC-7, Calu-3, and HaCaT cell lines. Gene expression was quantified by RT-qPCR in triplicate. Data represent the mean ± SEM from ( a ) 3 to 14 independent experiments using biological samples from different individuals and ( b ) 3 or 4 independent experiments from cultured cells. NHDF, normal human dermal fibroblast; NHEK, normal human epidermal keratinocyte; RHE, reconstructed human epidermis.

    Article Snippet: The following TaqMan MGB-FAM-labelled probes (Applied Biosystems, Thermo Fisher Scientific) were used for qPCR analysis: ACE2 (Hs01085340_m1), ACE2 + dACE2 (Hs01085333_m1), TMPRSS2 (Hs01120965_m1), NRP1 (Hs00826128_m1), CTSL (Hs00964650_m1), BSG (CD147) (Hs00936295_m1), DPP4 (Hs00897386_m1), AXL (Hs01064444_m1), KREMEN1 (Hs00230750_m1), ASGR1 (Hs01005019_m1), and reference gene GAPDH (Hs02758991_g1).

    Techniques: Gene Expression, Quantitative RT-PCR, Cell Culture

    Differential ACE2, TMPRSS2, NRP1, CTSL, CD147, AXL, and DPP4 protein expression. Whole-cell lysates of the indicated cells were analyzed by western blot using the following antibodies: ACE2 (mAb clone AC384), TMPRSS2 (mAb clone S20014A), NRP1 (mAb clone 14H4), CTSL (mAb clone 33/1), CD147 (mAb clone HIM6), AXL (polyclonal goat IgG, AF154), and DPP4 (polyclonal goat IgG, AF1180). ( a ) Representative immunoblots from 2 to 4 independent experiments. ( b ) Densitometric quantification normalized to actin, expressed as mean ± SEM from 2 to 4 independent experiments. CTSL, cathepsin L.

    Journal: JID Innovations

    Article Title: Human keratinocytes exhibit limited potential for SARS-CoV-2 infection despite ACE2 and mature cathepsin L expression

    doi: 10.1016/j.xjidi.2025.100447

    Figure Lengend Snippet: Differential ACE2, TMPRSS2, NRP1, CTSL, CD147, AXL, and DPP4 protein expression. Whole-cell lysates of the indicated cells were analyzed by western blot using the following antibodies: ACE2 (mAb clone AC384), TMPRSS2 (mAb clone S20014A), NRP1 (mAb clone 14H4), CTSL (mAb clone 33/1), CD147 (mAb clone HIM6), AXL (polyclonal goat IgG, AF154), and DPP4 (polyclonal goat IgG, AF1180). ( a ) Representative immunoblots from 2 to 4 independent experiments. ( b ) Densitometric quantification normalized to actin, expressed as mean ± SEM from 2 to 4 independent experiments. CTSL, cathepsin L.

    Article Snippet: The following TaqMan MGB-FAM-labelled probes (Applied Biosystems, Thermo Fisher Scientific) were used for qPCR analysis: ACE2 (Hs01085340_m1), ACE2 + dACE2 (Hs01085333_m1), TMPRSS2 (Hs01120965_m1), NRP1 (Hs00826128_m1), CTSL (Hs00964650_m1), BSG (CD147) (Hs00936295_m1), DPP4 (Hs00897386_m1), AXL (Hs01064444_m1), KREMEN1 (Hs00230750_m1), ASGR1 (Hs01005019_m1), and reference gene GAPDH (Hs02758991_g1).

    Techniques: Expressing, Western Blot

    Validation of flow cytometry protocols and anti-ACE2 antibodies. ( a ) Comparison of cell detachment protocols. ( b ) Comparison of anti-ACE2 antibody staining by flow cytometry. ( c, d ) Binding of 2019-nCoV Spike Protein S1 (RBD) protein and blocking with anti-ACE2 antibody (mAb clone AC384) assessed by ( c ) flow cytometry and ( d ) immunofluorescence (red). Cell nuclei are stained with DAPI (white). Bar = 10 μm. Data are representative of 3 independent experiments. ( e ) Cell surface expression of ACE2 (mAb clone Poly5036), TMPRSS2 (mAb clone S20014A), NRP1 (mAb clone U21-1283), CD147 (mAb clone HIM6), AXL (mAb clone 108724), and DPP4 (mAb clone BA5b) in A549 cells. Data are representative of 2 independent experiments.

    Journal: JID Innovations

    Article Title: Human keratinocytes exhibit limited potential for SARS-CoV-2 infection despite ACE2 and mature cathepsin L expression

    doi: 10.1016/j.xjidi.2025.100447

    Figure Lengend Snippet: Validation of flow cytometry protocols and anti-ACE2 antibodies. ( a ) Comparison of cell detachment protocols. ( b ) Comparison of anti-ACE2 antibody staining by flow cytometry. ( c, d ) Binding of 2019-nCoV Spike Protein S1 (RBD) protein and blocking with anti-ACE2 antibody (mAb clone AC384) assessed by ( c ) flow cytometry and ( d ) immunofluorescence (red). Cell nuclei are stained with DAPI (white). Bar = 10 μm. Data are representative of 3 independent experiments. ( e ) Cell surface expression of ACE2 (mAb clone Poly5036), TMPRSS2 (mAb clone S20014A), NRP1 (mAb clone U21-1283), CD147 (mAb clone HIM6), AXL (mAb clone 108724), and DPP4 (mAb clone BA5b) in A549 cells. Data are representative of 2 independent experiments.

    Article Snippet: The following TaqMan MGB-FAM-labelled probes (Applied Biosystems, Thermo Fisher Scientific) were used for qPCR analysis: ACE2 (Hs01085340_m1), ACE2 + dACE2 (Hs01085333_m1), TMPRSS2 (Hs01120965_m1), NRP1 (Hs00826128_m1), CTSL (Hs00964650_m1), BSG (CD147) (Hs00936295_m1), DPP4 (Hs00897386_m1), AXL (Hs01064444_m1), KREMEN1 (Hs00230750_m1), ASGR1 (Hs01005019_m1), and reference gene GAPDH (Hs02758991_g1).

    Techniques: Biomarker Discovery, Flow Cytometry, Comparison, Staining, Binding Assay, Blocking Assay, Immunofluorescence, Expressing

    Cell surface expression of ACE2, TMPRSS2, NRP1, CD147, AXL, and DPP4 receptors is associated with exclusive binding of SARS-CoV-2 Spike Protein S1 (RBD) to ACE2-expressing cells. ( a ) Flow cytometry analysis of cell surface expression of ACE2 (mAb clone Poly5036), TMPRSS2 (mAb clone S20014A), NRP1 (mAb clone U21-1283), CD147 (mAb clone HIM6), AXL (mAb clone 108724), and DPP4 (mAb clone BA5b) in the indicated cell lines and primary skin cells. Data are representative of 2–4 independent experiments. ( b, c ) Representative immunofluorescence microscopy images showing ( b ) ACE2 expression (mAb clone Poly5036) and ( c ) binding of 2019-nCoV Spike Protein S1 (RBD) in red. Cell nuclei are stained with DAPI (white). Bar = 10 μm. The proportions of cells expressing ACE2 and binding to spike are shown. Data are representative of at least 2 independent experiments. SARS-CoV-2, severe acute respiratory syndrome coronavirus 2.

    Journal: JID Innovations

    Article Title: Human keratinocytes exhibit limited potential for SARS-CoV-2 infection despite ACE2 and mature cathepsin L expression

    doi: 10.1016/j.xjidi.2025.100447

    Figure Lengend Snippet: Cell surface expression of ACE2, TMPRSS2, NRP1, CD147, AXL, and DPP4 receptors is associated with exclusive binding of SARS-CoV-2 Spike Protein S1 (RBD) to ACE2-expressing cells. ( a ) Flow cytometry analysis of cell surface expression of ACE2 (mAb clone Poly5036), TMPRSS2 (mAb clone S20014A), NRP1 (mAb clone U21-1283), CD147 (mAb clone HIM6), AXL (mAb clone 108724), and DPP4 (mAb clone BA5b) in the indicated cell lines and primary skin cells. Data are representative of 2–4 independent experiments. ( b, c ) Representative immunofluorescence microscopy images showing ( b ) ACE2 expression (mAb clone Poly5036) and ( c ) binding of 2019-nCoV Spike Protein S1 (RBD) in red. Cell nuclei are stained with DAPI (white). Bar = 10 μm. The proportions of cells expressing ACE2 and binding to spike are shown. Data are representative of at least 2 independent experiments. SARS-CoV-2, severe acute respiratory syndrome coronavirus 2.

    Article Snippet: The following TaqMan MGB-FAM-labelled probes (Applied Biosystems, Thermo Fisher Scientific) were used for qPCR analysis: ACE2 (Hs01085340_m1), ACE2 + dACE2 (Hs01085333_m1), TMPRSS2 (Hs01120965_m1), NRP1 (Hs00826128_m1), CTSL (Hs00964650_m1), BSG (CD147) (Hs00936295_m1), DPP4 (Hs00897386_m1), AXL (Hs01064444_m1), KREMEN1 (Hs00230750_m1), ASGR1 (Hs01005019_m1), and reference gene GAPDH (Hs02758991_g1).

    Techniques: Expressing, Binding Assay, Flow Cytometry, Immunofluorescence, Microscopy, Staining

    A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO-1 is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).

    Journal: bioRxiv

    Article Title: Characterizing the SASP-Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types

    doi: 10.64898/2026.02.10.705129

    Figure Lengend Snippet: A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO-1 is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).

    Article Snippet: Treatment with DPP4 inhibitor Sitagliptin (MedChemExpress, Catalog No. HY-13749) was used to eliminate DPP4-dependent cleavage and inactivation of CXCL12, which is a ligand of the CXCR7 receptor.

    Techniques: Activation Assay, RNA sequencing, Expressing, Standard Deviation

    Male WT (TN, n = 10; C, n = 11) and GLPDRKO mice (TN, n = 10; C, n = 8) were housed at TN (27 °C) or cold (6 °C) temperatures for 5 weeks. Fasting plasma a leptin levels. Body b weight, c lean mass, and d fat mass were measured at baseline and endpoint. Liver e mass and f triglyceride levels in WT (TN, n = 7; C, n = 7) and GLPDRKO mice (TN, n = 6; C, n = 5). After 2 weeks of temperature housing, WT (TN, n = 7; C, n = 7) and GLPDRKO mice (TN, n = 6; C, n = 5) were fasted for 5 h and administered a dietary fat challenge of 200 μL of olive oil. Fasting plasma g triglyceride levels. Lipid tolerance test plasma h triglyceride levels with AUC (inset). The P value indicates statistical differences among genotypes at TN. Plasma i GLP-1 and j GIP levels at baseline (0) and 10 min after the olive oil gavage (10). Fasting plasma k DPP4 activity. After 4 weeks of temperature housing, WT (TN, n = 7; C, n = 7) and GLPDRKO mice (TN, n = 6; C, n = 5) were fasted for 2 h and administered an oral gavage of carmine red. Intestinal l transit time was measured from gavage to the first red fecal pellet. Short-chain fatty acids were extracted from the feces of male WT (TN, n = 10; C, n = 11) and GLPDRKO mice (TN, n = 10; C, n = 7) for m butyrate measurements expressed as a percentage of total short-chain fatty acids. Two-way ANOVA with repeated measures and a Tukey test correction for multiple comparisons was used to determine statistical significance between housing temperature and genotype for both body weight and composition, as well as plasma GIP levels. Two-way ANOVA with a Tukey test correction for multiple comparisons was used to determine statistical significance between housing temperature and genotype. Data are shown as mean ± standard error of the mean (SEM).

    Journal: Communications Biology

    Article Title: Intestinal adaptation to cold-induced metabolic demand and feeding requires GLP-1R and GLP-2R signalling

    doi: 10.1038/s42003-025-09281-4

    Figure Lengend Snippet: Male WT (TN, n = 10; C, n = 11) and GLPDRKO mice (TN, n = 10; C, n = 8) were housed at TN (27 °C) or cold (6 °C) temperatures for 5 weeks. Fasting plasma a leptin levels. Body b weight, c lean mass, and d fat mass were measured at baseline and endpoint. Liver e mass and f triglyceride levels in WT (TN, n = 7; C, n = 7) and GLPDRKO mice (TN, n = 6; C, n = 5). After 2 weeks of temperature housing, WT (TN, n = 7; C, n = 7) and GLPDRKO mice (TN, n = 6; C, n = 5) were fasted for 5 h and administered a dietary fat challenge of 200 μL of olive oil. Fasting plasma g triglyceride levels. Lipid tolerance test plasma h triglyceride levels with AUC (inset). The P value indicates statistical differences among genotypes at TN. Plasma i GLP-1 and j GIP levels at baseline (0) and 10 min after the olive oil gavage (10). Fasting plasma k DPP4 activity. After 4 weeks of temperature housing, WT (TN, n = 7; C, n = 7) and GLPDRKO mice (TN, n = 6; C, n = 5) were fasted for 2 h and administered an oral gavage of carmine red. Intestinal l transit time was measured from gavage to the first red fecal pellet. Short-chain fatty acids were extracted from the feces of male WT (TN, n = 10; C, n = 11) and GLPDRKO mice (TN, n = 10; C, n = 7) for m butyrate measurements expressed as a percentage of total short-chain fatty acids. Two-way ANOVA with repeated measures and a Tukey test correction for multiple comparisons was used to determine statistical significance between housing temperature and genotype for both body weight and composition, as well as plasma GIP levels. Two-way ANOVA with a Tukey test correction for multiple comparisons was used to determine statistical significance between housing temperature and genotype. Data are shown as mean ± standard error of the mean (SEM).

    Article Snippet: Dpp4 , Mm01329189_m1.

    Techniques: Clinical Proteomics, Activity Assay

    Female WT (TN, n = 9; C, n = 8) and GLPDRKO (TN, n = 9; C, n = 10) mice were housed at TN (27 °C) or cold (6 °C) temperatures for 5 weeks. Fasting plasma a leptin levels. Body b weight, c lean mass, and d fat mass were measured at baseline and endpoint. Liver e mass and f triglyceride levels from female WT (TN, n = 6; C, n = 5) and GLPDRKO (TN, n = 5; C, n = 6). After 2 weeks of temperature housing, female WT (TN, n = 6; C, n = 5) and GLPDRKO (TN, n = 5; C, n = 6) mice were fasted for 5 h and administered a dietary fat challenge of 200 μL of olive oil. Fasting plasma g triglyceride levels. Lipid tolerance test plasma h triglyceride levels with AUC (inset). Plasma i GLP-1 and j GIP levels at baseline (0) and 10 min after the olive oil gavage (10). Fasting plasma k DPP4 activity. After 4 weeks of temperature housing, female WT (TN, n = 6; C, n = 5) and GLPDRKO (TN, n = 5; C, n = 6) mice were fasted for 2 h and administered an oral gavage of carmine red. Intestinal l transit time was measured from gavage to the first red fecal pellet. Short-chain fatty acids were extracted from the feces of female WT (TN, n = 6; C, n = 5) and GLPDRKO (TN, n = 6; C, n = 6) for (m) butyrate measurements expressed as a percentage of total short-chain fatty acids. Two-way ANOVA with a Tukey test correction for multiple comparisons was used to determine statistical significance between housing temperature, genotype, and time for both body weight and composition, as well as plasma GIP levels. Two-way ANOVA with a Tukey test correction for multiple comparisons was used to determine statistical significance between housing temperature and genotype. Data are shown as mean ± standard error of the mean (SEM).

    Journal: Communications Biology

    Article Title: Intestinal adaptation to cold-induced metabolic demand and feeding requires GLP-1R and GLP-2R signalling

    doi: 10.1038/s42003-025-09281-4

    Figure Lengend Snippet: Female WT (TN, n = 9; C, n = 8) and GLPDRKO (TN, n = 9; C, n = 10) mice were housed at TN (27 °C) or cold (6 °C) temperatures for 5 weeks. Fasting plasma a leptin levels. Body b weight, c lean mass, and d fat mass were measured at baseline and endpoint. Liver e mass and f triglyceride levels from female WT (TN, n = 6; C, n = 5) and GLPDRKO (TN, n = 5; C, n = 6). After 2 weeks of temperature housing, female WT (TN, n = 6; C, n = 5) and GLPDRKO (TN, n = 5; C, n = 6) mice were fasted for 5 h and administered a dietary fat challenge of 200 μL of olive oil. Fasting plasma g triglyceride levels. Lipid tolerance test plasma h triglyceride levels with AUC (inset). Plasma i GLP-1 and j GIP levels at baseline (0) and 10 min after the olive oil gavage (10). Fasting plasma k DPP4 activity. After 4 weeks of temperature housing, female WT (TN, n = 6; C, n = 5) and GLPDRKO (TN, n = 5; C, n = 6) mice were fasted for 2 h and administered an oral gavage of carmine red. Intestinal l transit time was measured from gavage to the first red fecal pellet. Short-chain fatty acids were extracted from the feces of female WT (TN, n = 6; C, n = 5) and GLPDRKO (TN, n = 6; C, n = 6) for (m) butyrate measurements expressed as a percentage of total short-chain fatty acids. Two-way ANOVA with a Tukey test correction for multiple comparisons was used to determine statistical significance between housing temperature, genotype, and time for both body weight and composition, as well as plasma GIP levels. Two-way ANOVA with a Tukey test correction for multiple comparisons was used to determine statistical significance between housing temperature and genotype. Data are shown as mean ± standard error of the mean (SEM).

    Article Snippet: Dpp4 , Mm01329189_m1.

    Techniques: Clinical Proteomics, Activity Assay