Fig 1: Modelling analysis with stepwise selection for peak fatty acid oxidation rate during fasted, incremental cycling (PFO), mean fatty acid oxidation during the first 30 min of prolonged, fed-state cycling (early FO), and mean fatty acid oxidation during 90–120 min of prolonged, fed-state cycling (late FO). Fitted model values compared with measured values are shown in (A), (C), and (E). Standardised coefficients with 95% confidence intervals are shown in (B), (D), and (F). Adj R2, Adjusted R2 value; CD36, cluster of differentiation 36/SR-B3 (previously SR-B2); CPT1, carnitine palmitoyltransferase 1; EE, energy expenditure; FABPpm, fatty acid binding protein plasma membrane; FATP1, fatty acid transport protein 1; FATP4, fatty acid transport protein 4; RMSE, root mean square error
Fig 2: Bivariate correlations between the peak fatty acid oxidation rate (PFO) measured during fasted, incremental cycling, fatty acid oxidation during the first 30 min of prolonged, fed-state cycling (early FO), and 90–120 min of prolonged, fed-state cycling (late FO) and vastus lateralis carnitine palmitoyltransferase 1 (CPT1), carnitine palmitoyltransferase 2 (CPT2), fatty acid binding protein 1 (FABPpm), cluster of differentiation 36 (CD36), fatty acid transporter 1 (FATP1), and fatty acid transport 4 (FATP4). Circles denote Pearson’s correlation coefficient, and triangles ‘?’ denote Spearman’s rank-order correlation coefficient, with 95% confidence intervals shown by the solid lines. Colours denote statistical significance (P < 0.05)
Fig 3: Schematic model of proteins involved in fatty acid transport in skeletal muscle. CD36, cluster of differentiation 36/SR-B3 (previously SR-B2); CPT1, carnitine palmitoyltransferase 1; CPT2, carnitine palmitoyltransferase 2; FABPpm, fatty acid binding protein plasma membrane, plasma membrane; FATP1, fatty acid transport protein 1; FATP4, fatty acid transport protein 4, FATP4; TCA, tricarboxylic acid. We acknowledge that the specific localisation of FATP1 is debated [14, 15, 48]
Fig 4: Atomoxetine and fluoxetine treatment induce mitochondrial CPT1 activity in SH-SY5Y (A, B) and U-87 MG (C, D) cell lines. Representative western blots of mitochondrial and cytosol fractions of SH-SY5Y (A) and U-87 MG (C) cells treated with 5 µg/mL atomoxetine and 5 µg/mL fluoxetine for 60 min. Measure of intracellular activity of CPT1 in mitochondrial and cytosol fractions of SH-SY5Y (B) and U-87 MG (D) cells treated with 5 µg/mL atomoxetine and 5 µg/mL fluoxetine for 30 min. Values are presented as means±SEM (N=3, *p<0.05; **p<0.01). C, vehicle control; A, atomoxetine; F, fluoxetine; CPT, carnitine palmitoyl transferase; SEM, standard error of the mean.
Fig 5: Proposed metabolic model for atomoxetine and fluoxetine effect on AMPK-ACC-CPT1 pathway in human SH-SY5Y and U-87 MG Cells. AMPK, adenosine monophosphate-activated protein kinase; ACC, acetyl-CoA carboxylase; CPT1, carnitine palmitoyl transferase 1; CaMKK, calcium/calmodulin-dependent kinase kinase; CoA, coenzyme A.
Supplier Page from MyBioSource.com for Human Carnitine palmitoyltransferase I ELISA Kit