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This in turn leads to the increased oxidation of fatty acids in other tissues such as muscle and liver. In the liver, the net result (due to increased acetyl-CoA levels) is the production of ketone bodies (see below). This would occur under conditions in which the carbohydrate stores and gluconeogenic precursors available in the liver are not sufficient to allow increased glucose production. The increased levels of fatty acid omega 3 fat that become available omega 3 fat in response to glucagon or epinephrine are assured of being completely oxidized, because PKA also phosphorylates ACC; the synthesis omega 3 fat of fatty acid is thereby inhibited. Insulin has the opposite effect to glucagon and epinephrine: it increases the synthesis of triacylglycerols (and glycogen). One of the many effects of insulin is to lower cAMP levels, which leads to increased dephosphorylation through the enhanced activity of protein phosphatases such as PP-1.
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