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Lipolysis and ketone bodies compensate norUDCA-induced defects in energy homeostasis and thermogenesis. A-G Mice were fed a regular chow (control), or chow diet supplemented with norUDCA for 1 day, 3 days or 7 days with housing at room temperature. A-C Circulating levels of glucose ( A ), non esterified fatty acids (NEFA) ( B ), and ketone bodies ( C ) were determined ( n = 7 ). D-G , Uptake of 3 H-deoxyglucose ( D, E ) and 14 C-hydroxybutyrate ( F, G ) by heart ( D, F ) and by BAT ( E, G ) was determined 15 min after intravenous administration ( n = 6 ). H Release of NEFA and glycerol from white adipose tissue explants isolated from mice fed a chow (control) or chow diet supplemented with norUDCA ( n = 3 ). I , Expression of lipogenic and lipolytic genes in white adipose tissues isolated from control and norUDCA-fed mice ( n = 7 ). J-K Indirect calorimetry was performed at room temperature in lipolysis-deficient <t>ATGL-MHC</t> and control mice fed a chow for 3 days followed by feeding a norUDCA-containing chow diet for 5 days ( n = 2-3 ). Consumption of O 2 ( J ) and production of CO 2 ( K ) are shown. L-N Indirect calorimetry was performed in wild type mice that were fed a low-carb diet or low-carb diet supplemented with norUDCA. Production of CO 2 ( L ), consumption of O 2 ( M ) and respiratory exchange ratio ( N ) were recorded at various housing temperatures as indicated by the red line ( n = 3 ). Error bars are shown as SEM. Statistical analysis was performed with one-way ANOVA ( A-G ), or Student's T-Test ( H–I ). ∗p < 0.05, ∗∗p < 0.01,∗∗∗p < 0.001.
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Lipolysis and ketone bodies compensate norUDCA-induced defects in energy homeostasis and thermogenesis. A-G Mice were fed a regular chow (control), or chow diet supplemented with norUDCA for 1 day, 3 days or 7 days with housing at room temperature. A-C Circulating levels of glucose ( A ), non esterified fatty acids (NEFA) ( B ), and ketone bodies ( C ) were determined ( n = 7 ). D-G , Uptake of 3 H-deoxyglucose ( D, E ) and 14 C-hydroxybutyrate ( F, G ) by heart ( D, F ) and by BAT ( E, G ) was determined 15 min after intravenous administration ( n = 6 ). H Release of NEFA and glycerol from white adipose tissue explants isolated from mice fed a chow (control) or chow diet supplemented with norUDCA ( n = 3 ). I , Expression of lipogenic and lipolytic genes in white adipose tissues isolated from control and norUDCA-fed mice ( n = 7 ). J-K Indirect calorimetry was performed at room temperature in lipolysis-deficient ATGL-MHC and control mice fed a chow for 3 days followed by feeding a norUDCA-containing chow diet for 5 days ( n = 2-3 ). Consumption of O 2 ( J ) and production of CO 2 ( K ) are shown. L-N Indirect calorimetry was performed in wild type mice that were fed a low-carb diet or low-carb diet supplemented with norUDCA. Production of CO 2 ( L ), consumption of O 2 ( M ) and respiratory exchange ratio ( N ) were recorded at various housing temperatures as indicated by the red line ( n = 3 ). Error bars are shown as SEM. Statistical analysis was performed with one-way ANOVA ( A-G ), or Student's T-Test ( H–I ). ∗p < 0.05, ∗∗p < 0.01,∗∗∗p < 0.001.

Journal: Molecular Metabolism

Article Title: The conjugation-resistant bile acid norUDCA cures liver fibrosis but impairs systemic energy metabolism

doi: 10.1016/j.molmet.2026.102363

Figure Lengend Snippet: Lipolysis and ketone bodies compensate norUDCA-induced defects in energy homeostasis and thermogenesis. A-G Mice were fed a regular chow (control), or chow diet supplemented with norUDCA for 1 day, 3 days or 7 days with housing at room temperature. A-C Circulating levels of glucose ( A ), non esterified fatty acids (NEFA) ( B ), and ketone bodies ( C ) were determined ( n = 7 ). D-G , Uptake of 3 H-deoxyglucose ( D, E ) and 14 C-hydroxybutyrate ( F, G ) by heart ( D, F ) and by BAT ( E, G ) was determined 15 min after intravenous administration ( n = 6 ). H Release of NEFA and glycerol from white adipose tissue explants isolated from mice fed a chow (control) or chow diet supplemented with norUDCA ( n = 3 ). I , Expression of lipogenic and lipolytic genes in white adipose tissues isolated from control and norUDCA-fed mice ( n = 7 ). J-K Indirect calorimetry was performed at room temperature in lipolysis-deficient ATGL-MHC and control mice fed a chow for 3 days followed by feeding a norUDCA-containing chow diet for 5 days ( n = 2-3 ). Consumption of O 2 ( J ) and production of CO 2 ( K ) are shown. L-N Indirect calorimetry was performed in wild type mice that were fed a low-carb diet or low-carb diet supplemented with norUDCA. Production of CO 2 ( L ), consumption of O 2 ( M ) and respiratory exchange ratio ( N ) were recorded at various housing temperatures as indicated by the red line ( n = 3 ). Error bars are shown as SEM. Statistical analysis was performed with one-way ANOVA ( A-G ), or Student's T-Test ( H–I ). ∗p < 0.05, ∗∗p < 0.01,∗∗∗p < 0.001.

Article Snippet: Quantitative real-time PCR was performed on a QuantStudioTM 5 Real-Time PCR System using the following TaqMan® on-demand primer sets (Invitrogen): Acaca : Mm01304285_m1, Acly : Mm00652520_m1, Ccl2 : Mm00441242_m1, Ccl5 : Mm01302428_m1, Cd68 : Mm03047343_m1, Col1a1 : Mm00801666_g1, Cpt1 : Mm00550438_m1, Cxcl10 : Mm00445235_m1, Fasn : Mm00662319_m1, Il1b :Mm00434228_m1, Lipe : Mm00495359_m1, Lpl : Mm00434764_m1, Mmp12 : Mm00500554_m1, Mmp13 : Mm00439491_m1), Pdk4 : Mm00443325_m1, Pfkfb4 : Mm00557176_m1, Pnpla2 : Mm00503040_m1, Ppargc1a : Mm00447183_m1, Scd1 : Mm00772290_m1, Slc2a1 (encoding Glut1): Mm00441480_m1, Slc2a4 (encoding Glut4): Mm01245502_m1, Tbp : Mm00446973_m1, Timp1 : Mm00441818_m1, Tnfa : Mm00443258_m1). mRNA levels were normalized to the level of the housekeeping gene TATA-box binding protein ( Tbp ) mRNA, and the results were displayed as relative gene expression normalized to the experimental control group, following calculations using the 2-ΔΔCt method.

Techniques: Control, Isolation, Expressing