De novo lipogenesis (DNL), the synthesis of saturated and monounsaturated fatty acids from acetyl-CoA, occurs in most, if not all mammalian cell types. The liver and the adipose tissue are the major sites of DNL where excess nutrients are converted into DNL-derived fatty acids that then become the energy supply of other organs or are stored as triglycerides. DNL in the adipose tissue has been studied to a lesser extent than hepatic DNL. Similar to hepatic DNL, it appears that insulin and a systemic surplus of monosaccharides are powerful stimulants of DNL in white and brown adipose tissue. Although DNL in the liver and adipose tissues share regulatory mechanisms, adipose tissue DNL appears to be a marker of metabolic health whereas hepatic DNL often is increased in unfavorable metabolic states. Here we will discuss mechanisms orchestrating DNL in WAT and BAT and in the liver in physiology and the dysregulation of DNL in obesity and related disorders. We will also review several bioactive lipids that are products of adipose tissue DNL and their role in metabolic health.
|Title of host publication||Hepatic De Novo Lipogenesis and Regulation of Metabolism|
|Publisher||Springer International Publishing|
|Number of pages||17|
|State||Published - 1 Jan 2015|