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High-fat diet induces cardiac remodelling and dysfunction: assessment of the role played by SIRT3 loss.

Zeng H, Vaka VR, He X, Booz GW, Chen JX - J. Cell. Mol. Med. (2015)

Bottom Line: HFD resulted in a significant reduction in SIRT3 expression in the heart.SIRT3 KO mice fed HFD showed greater ROS production and a further reduction in cardiac function compared to SIRT3 KO mice on ND.However, HFD did not further reduce capillary density in SIRT3 KO hearts, implicating SIRT3 loss in HFD-induced capillary rarefaction.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology and Toxicology, The University of Mississippi Medical Center, School of Medicine, Jackson, MS, USA.

No MeSH data available.


Related in: MedlinePlus

Accumulation of lipids in hearts of mice fed HFD. Ventricular slices were stained for lipids using Oil Red O. Representative images are shown for hearts from WT mice fed (A) ND, or (B) HFD and SIRT3 KO mice fed a (C) ND or (D) HFD.
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fig02: Accumulation of lipids in hearts of mice fed HFD. Ventricular slices were stained for lipids using Oil Red O. Representative images are shown for hearts from WT mice fed (A) ND, or (B) HFD and SIRT3 KO mice fed a (C) ND or (D) HFD.

Mentions: Feeding mice a HFD for 16 weeks lead to an accumulation of lipids in the hearts of both WT and SIRT3 KO mice (Fig.2). In addition, hearts from mice fed with HFD for 16 weeks exhibited a significant increase in DHE staining, indicating increased ROS levels, compared to mice fed with ND (Fig.3A and B). There was a trend towards increased ROS levels in hearts of SIRT3 KO mice on ND compared to WT mice on ND, but this did not reach significance. However, SIRT3 KO mice fed HFD exhibited a significant increase in DHE staining in the heart (Fig.3A and B). No interaction was observed between HFD and SIRT3 loss on ROS formation in the heart; however, the consequences of HFD on oxidative stress in the heart were enhanced by SIRT3 loss.


High-fat diet induces cardiac remodelling and dysfunction: assessment of the role played by SIRT3 loss.

Zeng H, Vaka VR, He X, Booz GW, Chen JX - J. Cell. Mol. Med. (2015)

Accumulation of lipids in hearts of mice fed HFD. Ventricular slices were stained for lipids using Oil Red O. Representative images are shown for hearts from WT mice fed (A) ND, or (B) HFD and SIRT3 KO mice fed a (C) ND or (D) HFD.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4549035&req=5

fig02: Accumulation of lipids in hearts of mice fed HFD. Ventricular slices were stained for lipids using Oil Red O. Representative images are shown for hearts from WT mice fed (A) ND, or (B) HFD and SIRT3 KO mice fed a (C) ND or (D) HFD.
Mentions: Feeding mice a HFD for 16 weeks lead to an accumulation of lipids in the hearts of both WT and SIRT3 KO mice (Fig.2). In addition, hearts from mice fed with HFD for 16 weeks exhibited a significant increase in DHE staining, indicating increased ROS levels, compared to mice fed with ND (Fig.3A and B). There was a trend towards increased ROS levels in hearts of SIRT3 KO mice on ND compared to WT mice on ND, but this did not reach significance. However, SIRT3 KO mice fed HFD exhibited a significant increase in DHE staining in the heart (Fig.3A and B). No interaction was observed between HFD and SIRT3 loss on ROS formation in the heart; however, the consequences of HFD on oxidative stress in the heart were enhanced by SIRT3 loss.

Bottom Line: HFD resulted in a significant reduction in SIRT3 expression in the heart.SIRT3 KO mice fed HFD showed greater ROS production and a further reduction in cardiac function compared to SIRT3 KO mice on ND.However, HFD did not further reduce capillary density in SIRT3 KO hearts, implicating SIRT3 loss in HFD-induced capillary rarefaction.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology and Toxicology, The University of Mississippi Medical Center, School of Medicine, Jackson, MS, USA.

No MeSH data available.


Related in: MedlinePlus