| First Author | Benziane B | Year | 2017 |
| Journal | J Lipid Res | Volume | 58 |
| Issue | 12 | Pages | 2324-2333 |
| PubMed ID | 29066466 | Mgi Jnum | J:256898 |
| Mgi Id | MGI:6098771 | Doi | 10.1194/jlr.M079723 |
| Citation | Benziane B, et al. (2017) DGKzeta deficiency protects against peripheral insulin resistance and improves energy metabolism. J Lipid Res 58(12):2324-2333 |
| abstractText | Diacylglycerol kinases (DGKs) regulate the balance between diacylglycerol (DAG) and phosphatidic acid. DGKzeta is highly abundant in skeletal muscle and induces fiber hypertrophy. We hypothesized that DGKzeta influences functional and metabolic adaptations in skeletal muscle and whole-body fuel utilization. DAG content was increased in skeletal muscle and adipose tissue, but unaltered in liver of DGKzeta KO mice. Linear growth, body weight, fat mass, and lean mass were reduced in DGKzeta KO versus wild-type mice. Conversely, male DGKzeta KO and wild-type mice displayed a similar robust increase in plantaris weight after functional overload, suggesting that DGKzeta is dispensable for muscle hypertrophy. Although glucose tolerance was similar, insulin levels were reduced in high-fat diet (HFD)-fed DGKzeta KO versus wild-type mice. Submaximal insulin-stimulated glucose transport and p-Akt Ser(473) were increased, suggesting enhanced skeletal muscle insulin sensitivity. Energy homeostasis was altered in DGKzeta KO mice, as evidenced by an elevated respiratory exchange ratio, independent of altered physical activity or food intake. In conclusion, DGKzeta deficiency increases tissue DAG content and leads to modest growth retardation, reduced adiposity, and protection against insulin resistance. DGKzeta plays a role in the control of growth and metabolic processes, further highlighting specialized functions of DGK isoforms in type 2 diabetes pathophysiology. |
