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Thermo Fisher gene exp slc5a1 mm00451203 m1
The sweet receptor interfaces with a metabolic oral glucosensor. ( A-B ) Sweet sensitive B6 (A) had more Gck mRNA transcripts (red dots) in the circumvallate after overnight food restriction than in a fed state while T1R2+3 KO (B) showed no such effect. Representative taste buds are outlined in the white dash; examples of counted dots are indicated by white arrows. Unpaired t-test: ∗p < 0.05; n = 6–9 mice/group (each data point represents the average number of glucokinase dots per taste bud per mouse, using ≈ 17 taste buds/CV section and 2 CV sections/mouse). ( C-D ) Gck and <t>Sglt1</t> mRNA was almost significantly higher in the circumvallate of naïve T1R2+3 KO relative to B6 mice (C). Experience with sugars modified this pattern of expression with a lower Gck mRNA expression and a higher Sglt1 mRNA expression in sugar-exposed T1R2+3 KO relative to B6 mice (D). One sample t-test vs 1.0: ∗p < 0.05; n = 6–9/group. ( E ) Tas1r3 , Tas1r2 and Gck , but not Sglt1 mRNA, was lower in the circumvallate following acute lingual Tas1r3 knockdown (T1R3 KD) than control. One sample t-test vs 1.0: ∗p < 0.05; ∗∗p < 0.01; n = 5–7/group.
Gene Exp Slc5a1 Mm00451203 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Thermo Fisher gene exp slc5a1 hs01573793 m1
Inflammation upregulates <t>SGLT1,</t> ACE2 and TMPRSS2 in Caco-2/TC7 cells. ( A ) Graphical illustration of the experimental protocol for the standard and inflamed Caco-2/TC7 cell models. Cells were differentiated in 25 mM glucose until day 7, then in 5.5 mM glucose until day 14. Cells were differentiated for 14 days from confluence and treated with dexamethasone (DEX) or 0.1% (v/v) DMSO (vehicle control) up to twice daily for 60 h, 24 h, or 4 h. For the inflamed model, a cytokine cocktail containing IL-1β (25 ng/mL) and TNF-α (50 ng/mL) was added to the basolateral (BL) once daily for 72 h. Finally, cell culture media from both apical (AP) and BL compartments were collected from the inflamed cells for IL-8 quantification. mRNA and protein were extracted from cells in both the standard and inflamed models and analysed through ddPCR and ELISA, respectively. A comparison of ( B ) IL-8 secretion and ( C ) SGLT1, ( D ) GLUT2, ( E ) ACE2 and ( F ) TMPRSS2 mRNA expression between standard (grey) and inflamed (blue) Caco-2/TC7 cells is shown. Total RNA was extracted and reverse transcribed, and absolute copies of SGLT1, GLUT2, ACE2 or TMPRSS2 cDNA measured by ddPCR are expressed relative to the housekeeping gene TBP. For IL-8 detection, cell culture media were processed, and IL-8 measured using ELISA and corrected for total protein measured by Bradford assay. Data are presented as mean ± SD (n = 6 technical replicates from N = 3 biological replicates). Differences between cells in the standard and inflamed environments in B-F were determined by unpaired t -test with Welch’s correction; ns—not significant, ** P < 0.01, *** P < 0.001. A —created with BioRender.com ( https://BioRender.com/r16s632 ); B-F —created with GraphPad Prism version 9.0.1.
Gene Exp Slc5a1 Hs01573793 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Thermo Fisher gene exp slc5a1 rn01640634 m1
Tissue distribution of TRs and expression of <t>SGLT1</t> in the small intestine and other tissues. ( A ) mRNA expression levels of TRA and TRB relative to GAPDH in various organs (liver, heart, pituitary, and small intestine) from mice. Data are shown as mean ± SEM. ( B ) After rats were injected daily with T4 (1.5 μg of T4/100 g body weight) overnight, the total serum thyroxine (T4) concentration was measured using an ECLIA. These data are presented as dosing validation to confirm effective induction of a hyperthyroid state, rather than as mechanistic evidence. Data are shown as mean ± SEM. ( C ) Rats were injected with T4 (1.5 μg of T4/100 g body weight) overnight and then sacrificed. Their small intestines were then harvested and divided into three sections: proximal (corresponding to the upper jejunum), middle (lower jejunum), and distal (ileum), starting from the stomach side. The expression of SGLT1 mRNAs was determined using qRT-PCR. In each experiment, four to six mice were used. Data are shown as mean ± SEM.
Gene Exp Slc5a1 Rn01640634 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Huabio Inc primary antibodies against slc5a1 cat. er191651
Tissue distribution of TRs and expression of <t>SGLT1</t> in the small intestine and other tissues. ( A ) mRNA expression levels of TRA and TRB relative to GAPDH in various organs (liver, heart, pituitary, and small intestine) from mice. Data are shown as mean ± SEM. ( B ) After rats were injected daily with T4 (1.5 μg of T4/100 g body weight) overnight, the total serum thyroxine (T4) concentration was measured using an ECLIA. These data are presented as dosing validation to confirm effective induction of a hyperthyroid state, rather than as mechanistic evidence. Data are shown as mean ± SEM. ( C ) Rats were injected with T4 (1.5 μg of T4/100 g body weight) overnight and then sacrificed. Their small intestines were then harvested and divided into three sections: proximal (corresponding to the upper jejunum), middle (lower jejunum), and distal (ileum), starting from the stomach side. The expression of SGLT1 mRNAs was determined using qRT-PCR. In each experiment, four to six mice were used. Data are shown as mean ± SEM.
Primary Antibodies Against Slc5a1 Cat. Er191651, supplied by Huabio Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The sweet receptor interfaces with a metabolic oral glucosensor. ( A-B ) Sweet sensitive B6 (A) had more Gck mRNA transcripts (red dots) in the circumvallate after overnight food restriction than in a fed state while T1R2+3 KO (B) showed no such effect. Representative taste buds are outlined in the white dash; examples of counted dots are indicated by white arrows. Unpaired t-test: ∗p < 0.05; n = 6–9 mice/group (each data point represents the average number of glucokinase dots per taste bud per mouse, using ≈ 17 taste buds/CV section and 2 CV sections/mouse). ( C-D ) Gck and Sglt1 mRNA was almost significantly higher in the circumvallate of naïve T1R2+3 KO relative to B6 mice (C). Experience with sugars modified this pattern of expression with a lower Gck mRNA expression and a higher Sglt1 mRNA expression in sugar-exposed T1R2+3 KO relative to B6 mice (D). One sample t-test vs 1.0: ∗p < 0.05; n = 6–9/group. ( E ) Tas1r3 , Tas1r2 and Gck , but not Sglt1 mRNA, was lower in the circumvallate following acute lingual Tas1r3 knockdown (T1R3 KD) than control. One sample t-test vs 1.0: ∗p < 0.05; ∗∗p < 0.01; n = 5–7/group.

Journal: Molecular Metabolism

Article Title: Nutritional regulation of metabolism-dependent and-independent glucosensing in the mammalian taste system

doi: 10.1016/j.molmet.2025.102280

Figure Lengend Snippet: The sweet receptor interfaces with a metabolic oral glucosensor. ( A-B ) Sweet sensitive B6 (A) had more Gck mRNA transcripts (red dots) in the circumvallate after overnight food restriction than in a fed state while T1R2+3 KO (B) showed no such effect. Representative taste buds are outlined in the white dash; examples of counted dots are indicated by white arrows. Unpaired t-test: ∗p < 0.05; n = 6–9 mice/group (each data point represents the average number of glucokinase dots per taste bud per mouse, using ≈ 17 taste buds/CV section and 2 CV sections/mouse). ( C-D ) Gck and Sglt1 mRNA was almost significantly higher in the circumvallate of naïve T1R2+3 KO relative to B6 mice (C). Experience with sugars modified this pattern of expression with a lower Gck mRNA expression and a higher Sglt1 mRNA expression in sugar-exposed T1R2+3 KO relative to B6 mice (D). One sample t-test vs 1.0: ∗p < 0.05; n = 6–9/group. ( E ) Tas1r3 , Tas1r2 and Gck , but not Sglt1 mRNA, was lower in the circumvallate following acute lingual Tas1r3 knockdown (T1R3 KD) than control. One sample t-test vs 1.0: ∗p < 0.05; ∗∗p < 0.01; n = 5–7/group.

Article Snippet: The following TaqMan Gene Expression Assays (ThermoFisher Scientific) were used: mouse β-actin (Actb, Mm02619580_g1), glucokinase (Gck, Mm00439129_m1), T1R2 (Tas1r2, Mm00499716_m1), T1R3 (Tas1r3, Mm00473459_g1) and SGLT1 (Slc5a1, Mm00451203_m1).

Techniques: Modification, Expressing, Knockdown, Control

Inflammation upregulates SGLT1, ACE2 and TMPRSS2 in Caco-2/TC7 cells. ( A ) Graphical illustration of the experimental protocol for the standard and inflamed Caco-2/TC7 cell models. Cells were differentiated in 25 mM glucose until day 7, then in 5.5 mM glucose until day 14. Cells were differentiated for 14 days from confluence and treated with dexamethasone (DEX) or 0.1% (v/v) DMSO (vehicle control) up to twice daily for 60 h, 24 h, or 4 h. For the inflamed model, a cytokine cocktail containing IL-1β (25 ng/mL) and TNF-α (50 ng/mL) was added to the basolateral (BL) once daily for 72 h. Finally, cell culture media from both apical (AP) and BL compartments were collected from the inflamed cells for IL-8 quantification. mRNA and protein were extracted from cells in both the standard and inflamed models and analysed through ddPCR and ELISA, respectively. A comparison of ( B ) IL-8 secretion and ( C ) SGLT1, ( D ) GLUT2, ( E ) ACE2 and ( F ) TMPRSS2 mRNA expression between standard (grey) and inflamed (blue) Caco-2/TC7 cells is shown. Total RNA was extracted and reverse transcribed, and absolute copies of SGLT1, GLUT2, ACE2 or TMPRSS2 cDNA measured by ddPCR are expressed relative to the housekeeping gene TBP. For IL-8 detection, cell culture media were processed, and IL-8 measured using ELISA and corrected for total protein measured by Bradford assay. Data are presented as mean ± SD (n = 6 technical replicates from N = 3 biological replicates). Differences between cells in the standard and inflamed environments in B-F were determined by unpaired t -test with Welch’s correction; ns—not significant, ** P < 0.01, *** P < 0.001. A —created with BioRender.com ( https://BioRender.com/r16s632 ); B-F —created with GraphPad Prism version 9.0.1.

Journal: Scientific Reports

Article Title: Dexamethasone enhances intestinal glucose absorption and TMPRSS2 expression with implications for hyperglycaemia and infection risk

doi: 10.1038/s41598-025-22312-8

Figure Lengend Snippet: Inflammation upregulates SGLT1, ACE2 and TMPRSS2 in Caco-2/TC7 cells. ( A ) Graphical illustration of the experimental protocol for the standard and inflamed Caco-2/TC7 cell models. Cells were differentiated in 25 mM glucose until day 7, then in 5.5 mM glucose until day 14. Cells were differentiated for 14 days from confluence and treated with dexamethasone (DEX) or 0.1% (v/v) DMSO (vehicle control) up to twice daily for 60 h, 24 h, or 4 h. For the inflamed model, a cytokine cocktail containing IL-1β (25 ng/mL) and TNF-α (50 ng/mL) was added to the basolateral (BL) once daily for 72 h. Finally, cell culture media from both apical (AP) and BL compartments were collected from the inflamed cells for IL-8 quantification. mRNA and protein were extracted from cells in both the standard and inflamed models and analysed through ddPCR and ELISA, respectively. A comparison of ( B ) IL-8 secretion and ( C ) SGLT1, ( D ) GLUT2, ( E ) ACE2 and ( F ) TMPRSS2 mRNA expression between standard (grey) and inflamed (blue) Caco-2/TC7 cells is shown. Total RNA was extracted and reverse transcribed, and absolute copies of SGLT1, GLUT2, ACE2 or TMPRSS2 cDNA measured by ddPCR are expressed relative to the housekeeping gene TBP. For IL-8 detection, cell culture media were processed, and IL-8 measured using ELISA and corrected for total protein measured by Bradford assay. Data are presented as mean ± SD (n = 6 technical replicates from N = 3 biological replicates). Differences between cells in the standard and inflamed environments in B-F were determined by unpaired t -test with Welch’s correction; ns—not significant, ** P < 0.01, *** P < 0.001. A —created with BioRender.com ( https://BioRender.com/r16s632 ); B-F —created with GraphPad Prism version 9.0.1.

Article Snippet: High Capacity RNA-to-cDNA reverse transcription kits, and FAM- or VIC-labelled TaqMan primers for ACE2 (Hs01085333_m1), SGLT1 (Hs01573793_m1), GLUT2 (Hs01096908_m1), TMPRSS2 (Hs01122322_m1) and TBP (Hs00427620_m1) were also from Thermo Fisher Scientific.

Techniques: Control, Cell Culture, Enzyme-linked Immunosorbent Assay, Comparison, Expressing, Reverse Transcription, Bradford Assay

Gene expression changes in dexamethasone-treated and untreated normal and inflamed enterocytes from wild-type C57BL/6 J mice. ( A ) A summary of the GSE113691 study and the samples considered for analysis. Raw counts obtained from the NCBI GEO database ( GSE113691 ) were filtered (< 1 count per million in at least 3 samples) and were normalised using the trimmed mean of m-values (TMM). Differences in ( B ) SGLT1, ( C ) TMPRSS2, ( D ) GLUT2, ( E ) ACE2 gene expression in enterocytes from normal mice (NM) and inflamed mice (IF) between dexamethasone-treated (NM-D, IF-D) and untreated mice (NM-C, IF-C). Volcano plot showing ( F ) 910 differentially expressed genes between NM-D and NM-C and ( I ) 386 differentially expressed genes between IF-D and IF-C. Venn diagrams depicting upregulated and downregulated genes in ( G ) NM-D and ( J ) IF-D treatment groups compared to controls NM-C and IF-C, respectively. Red indicates upregulation and blue indicates downregulation (log 2 FC ≥ 1, FDR ≤ 0.05), overlapping indicates the unchanged number of genes. ( H ) Log 2 FC of SGLT1, TMPRSS2, GLUT2, and ACE2 between NM-D vs. NM-C and IF-D vs. IF-C (*indicates significantly differentially expressed genes (log 2 FC ≥ 1, FDR ≤ 0.05)). Gene Set Enrichment Analysis on the mouse Hallmark signature collection, showing positively and negatively enriched gene sets in ( K ) NM-D vs. NM-C and ( L ) IF-D vs. IF-C. Orange bars indicate gene sets enriched in both groups. ( M ) Pearson correlation matrix showing associations between SGLT1, TMPRSS2, GLUT2, and ACE2 mRNA expression in mouse intestinal epithelial cells. Blue represents positive correlation, red represents negative correlation. ( B-E ) Data are presented as mean ± SD (N = 3). ( B-E ) Significant differences were determined using one-way ANOVA with Fisher’s LSD multiple comparisons test. ns—not significant, * P < 0.05, ** P < 0.01, *** P < 0.001. DEX—dexamethasone, NM-C—normal mouse control, NM-D—normal mouse treated with dexamethasone, IF-C—inflamed mouse control, IF-D—inflamed mouse treated with dexamethasone, NES—normalised enrichment score.

Journal: Scientific Reports

Article Title: Dexamethasone enhances intestinal glucose absorption and TMPRSS2 expression with implications for hyperglycaemia and infection risk

doi: 10.1038/s41598-025-22312-8

Figure Lengend Snippet: Gene expression changes in dexamethasone-treated and untreated normal and inflamed enterocytes from wild-type C57BL/6 J mice. ( A ) A summary of the GSE113691 study and the samples considered for analysis. Raw counts obtained from the NCBI GEO database ( GSE113691 ) were filtered (< 1 count per million in at least 3 samples) and were normalised using the trimmed mean of m-values (TMM). Differences in ( B ) SGLT1, ( C ) TMPRSS2, ( D ) GLUT2, ( E ) ACE2 gene expression in enterocytes from normal mice (NM) and inflamed mice (IF) between dexamethasone-treated (NM-D, IF-D) and untreated mice (NM-C, IF-C). Volcano plot showing ( F ) 910 differentially expressed genes between NM-D and NM-C and ( I ) 386 differentially expressed genes between IF-D and IF-C. Venn diagrams depicting upregulated and downregulated genes in ( G ) NM-D and ( J ) IF-D treatment groups compared to controls NM-C and IF-C, respectively. Red indicates upregulation and blue indicates downregulation (log 2 FC ≥ 1, FDR ≤ 0.05), overlapping indicates the unchanged number of genes. ( H ) Log 2 FC of SGLT1, TMPRSS2, GLUT2, and ACE2 between NM-D vs. NM-C and IF-D vs. IF-C (*indicates significantly differentially expressed genes (log 2 FC ≥ 1, FDR ≤ 0.05)). Gene Set Enrichment Analysis on the mouse Hallmark signature collection, showing positively and negatively enriched gene sets in ( K ) NM-D vs. NM-C and ( L ) IF-D vs. IF-C. Orange bars indicate gene sets enriched in both groups. ( M ) Pearson correlation matrix showing associations between SGLT1, TMPRSS2, GLUT2, and ACE2 mRNA expression in mouse intestinal epithelial cells. Blue represents positive correlation, red represents negative correlation. ( B-E ) Data are presented as mean ± SD (N = 3). ( B-E ) Significant differences were determined using one-way ANOVA with Fisher’s LSD multiple comparisons test. ns—not significant, * P < 0.05, ** P < 0.01, *** P < 0.001. DEX—dexamethasone, NM-C—normal mouse control, NM-D—normal mouse treated with dexamethasone, IF-C—inflamed mouse control, IF-D—inflamed mouse treated with dexamethasone, NES—normalised enrichment score.

Article Snippet: High Capacity RNA-to-cDNA reverse transcription kits, and FAM- or VIC-labelled TaqMan primers for ACE2 (Hs01085333_m1), SGLT1 (Hs01573793_m1), GLUT2 (Hs01096908_m1), TMPRSS2 (Hs01122322_m1) and TBP (Hs00427620_m1) were also from Thermo Fisher Scientific.

Techniques: Gene Expression, Expressing, Control

Dexamethasone upregulates SGLT1 mRNA in Caco-2/TC7 cells. The acute and chronic effect of dexamethasone (DEX) on SGLT1 mRNA expression was assessed in 14-day differentiated Caco-2/TC7 cells, under either standard conditions (Panel 1) or an inflamed state induced by daily exposure to IL-1β and TNF-α during the final 72 h (Panel 2). Cells were treated with dexamethasone (5, 10, 20 µM) or 0.1% (v/v) DMSO vehicle control for different time durations: ( A, D ) 4 h, ( B, E ) 24 h and ( C, F ) 60 h. A comparison of the effect of dexamethasone between standard (grey) and inflamed (blue) conditions is shown in Panel 3 ( G —4 h, H —24 h, I —60 h). Total RNA was extracted and reverse transcribed, and absolute copies of SGLT1 cDNA measured by ddPCR are expressed relative to the housekeeping gene TBP. Values represent mean fold change compared to DMSO vehicle control (Panel 1) or cytokine-treated DMSO vehicle control (Panel 2). Data are presented as mean ± SD (n = 6 technical replicates from N = 3 biological replicates). Differences were determined as follows: A, D, G —unpaired t -test with Welch’s correction; B-C , E–F —one-way ANOVA with Fisher’s LSD multiple comparisons test; H, I —two-way ANOVA with Fisher’s LSD multiple comparisons test. ns—not significant, ** P < 0.01, *** P < 0.001. Graphs created with GraphPad Prism version 9.0.1.

Journal: Scientific Reports

Article Title: Dexamethasone enhances intestinal glucose absorption and TMPRSS2 expression with implications for hyperglycaemia and infection risk

doi: 10.1038/s41598-025-22312-8

Figure Lengend Snippet: Dexamethasone upregulates SGLT1 mRNA in Caco-2/TC7 cells. The acute and chronic effect of dexamethasone (DEX) on SGLT1 mRNA expression was assessed in 14-day differentiated Caco-2/TC7 cells, under either standard conditions (Panel 1) or an inflamed state induced by daily exposure to IL-1β and TNF-α during the final 72 h (Panel 2). Cells were treated with dexamethasone (5, 10, 20 µM) or 0.1% (v/v) DMSO vehicle control for different time durations: ( A, D ) 4 h, ( B, E ) 24 h and ( C, F ) 60 h. A comparison of the effect of dexamethasone between standard (grey) and inflamed (blue) conditions is shown in Panel 3 ( G —4 h, H —24 h, I —60 h). Total RNA was extracted and reverse transcribed, and absolute copies of SGLT1 cDNA measured by ddPCR are expressed relative to the housekeeping gene TBP. Values represent mean fold change compared to DMSO vehicle control (Panel 1) or cytokine-treated DMSO vehicle control (Panel 2). Data are presented as mean ± SD (n = 6 technical replicates from N = 3 biological replicates). Differences were determined as follows: A, D, G —unpaired t -test with Welch’s correction; B-C , E–F —one-way ANOVA with Fisher’s LSD multiple comparisons test; H, I —two-way ANOVA with Fisher’s LSD multiple comparisons test. ns—not significant, ** P < 0.01, *** P < 0.001. Graphs created with GraphPad Prism version 9.0.1.

Article Snippet: High Capacity RNA-to-cDNA reverse transcription kits, and FAM- or VIC-labelled TaqMan primers for ACE2 (Hs01085333_m1), SGLT1 (Hs01573793_m1), GLUT2 (Hs01096908_m1), TMPRSS2 (Hs01122322_m1) and TBP (Hs00427620_m1) were also from Thermo Fisher Scientific.

Techniques: Expressing, Control, Comparison, Reverse Transcription

Pearson correlation analysis. ( A ) Pearson correlation matrix showing the association between variables. Blue represents a positive correlation, and red represents a negative correlation. ( B ) Table showing the statistical significance of the relationship between variables examined by Pearson correlation analysis. ACE2, TMPRSS2, SGLT1 and GLUT2 are mRNA expression levels; IL-8 is a secreted protein. The correlation matrix was created with GraphPad Prism version 9.0.1. ns—not significant; *** P < 0.001.

Journal: Scientific Reports

Article Title: Dexamethasone enhances intestinal glucose absorption and TMPRSS2 expression with implications for hyperglycaemia and infection risk

doi: 10.1038/s41598-025-22312-8

Figure Lengend Snippet: Pearson correlation analysis. ( A ) Pearson correlation matrix showing the association between variables. Blue represents a positive correlation, and red represents a negative correlation. ( B ) Table showing the statistical significance of the relationship between variables examined by Pearson correlation analysis. ACE2, TMPRSS2, SGLT1 and GLUT2 are mRNA expression levels; IL-8 is a secreted protein. The correlation matrix was created with GraphPad Prism version 9.0.1. ns—not significant; *** P < 0.001.

Article Snippet: High Capacity RNA-to-cDNA reverse transcription kits, and FAM- or VIC-labelled TaqMan primers for ACE2 (Hs01085333_m1), SGLT1 (Hs01573793_m1), GLUT2 (Hs01096908_m1), TMPRSS2 (Hs01122322_m1) and TBP (Hs00427620_m1) were also from Thermo Fisher Scientific.

Techniques: Expressing

Tissue distribution of TRs and expression of SGLT1 in the small intestine and other tissues. ( A ) mRNA expression levels of TRA and TRB relative to GAPDH in various organs (liver, heart, pituitary, and small intestine) from mice. Data are shown as mean ± SEM. ( B ) After rats were injected daily with T4 (1.5 μg of T4/100 g body weight) overnight, the total serum thyroxine (T4) concentration was measured using an ECLIA. These data are presented as dosing validation to confirm effective induction of a hyperthyroid state, rather than as mechanistic evidence. Data are shown as mean ± SEM. ( C ) Rats were injected with T4 (1.5 μg of T4/100 g body weight) overnight and then sacrificed. Their small intestines were then harvested and divided into three sections: proximal (corresponding to the upper jejunum), middle (lower jejunum), and distal (ileum), starting from the stomach side. The expression of SGLT1 mRNAs was determined using qRT-PCR. In each experiment, four to six mice were used. Data are shown as mean ± SEM.

Journal: International Journal of Molecular Sciences

Article Title: Thyroid Hormones Regulate Postprandial Glucose Metabolism by Regulating SGLT1 Expression in the Small Intestine in Rats and Mice

doi: 10.3390/ijms26188854

Figure Lengend Snippet: Tissue distribution of TRs and expression of SGLT1 in the small intestine and other tissues. ( A ) mRNA expression levels of TRA and TRB relative to GAPDH in various organs (liver, heart, pituitary, and small intestine) from mice. Data are shown as mean ± SEM. ( B ) After rats were injected daily with T4 (1.5 μg of T4/100 g body weight) overnight, the total serum thyroxine (T4) concentration was measured using an ECLIA. These data are presented as dosing validation to confirm effective induction of a hyperthyroid state, rather than as mechanistic evidence. Data are shown as mean ± SEM. ( C ) Rats were injected with T4 (1.5 μg of T4/100 g body weight) overnight and then sacrificed. Their small intestines were then harvested and divided into three sections: proximal (corresponding to the upper jejunum), middle (lower jejunum), and distal (ileum), starting from the stomach side. The expression of SGLT1 mRNAs was determined using qRT-PCR. In each experiment, four to six mice were used. Data are shown as mean ± SEM.

Article Snippet: TaqMan Gene Expression Assay Probes (Applied Biosystems) were used for SGLT1 (Rn01640634_m1 for rat, Mm00451203_m1 for mouse), SGLT2 (Rn00574917_m1 for rat, Mm00453831_m1 for mouse), Thra (Mm00579691_m1), Thrb (Mm00437044_m1), and Gapdh (Rn01775763_g1 for rat, Mm99999915_g1 for mouse).

Techniques: Expressing, Injection, Concentration Assay, Biomarker Discovery, Quantitative RT-PCR

Hyperthyroid treatment uniquely elevates blood glucose levels during OGTT, attributed to heightened SGLT1 expression. ( A ) After mice were injected daily with T4 (1.5 μg of T4/100 g body weight) for 14 days, the total serum thyroxine (T4) concentration was measured using an ECLIA. Data are shown as mean ± SEM. ( B ) After mice were injected daily with T4 (1.5 μg of T4/100 g body weight) for 14 days, IPGTT was performed, followed by glucose measurements. Data are shown as mean ± SEM. ( C ) The area under the curve (AUC) was calculated with or without T4 treatment. ( D ) After mice were injected daily with T4 (1.5 μg of T4/100 g body weight) for 14 days, an OGTT was performed, followed by glucose measurements. Data are shown as mean ± SEM, * p = 0.033 ( E ) AUC was calculated with or without T4 treatment. ( F ) After mice were injected daily with T4 (1.5 μg of T4/100 g body weight) for 14 days, the expression of SGLT1 mRNAs was determined with qRT-PCR. In each experiment, four to six mice were used. Data are shown as mean ± SEM.

Journal: International Journal of Molecular Sciences

Article Title: Thyroid Hormones Regulate Postprandial Glucose Metabolism by Regulating SGLT1 Expression in the Small Intestine in Rats and Mice

doi: 10.3390/ijms26188854

Figure Lengend Snippet: Hyperthyroid treatment uniquely elevates blood glucose levels during OGTT, attributed to heightened SGLT1 expression. ( A ) After mice were injected daily with T4 (1.5 μg of T4/100 g body weight) for 14 days, the total serum thyroxine (T4) concentration was measured using an ECLIA. Data are shown as mean ± SEM. ( B ) After mice were injected daily with T4 (1.5 μg of T4/100 g body weight) for 14 days, IPGTT was performed, followed by glucose measurements. Data are shown as mean ± SEM. ( C ) The area under the curve (AUC) was calculated with or without T4 treatment. ( D ) After mice were injected daily with T4 (1.5 μg of T4/100 g body weight) for 14 days, an OGTT was performed, followed by glucose measurements. Data are shown as mean ± SEM, * p = 0.033 ( E ) AUC was calculated with or without T4 treatment. ( F ) After mice were injected daily with T4 (1.5 μg of T4/100 g body weight) for 14 days, the expression of SGLT1 mRNAs was determined with qRT-PCR. In each experiment, four to six mice were used. Data are shown as mean ± SEM.

Article Snippet: TaqMan Gene Expression Assay Probes (Applied Biosystems) were used for SGLT1 (Rn01640634_m1 for rat, Mm00451203_m1 for mouse), SGLT2 (Rn00574917_m1 for rat, Mm00453831_m1 for mouse), Thra (Mm00579691_m1), Thrb (Mm00437044_m1), and Gapdh (Rn01775763_g1 for rat, Mm99999915_g1 for mouse).

Techniques: Expressing, Injection, Concentration Assay, Quantitative RT-PCR

( A ) Total serum thyroxine (T4) concentration was measured using an ECLIA. Data are shown as mean ± SEM. ( B ) IPGTT was performed, followed by glucose measurements. Data are shown as mean ± SEM. ( C ) AUC was calculated either in WT or TRβΔ337T knock-in mice. ( D ) OGTT was performed, followed by glucose measurements. Data are shown as mean ± SEM, * p < 0.001. ( E ) Area under the curve (AUC) was calculated in WT or TRβΔ337T knock-in mice. ( F ) The expression of SGLT1 mRNAs was determined using qRT-PCR. Data are shown as mean ± SEM. ( G ) Small intestines were harvested and divided into two sections, A and B, starting from the stomach side. The expression of SGLT1 mRNAs was determined using qRT-PCR. In each experiment, three to six mice were used. Data are shown as mean ± SEM.

Journal: International Journal of Molecular Sciences

Article Title: Thyroid Hormones Regulate Postprandial Glucose Metabolism by Regulating SGLT1 Expression in the Small Intestine in Rats and Mice

doi: 10.3390/ijms26188854

Figure Lengend Snippet: ( A ) Total serum thyroxine (T4) concentration was measured using an ECLIA. Data are shown as mean ± SEM. ( B ) IPGTT was performed, followed by glucose measurements. Data are shown as mean ± SEM. ( C ) AUC was calculated either in WT or TRβΔ337T knock-in mice. ( D ) OGTT was performed, followed by glucose measurements. Data are shown as mean ± SEM, * p < 0.001. ( E ) Area under the curve (AUC) was calculated in WT or TRβΔ337T knock-in mice. ( F ) The expression of SGLT1 mRNAs was determined using qRT-PCR. Data are shown as mean ± SEM. ( G ) Small intestines were harvested and divided into two sections, A and B, starting from the stomach side. The expression of SGLT1 mRNAs was determined using qRT-PCR. In each experiment, three to six mice were used. Data are shown as mean ± SEM.

Article Snippet: TaqMan Gene Expression Assay Probes (Applied Biosystems) were used for SGLT1 (Rn01640634_m1 for rat, Mm00451203_m1 for mouse), SGLT2 (Rn00574917_m1 for rat, Mm00453831_m1 for mouse), Thra (Mm00579691_m1), Thrb (Mm00437044_m1), and Gapdh (Rn01775763_g1 for rat, Mm99999915_g1 for mouse).

Techniques: Concentration Assay, Knock-In, Expressing, Quantitative RT-PCR