Data on triiodothyronine treated peroxisome proliferator-activated receptor-alpha-null mouse hearts using magnetic resonance imaging and magnetic resonance spectroscopy

This data contain left ventricular end-diastolic volumes, end-systolic volumes, stroke volumes, ejection fractions, cardiac outputs, heart rates, phosphocreatine concentrations, adenosine 5’-triphosphate (ATP) concentrations, total creatine concentrations, citrate synthase activities and heart weights for wild-type and peroxisome proliferator-activated receptor-alpha-null mouse hearts without and with triiodothyronine treatment.


a b s t r a c t
This data contain left ventricular end-diastolic volumes, end-systolic volumes, stroke volumes, ejection fractions, cardiac outputs, heart rates, phosphocreatine concentrations, adenosine 5'-triphosphate (ATP) concentrations, total creatine concentrations, citrate synthase activities and heart weights for wild-type and peroxisome proliferator-activated receptor-alpha-null mouse hearts without and with triiodothyronine treatment.

Value of the Data
The data can be used to further investigate whether the cross-talk between peroxisome proliferator-activated receptor-alpha and triiodothyronine signaling pathways in vitro happens in hearts in vivo.
The data can be used to investigate how peroxisome proliferator-activated receptor-alpha and triiodothyronine regulate mitochondrial contents in hearts.
The data can be used to investigate the role of peroxisome proliferator-activated receptor-alpha in left ventricular dysfunction in human non-alcoholic fatty liver disease and in pharmaceutical area.

Data
Triiodothyronine treatment causes abnormal decrease of left ventricular stroke volumes, phosphocreatine concentrations and ATP concentrations associated with abnormal increase of heart weights and citrate synthase activities in peroxisome proliferator-activated receptor-alpha-null mouse hearts (Fig. 1).

Acknowledgments
Wen Zhang acknowledges Clarendon Scholarships from University of Oxford and Hong Kong Oxford Scholarship for supporting her DPhil studies.

Funding resources
This work is part of Wen Zhang's DPhil thesis and was supported by the British Heart Foundation (grant reference PG/07/030/22667).

Transparency document. Supporting information
Transparency data associated with this article can be found in the online version at https://doi.org/ 10.1016/j.dib.2018.08.009.