As fasting continues into early starvation and beyond, the kidney plays important roles. The kidney expresses the enzymes of gluconeogenesis, including glucose 6-phosphatase, and in late fasting about 50% of gluconeogenesis occurs here.
KIDNEY IN LONG-TERM FASTING
As fasting continues
into early starvation and beyond, the kidney plays important roles. The kidney
expresses the enzymes of gluconeogenesis, including glucose 6-phosphatase, and
in late fasting about 50% of gluconeogenesis occurs here. [Note: A portion of
this glucose is used by the kidney itself.] The kidney also provides
compensation for the acidosis that accompanies the increased production of
ketone bodies (organic acids). The glutamine released from the muscle’s
metabolism of BCAAs is taken up by the kidney and acted upon by renal
glutaminase and glutamate dehydrogenase, producing α-ketoglutarate that can be
used as a substrate for gluconeogenesis, plus ammonia (NH3). The NH3
picks up protons from ketone body dissociation and is excreted in the urine as
ammonium (NH4+), thereby decreasing the acid load in the body (Figure 24.18).
In long-term fasting, then, there is a switch from nitrogen disposal in the
form of urea to disposal in the form of ammonia. [Note: As ketone body
concentration rises, enterocytes, typically consumers of glutamine, become
consumers of ketone bodies. This allows more glutamine to be available to the kidney.]
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