Key result
Angiopoietin-like 4 (Angptl4) stimulates intracellular adipocyte lipolysis and cAMP-dependent PKA signaling, in addition to its known ability to inhibit lipoprotein lipase.
Angptl4 is identified as a novel stimulator of intracellular adipocyte lipolysis via cAMP-dependent PKA signaling, in addition to its known role in inhibiting lipoprotein lipase.
Hypothesis-generating in adipocytes; leaves open Angptl4's relevance to human lipid disorders or cardiovascular risk.
Angiopoietin-like 4 (Angptl4) is a secreted protein modulating triacylglycerol homeostasis. Its transcription is induced by glucocorticoids, which act to elevate circulating Angptl4 levels during fasting. In investigating the role of Angptl4 in glucocorticoid action, we identified that in addition to its known ability to inhibit lipoprotein lipase, Angptl4 stimulates intracellular adipocyte lipolysis. Fatty acid release by murine adipocytes following fasting or treatment with glucocorticoids or catecholamines is highly Angptl4-dependent. In fact, Angptl4 can directly stimulate cAMP-dependent PKA signaling and lipolysis when added to adipocytes. Here, we detail this novel Angptl4-dependent lipolytic regulatory mechanism and discuss its physiological and therapeutic implications.
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Koliwad et al. (2012) conducted a review in Triacylglycerol homeostasis. Angiopoietin-like 4 (Angptl4) was evaluated. Angiopoietin-like 4 (Angptl4) stimulates intracellular adipocyte lipolysis and cAMP-dependent PKA signaling, in addition to its known ability to inhibit lipoprotein lipase.
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