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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells <t>using</t> <t>Dunnett's</t> test or two-way <t>ANOVA</t> followed by Dunnett's test, respectively (p < 0.05).
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Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells using Dunnett's test or two-way ANOVA followed by Dunnett's test, respectively (p < 0.05).

Journal: Biochemistry and Biophysics Reports

Article Title: Effects of ethanol or ethylene glycol exposure on PPARγ and aromatase expression in adipose tissue

doi: 10.1016/j.bbrep.2024.101742

Figure Lengend Snippet: Lipid accumulation and adipogenic marker mRNA in response to chemical exposure during adipocyte differentiation . C3H10T1/2 cells were differentiated for 6 days in the presence of 0, 0.3, or 1 % ( A ) ethanol or ( B ) ethylene glycol. Cells were compared to an undifferentiated control. Gene expression analysis by RT-qPCR was performed for adipocyte markers ( Pparg2 , Adipoq , Fabp4 , Slc2a4 ) using SYBR Green assay ( n = 4). ( C ) Differentiation of human ASCs was induced with either high (2 μM) or low (0.1 μM) concentrations of rosiglitazone in the adipogenic medium. During differentiation, cells were exposed to 0, 0.3, or 1 % ethanol. Lipids were stained with Oil Red O at day 12 of differentiation, visualized by microscopy, and quantified ( n = 4). The graphs show means ± SEM. Asterisk (*) and hash (#) indicate statistically significant differences compared to the differentiated unexposed control cells using Dunnett's test or two-way ANOVA followed by Dunnett's test, respectively (p < 0.05).

Article Snippet: Statistical significance was assessed by Dunnett's multiple comparisons test or two-way analysis of variance (ANOVA) using GraphPad Prism 10.1.2, depending on the number of variables.

Techniques: Marker, Control, Gene Expression, Quantitative RT-PCR, SYBR Green Assay, Staining, Microscopy

Aromatase mRNA level in response to ethanol or ethylene glycol exposure . Gene expression analysis of aromatase ( CYP19A1 ) and adipocyte markers ( ADIPOQ and FASN ) was performed by RT-qPCR using SYBR Green assay. ( A ) Undifferentiated or ( B ) differentiated A41 cells were exposed to 1 % ethanol or ethylene glycol for 24 h (both panels). The graphs present means ± SEM ( n = 3). Asterisk (*) and hash (#) indicate statistically significant differences compared to control cells using Dunnett's test or two-way ANOVA followed by Dunnett's test, respectively ( p < 0.05).

Journal: Biochemistry and Biophysics Reports

Article Title: Effects of ethanol or ethylene glycol exposure on PPARγ and aromatase expression in adipose tissue

doi: 10.1016/j.bbrep.2024.101742

Figure Lengend Snippet: Aromatase mRNA level in response to ethanol or ethylene glycol exposure . Gene expression analysis of aromatase ( CYP19A1 ) and adipocyte markers ( ADIPOQ and FASN ) was performed by RT-qPCR using SYBR Green assay. ( A ) Undifferentiated or ( B ) differentiated A41 cells were exposed to 1 % ethanol or ethylene glycol for 24 h (both panels). The graphs present means ± SEM ( n = 3). Asterisk (*) and hash (#) indicate statistically significant differences compared to control cells using Dunnett's test or two-way ANOVA followed by Dunnett's test, respectively ( p < 0.05).

Article Snippet: Statistical significance was assessed by Dunnett's multiple comparisons test or two-way analysis of variance (ANOVA) using GraphPad Prism 10.1.2, depending on the number of variables.

Techniques: Gene Expression, Quantitative RT-PCR, SYBR Green Assay, Control