Lipotoxicity: when tissues overeat

By J. Schaffer. Current Opinion in Lipidology, 2003

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Hepatic lipotoxicity and the pathogenesis of nonalcoholic steatohepatitis: The central role of nontriglyceride fatty acid metabolites (2010, background): “Because fatty acids can be shuttled off to so many metabolic pathways, it has been difficult to prove whether free fatty acids or their metabolites are responsible for the cellular injury seen in lipotoxicity.(38) Saturated fatty acids can serve as activating ligands for toll-like receptor-4, leadin”
Lipolysis – A highly regulated multi-enzyme complex mediates the catabolism of cellular fat stores (2011, background): “Additionally, it compromises insulin signaling and cell function, a process which is often referred to as lipotoxicity [161].”
Adipose triglyceride lipase-mediated lipolysis of cellular fat stores is activated by CGI-58 and defective in Chanarin-Dorfman Syndrome. (2006, background): “Lipolytic activities in adipose tissue modulate the concentration of FFA in plasma, which, when chronically elevated, exert a lipotoxic effect on many nonadipose tissues (Schaffer, 2003; Unger, 2002) and contribute to the development of insulin resistance (Boden and Shulman, 2002).”