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Fig. 8 | Cell & Bioscience

Fig. 8

From: WRN loss accelerates abnormal adipocyte metabolism in Werner syndrome

Fig. 8

Nicotinamide riboside (NR) normalizes metabolism in WRN KO adipocytes. a–h qTR-PCR analysis of selected adipogenic genes PPARγ (a), CEBPα (b), UCP1 (c), PGC (d), FABP4 (e), ADIPQ (f), ACACA (g), and ELOVL 6 (h) among WT, WRN KO (veh), and WRN KO (NR) in hMSCs (N = 3 biological replicates). i–l qTR-PCR analysis of selected adipogenic circadian genes RORB (i), CYP1B1 (j), ME1 (k), and LAMA2 (l) among WT, WRN KO (veh), and WRN KO (NR) (N = 3 biological replicates). m–p qTR-PCR analysis of selected adipogenic circadian genes pparγ (m), cebpα (n), per1a (o), and rorb (p) among wildtype, wrn−/− mutant zebrafish (veh), and wrn−/− mutant zebrafish (NR) (N = 3 biological replicates). q, r qTR-PCR analysis of SMARCA5 on day 1 (q) and day 5 (r) during adipogenesis (N = 3 biological replicates). s qTR-PCR analysis of SIRT1 on day 5 during adipogenesis (N = 3 biological replicates). t qTR-PCR analysis of sirt1 at 2 dpf, 4 dpf, and 14 dpf in zebrafish (N = 3 biological replicates). Data are presented as the mean ± S.D. Statistical analysis was performed using two-tailed unpaired Student’s t-test. *P < 0.05, **P < 0.01, ***P < 0.001

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