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. 2012 Mar 7;15(3):279–291. doi: 10.1016/j.cmet.2011.12.018

Figure 1.

Figure 1

Lipolysis in Adipose and Oxidative Tissues during Fasting

In adipose tissues, beta-adrenergic stimulation of lipolysis leads to the consecutive hydrolysis of TG and the formation of FAs and glycerol. The process requires three enzymes: ATGL cleaves the first esterbond in TGs, HSL hydrolyzes DGs, and MGL MGs. For full hydrolytic activity, ATGL interacts with its coactivator protein CGI-58, whereas HSL is phosphorylated, translocates to the LD, and interacts with phosphorylated PLIN-1. Expression of the ATGL inhibitor G0S2 during fasting is low in adipose and high in oxidative tissues (e.g., liver). In oxidative tissues PLIN-1 is not present on LDs. Instead, PLIN-5 is expressed and interacts with both ATGL and CGI-58, facilitating LD localization of these proteins. ATGL, adipose triglyceride lipase; CGI-58, comparative gene identification-58; DG, diacylglycerol; FA, fatty acid; G, glycerol; G0S2, G0/G1 switch gene 2; HSL, hormone-sensitive lipase; MG, monoacylglycerol; MGL, monoglyceride lipase; PLIN-1, perilipin-1; PLIN-5, perilipin-5; TG, triacylglycerol.