The Reaction OfAdipose Tissue During the Postabsorptive Phase Is to Mobilize Fatty Acids
Fatty acids are released from adipose tissue because of the action of the phosphorylation-stimulated enzyme Iwrnione- sensitive lipase (HSL). This enzyme is stimulated by the relative lack of insulin in the postabsorptive period; insulin suppresses the action of HSL by promoting its dephosphorylation.
Glucagon may have some adipose tissue activity in promoting triglyceride breakdown by stimulating the phosphorylation and activation of HSL. More likely, however, glucagon’s effects are restricted to the liver, and the normal stimulation of HSL comes from epinephrine or norepinephrine; norepinephrine originates from sympathetic nerves in the adipose tissue. The exact means by which sympathetic nerve activity in adipose tissue is coordinated with body fuel availability is not well established, but the catecholamine hormones and neuroregulators appear to be the primary positive stimulus for breakdown of adipose triglyceride. However, the negative stimulus provided by the absence of insulin may be the most important regulator of adipose fat mobilization.Stimulation of HSL in the postabsorptive state leads to the release of fatty acids from adipose tissue into the blood. Fatty acids in blood are reversibly bound to albumin because they are not otherwise soluble in water. Albuminbound fatty acids in blood are usually referred to as Iionesterified fatty acids (NEFAs) to distinguish them from triglyceride fatty acids in chylomicrons and lipoproteins. NEFAs in blood may be used directly for energy by many tissues. However, many NEFAs are taken up by the liver and used for either ketone body production or VLDL synthesis, as discussed in the next section.