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The role of CaMKII activation in the regulation of carnitine palmitoyl transferase and lipid oxidation in rats muscle
Author(s) -
Mukwevho Emmanuel
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb667
Subject(s) - carnitine , chemistry , skeletal muscle , medicine , endocrinology , beta oxidation , lipid metabolism , gastrocnemius muscle , insulin resistance , fatty acid , downregulation and upregulation , metabolism , biochemistry , insulin , biology , gene
The mismatch between high fatty acids supply and mitochondrial fatty acid oxidation in skeletal muscle has been associated with insulin resistance, the hallmark of type II diabetes (Holloway et al., 2009). In this study we wanted to investigate the role of CaMKII activation in the reduction of lipids and whether carnitine palmitoyl transferase (CPT)‐1, the rate limiting step oxidation was involved. Improved mitochondrial fatty acid oxidation is seen as a crucial step in the reduction of lipids that interferes with insulin signaling pathway. In this study, male Wistar rats were used. The exercise regime was designed for 5 days, where each session per day was 5 × 12 min with 3 minutes rests, after which gastrocnemius muscle was excised after 18h of the 5 th day. Using GC‐MS (Gas chromatography mass spectroscopy) with flame ionization detector (FID), we found that CaMKII activation resulted in significant reduction in total lipid content. When KN93 (CaMKII inhibitor) was injected in the muscle prior exercise, the content of lipid was significantly higher than of muscle of the exercised rat without KN93, however similar to that of non‐exercised rat muscle. Exercise also resulted in increased CPT‐1 protein content whereas inclusion of KN93 prior exercise significantly altered the observed CPT‐1 upregulation. These observations indicate that CaMKII plays a significant role in lipid oxidation metabolism.