Premium
Rosmarinic Acid Mediates Mitochondrial Biogenesis in Insulin Resistant Skeletal Muscle Through Activation of AMPK
Author(s) -
Jayanthy Govindaraj,
Roshana Devi Vellai,
Ilango Kaliappan,
Subramanian Sorimuthu Pillai
Publication year - 2017
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.25869
Subject(s) - mitochondrial biogenesis , skeletal muscle , insulin resistance , ampk , tfam , medicine , endocrinology , glucose uptake , insulin , chemistry , myogenesis , mitochondrion , microbiology and biotechnology , biology , phosphorylation , protein kinase a
Rosmarinic acid (RA), a polyphenol, is known to improve hepatic insulin sensitivity in experimental type 2 diabetes. However, its effect on skeletal muscle insulin resistance is meagerly understood. The present study was aimed to investigate the up‐ and downstream mediators of the molecular targets of RA in attenuating insulin resistance in the skeletal muscle both in vivo and in vitro. We found that supplementation of RA increased the expression of key genes involved in the mitochondrial biogenesis like PGC‐1α, SIRT‐1, and TFAM via activation of AMPK in the skeletal muscle of insulin resistant rats as well as in L6 myotubes. Further, RA treatment increased the glucose uptake and decreased the phosphorylation of serine IRS‐1 while increasing the translocation of GLUT 4. Together, our findings evidenced that RA treatment significantly inhibit insulin resistance in skeletal muscle cells by enhancing mitochondrial biogenesis. J. Cell. Biochem. 118: 1839–1848, 2017. © 2017 Wiley Periodicals, Inc.