Key result
Digoxin reduces cardiac lipid deposition in diabetic rats via calcium-triggered signals regulating fatty acid oxidation.
Why the study?
The mediation of PPARδ in lipid metabolism improvement by digoxin in the heart of diabetic rats and hyperglycemia-treated cardiomyocytes was not fully understood.
Digoxin improves lipid metabolism in the diabetic rat heart by upregulating PPARδ and fatty acid oxidation genes through calcium-dependent signaling.
Should not alter clinical practice; hypothesis-generating for PPARδ-targeted effects of digoxin in diabetic cardiomyopathy.
Increase of peroxisome proliferator-activated receptor δ (PPARδ) expression by digoxin in the heart of diabetic rats has been documented. The present study investigated the mediation of PPARδ in lipid metabolism improved by digoxin in the heart of diabetic rats and in the hyperglycemia-treated cardiomyocytes using the primary cultured cardiomyocytes from neonatal rat. The lipid deposition within the heart section was assessed in diabetic rats by oil red O staining. The fatty acid oxidation genes in cardiomyocytes were also examined. Inhibitor of calcium ions and siRNA-PPARδ were employed to investigate the potential mechanisms. After a 20-day digoxin treatment, the PPARδ expression was elevated in hearts of diabetic rats while the cardiac lipid deposition was reduced. In neonatal cardiomyocytes, digoxin also caused an increase in expressions of PPARδ and fatty acid oxidation genes. But both actions of digoxin were blocked by BAPTA-AM to chelate calcium ions and by siRNA-PPARδ in cardiomyocytes. The obtained results show that increase of PPARδ by digoxin is related to regulation of fatty acid oxidation genes in cardiac cells mediated by calcium-triggered signals.
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Chen et al. (2012) studied Diabetic rats and hyperglycemia-treated cardiomyocytes. Digoxin was evaluated on PPARδ expression and cardiac lipid deposition. A 20-day digoxin treatment elevated PPARδ expression and reduced cardiac lipid deposition in diabetic rats, mediated by calcium-triggered signals regulating fatty acid oxidation.
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