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Postabsorptive (fasting) state
Body_ID: HC020031
In the clinical jargon the postabsorptive state is often referred to as 'fasting'. During the postabsorptive state, glucoseView drug information metabolism approaches a steady state (i.e. hepatic glucoseView drug information production, largely from glycogenolysis, equals its tissue uptake). After an overnight fast, insulin secretion decreases and glucagon secretion increases. This leads to a decrease in glycogen synthesis and to an increase in glycogenolysis (Fig. 20.12); the liver gradually becomes a glucose-producing organ.
Body_ID: P020041
In the postabsorptive state, approximately 80% of all glucoseView drug information is taken up by insulin-independent tissues. Of this, 50% goes to the brain and 20% to the erythrocytes. In the postabsorptive state insulin-dependent tissues use little glucoseView drug information - muscle and adipose tissue together are responsible for just about 20% of total glucoseView drug information utilization.
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After a 12h fast, 65-75% of endogenous glucoseView drug information is derived from glycogen, and the rest from gluconeogenesis. The contribution of gluconeogenesis, however, increases. Muscle releases lactate which, after being oxidized to pyruvate, enters gluconeogenesis. GlucoseView drug information that is formed returns to the skeletal muscle; this is known as the Cori cycle. Low insulin level also stimulates proteolysis. The two main amino acidsView drug information released from muscle are alanine and glutamine. A cycle analogous to the Cori cycle, involving alanine, operates between muscle and the liver: it is known as the glucose-alanine cycle. Alanine released from muscle enters gluconeogenesis in the liver after being converted to pyruvate (Fig. 20.13).
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Glucagon activates lipolysis in adipose tissue
Body_ID: HC020033
In the liver, glucagon stimulates lipolysis by acting on hormone-sensitive lipase. This releases glycerol, the third major gluconeogenic substrate, and provides free fatty acids for energy metabolism in muscle. Activation of lipolysis in the liver secondarily stimulates ketogenesis from acetyl-CoA, yielding acetoacetate, hydroxybutyrate, and the product of spontaneous decarboxylation of acetoacetate, acetone. The three metabolites are known as ketone bodies and are oxidized in heart and skeletal muscle.
Body_ID: P020044
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