Fig. 7: The effect and mechanism of FGF21 on diabetes-induced lipid accumulation in the heart. | Cell Death & Disease

Fig. 7: The effect and mechanism of FGF21 on diabetes-induced lipid accumulation in the heart.

From: Fibroblast growth factor-21 prevents diabetic cardiomyopathy via AMPK-mediated antioxidation and lipid-lowering effects in the heart

Fig. 7

The slices of the heart from both WT and FGF21-KO mice were used for oil-O-red staining to evaluate lipid accumulation in the myocardium (a). Meanwhile, triglyceride levels of both the heart and plasma were examined by ELISA (b, c). Cardiac tissue was used for measuring ACC phosphorylation (d) and CPT-1 expression (e) by western blot to evaluate the activity of fatty acid β-oxidation pathway. Primary cardiomyocytes from AMPK-knockdown study were collected for detecting triglyceride by ELISA assay (f), as well as ACC phosphorylation (g) and CPT-1 expression (h) by western blot assay. Fatty acid β-oxidation inhibitor (TMZ) was used to identify the role of AMPK-mediated β-oxidation in FGF21-induced cardiomyocyte protection by detecting cleaved-caspase-3 level (i), ANP (j), and CTGF expressions (k) by western blot. For in vivo study (a−e), data are presented as means ± SD, n = 8/group. *P < 0.05 vs. the Con group in WT mice; #P < 0.05 vs. the DM group in WT mice; @P < 0.05 vs. the Con group in FGF21-KO mice; &P < 0.05 vs. the DM group in FGF21-KO mice. For in vitro study (f−h), data were collected from at least three independent experiments and presented as mean ± SD. *P < 0.05 vs. control in the Con-siRNA group; #P < 0.05 vs. HG/Pal in the Con-siRNA group; @P < 0.05 vs. control in the AMPK-siRNA group; #P < 0.05 vs. HG/Pal in the AMPK-siRNA group. For in vitro study (i−k), data were collected from at least three independent experiments and presented as mean ± SD. *P < 0.05 vs. control; #P < 0.05 vs. HG/Pal; $P < 0.05 vs. HG/Pal/FGF21

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