The mitochondrial DNA copy number and the citrate synthase activity have been studied in rat model of nonalcoholic fatty liver disease induced by a high-fat plus fructose (HF-F) diet which mimics a typical unhealthy Western diet. Rats treated by adding dehydroepiandrosterone (DHEA) to the diet were also studied to investigate on the protective effects of DHEA, a compound of physiological origin with multitargeted antioxidant properties. An HF-F diet, fortified or not with DHEA (0.01%, w/w), was administered for 15 weeks to male Wistar rats. After HF-F the rat liver showed a decrease of mtDNA content and of citrate synthase activity probably as results of oxidative stress. The addition of DHEA to the diet restored the activity of citrate synthase whereas it was unable to prevent the loss of mtDNA.

Mitochondrial DNA copy number and citrate synthase activity in nonalcoholic fatty liver disease induced in rats by a high-fat plus fructose diet fortified or not with dehydroepiandrosterone(DHEA)

LEZZA, Angela Maria Serena;PESCE, VITO;
2009-01-01

Abstract

The mitochondrial DNA copy number and the citrate synthase activity have been studied in rat model of nonalcoholic fatty liver disease induced by a high-fat plus fructose (HF-F) diet which mimics a typical unhealthy Western diet. Rats treated by adding dehydroepiandrosterone (DHEA) to the diet were also studied to investigate on the protective effects of DHEA, a compound of physiological origin with multitargeted antioxidant properties. An HF-F diet, fortified or not with DHEA (0.01%, w/w), was administered for 15 weeks to male Wistar rats. After HF-F the rat liver showed a decrease of mtDNA content and of citrate synthase activity probably as results of oxidative stress. The addition of DHEA to the diet restored the activity of citrate synthase whereas it was unable to prevent the loss of mtDNA.
2009
978-960-474-141-0
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11586/19026
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