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Similarly, pharmacological inhibition of HSL and knockdown of PNPLA2 reduced the expression of known PPAR target genes in which LDs were shown to be a source of PPARα and PPARδ ligands that could be generated within minutes of stimulating lipolysis (3)

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β1, β2, and β3-ARs, which are coupled to G s , lead to activation of adenylyl cyclase, increasing levels of the second messenger cyclic AMP (cAMP) to promote Protein kinase A (PKA) activation (83) (Figure 2)