Limits...
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

Effect of HFD on bws and fasting blood glucose levels in mice. WT and SIRT3 KO mice were fed a HFD and ND for 16 weeks. (A) Body weight curves over 16 weeks are shown. Values are shown as mean ± SD, n = 10 mice per group. PI ≤ 0.01; **P ≤ 0.01 WT-ND versus WT-HFD; ##P ≤ 0.01 WT-HFD versus WT-ND, KO-HFD versus KO-ND, and WT-HFD versus KO-HFD. (B) Blood glucose measurements were made in WT and SIRT3 KO mice fasted for 24 hrs. Measurements were made in individual mice on ND and following 16 weeks of HFD (10 mice per group).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4549035&req=5

fig04: Effect of HFD on bws and fasting blood glucose levels in mice. WT and SIRT3 KO mice were fed a HFD and ND for 16 weeks. (A) Body weight curves over 16 weeks are shown. Values are shown as mean ± SD, n = 10 mice per group. PI ≤ 0.01; **P ≤ 0.01 WT-ND versus WT-HFD; ##P ≤ 0.01 WT-HFD versus WT-ND, KO-HFD versus KO-ND, and WT-HFD versus KO-HFD. (B) Blood glucose measurements were made in WT and SIRT3 KO mice fasted for 24 hrs. Measurements were made in individual mice on ND and following 16 weeks of HFD (10 mice per group).

Mentions: A diet of 60% fat caused a notable increase in bw in WT mice over the course of 16 weeks (Fig.4A). Body weight increased as well in SIRT3 KO mice on HFD, although to a lesser degree (PI ≤ 0.01). In contrast, others reported that feeding SIRT3 KO mice a so-called Western diet of high fat (42% kcal) and high carbohydrate (42.7% kcal), more than 2× the carbohydrate content of our diet, accelerated obesity and led to development of the metabolic syndrome 9. Mitochondrial dysfunction at basal conditions in SIRT3 KO may explain why SIRT3 KO mice gained less bw with HFD (mitochondrial stress) than WT mice as fatty acid oxidation would be more prominent in our study. No difference was seen over the 16 weeks in bw between WT and SIRT3 KO mice fed ND. Neither HFD nor SIRT3 KO induced diabetes. Fasting glucose levels were not increased in either WT or SIRT3 KO mice on HFD compared to ND (Fig.4B). Others have noted that the ability of HFD to induce diabetes in mice is strain-dependent 10. Of note, SIRT3 KO mice exhibited significantly lower fasting blood glucose levels than WT mice on the same diet (P ≤ 0.01); lower blood glucose levels may explain as well why SIRT3 KO mice gained less weight with HFD than WT mice.


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)

Effect of HFD on bws and fasting blood glucose levels in mice. WT and SIRT3 KO mice were fed a HFD and ND for 16 weeks. (A) Body weight curves over 16 weeks are shown. Values are shown as mean ± SD, n = 10 mice per group. PI ≤ 0.01; **P ≤ 0.01 WT-ND versus WT-HFD; ##P ≤ 0.01 WT-HFD versus WT-ND, KO-HFD versus KO-ND, and WT-HFD versus KO-HFD. (B) Blood glucose measurements were made in WT and SIRT3 KO mice fasted for 24 hrs. Measurements were made in individual mice on ND and following 16 weeks of HFD (10 mice per group).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig04: Effect of HFD on bws and fasting blood glucose levels in mice. WT and SIRT3 KO mice were fed a HFD and ND for 16 weeks. (A) Body weight curves over 16 weeks are shown. Values are shown as mean ± SD, n = 10 mice per group. PI ≤ 0.01; **P ≤ 0.01 WT-ND versus WT-HFD; ##P ≤ 0.01 WT-HFD versus WT-ND, KO-HFD versus KO-ND, and WT-HFD versus KO-HFD. (B) Blood glucose measurements were made in WT and SIRT3 KO mice fasted for 24 hrs. Measurements were made in individual mice on ND and following 16 weeks of HFD (10 mice per group).
Mentions: A diet of 60% fat caused a notable increase in bw in WT mice over the course of 16 weeks (Fig.4A). Body weight increased as well in SIRT3 KO mice on HFD, although to a lesser degree (PI ≤ 0.01). In contrast, others reported that feeding SIRT3 KO mice a so-called Western diet of high fat (42% kcal) and high carbohydrate (42.7% kcal), more than 2× the carbohydrate content of our diet, accelerated obesity and led to development of the metabolic syndrome 9. Mitochondrial dysfunction at basal conditions in SIRT3 KO may explain why SIRT3 KO mice gained less bw with HFD (mitochondrial stress) than WT mice as fatty acid oxidation would be more prominent in our study. No difference was seen over the 16 weeks in bw between WT and SIRT3 KO mice fed ND. Neither HFD nor SIRT3 KO induced diabetes. Fasting glucose levels were not increased in either WT or SIRT3 KO mice on HFD compared to ND (Fig.4B). Others have noted that the ability of HFD to induce diabetes in mice is strain-dependent 10. Of note, SIRT3 KO mice exhibited significantly lower fasting blood glucose levels than WT mice on the same diet (P ≤ 0.01); lower blood glucose levels may explain as well why SIRT3 KO mice gained less weight with HFD than WT mice.

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