During the postabsorptive phase A

muscles release mainly Gln and Ala. The gastrointestinal tract, too, absorbs Gln, releasing Ala and cirtulline in turn. All AA are absorbed by the liver, the N released as ammonia, and the carbon skeleton processed for further use.

Acidosis causes inhibition of hepatic Gln uptake. The kidneys then pick up Gln and convert it to ammonia, which combines with H+ ions that need to be excreted, forming NH4+. All H+ ions that need to be excreted due to acidosis are removed in this form. The AA Arg and Leu stimulate insulin secretion, others (e. g., Asn, Gly) stimulate glucagon secretion. Insulin enhances muscle protein synthesis, while glucagon enhances gluconeogenesis from AA in the liver. Since both hormones are, therefore, stimulated post-prandially, their concerted effects contribute significantly to the effective reduction of plasma AA concentrations after influx from the intestine.

The liver eliminates most of the N (B). Under physiological conditions, only small amounts of it are excreted by the kidneys as NH4+. Ammonia produced during cellular AA breakdown is transported as Gln. In the liver, all the NH4+ derived from AA degradation is converted to urea at a high energy cost. The body uses this somewhat wasteful urea cycle since urea has several distinct advantages over ammonia: it is relatively nontoxic and highly water-soluble, and can therefore easily be transported to the kidneys via the bloodstream for excretion.

Amino Acid Homeostasis 127

A. Postabsorptive Amino Acid Metabolism

Amino Acid Homeostasis 127

A. Postabsorptive Amino Acid Metabolism

Postabsorptive Phase
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