Open AccessCD 36 is essential for endurance improvement, changes in whole‐body metabolism, and efficient PPAR ‐related transcriptional responses in the muscle with exercise training
Author(s) -
Manio Mark Christian C.,
Matsumura Shigenobu,
Masuda Daisaku,
Inoue Kazuo
Publication year - 2017
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.13282
Subject(s) - cd36 , downregulation and upregulation , peroxisome , beta oxidation , glycogen , endocrinology , peroxisome proliferator activated receptor , medicine , fatty acid metabolism , fatty acid , lipid metabolism , endurance training , biology , metabolism , receptor , chemistry , biochemistry , gene
Although circulating fatty acids are utilized as energy substrates, they also function as ligands to the peroxisome‐proliferator activated receptors ( PPAR s), a family of fatty acid sensing transcription factors. Exercise training leads to various adaptations in the muscle such as elevation of glycogen content, mitochondrial number as well as upregulation of fatty acid uptake and utilization through downstream transcriptional adaptations. In line with this, CD 36 has been shown to be critical in controlling fatty acid uptake and consequently, fatty acid oxidation. We show that exercise training could not ameliorate impaired endurance performance in CD 36 KO mice despite intact adaptations in muscle glycogen storage and mitochondrial function. Changes in whole‐body metabolism at rest and during exercise were also suppressed in these animals. Furthermore, there was inefficient upregulation of PPAR and PPAR ‐related exercise‐responsive genes with chronic training in CD 36 KO mice despite normal upregulation of Pgc1a and mitochondrial genes. Our findings supplement previous observations and emphasize the importance of CD 36 in endurance performance, energy production and efficient downstream transcriptional regulation by PPAR s.