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Fig. 1 | Journal of Translational Medicine

Fig. 1

From: Deficiency in interleukin-18 promotes differentiation of brown adipose tissue resulting in fat accumulation despite dyslipidemia

Fig. 1

Brown adipose precursor cells from Il18−/− mice differentiate much more than cells from Il18+/+ mice. a Histopathological analysis of differentiated BAs with Oil Red O staining. b, c The protein expression of differentiation and thermogenic markers in each group was compared. d The expression of lipolysis markers. e The expression of other molecules related to BA function in Il18−/− and Il18+/+ mice. Data are presented as mean ± SD (b–e; n = 3 per group), *p < 0.05. All experiments were repeated at least three times. Scale bars, 50 μm (a). ACTB: β-actin; Adrb3: adrenergic receptor β 3; ATGL: adipose triglyceride lipase; Cd36: cluster of differentiation 36; Cebpb: CCAAT/enhancer binding protein (C/EBP) beta; Dio2: type II iodothyronine deiodinase; Elovl3: elongation of very long chain fatty acids protein 3; FABP4: fatty acid-binding protein 4; FGF21: fibroblast growth factor 21; Lep: leptin; PGC1α: peroxisome proliferator-activated receptor γ coactivator 1-α; Pgc1b: peroxisome proliferator-activated receptor γ coactivator 1-β; pHSL563: phospho-HSL (Ser563); pHSL565: phospho-HSL (Ser565); PPARγ: peroxisome proliferator-activated receptor γ; PRDM16: PR domain containing 16; UCP1: uncoupling protein 1; Ucp3: uncoupling protein 3

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