CLINICAL CASES
331
FA + Gtyoerot
ADIPOSE
Insulin
Glucagon, Epi. Lipolytic Hs
Glucose
85 mg/dL
Glycerol
100 pM
f-F
-A
h(K) pM
|vOH-butyrate
0.01 pM
POSTFEEDING FAST (16-20hr)
MUSCLE
Glycogen
o RBCs & Brain
Glu-1-P
Glycogen
LIVER
Glu-6-P — * G ucose
Glucose
Okl B P
F-1-6-P
FACoA
AC A
NADH.FADH
CoA
setone bodies
mino
m
m
protein
Figure 36-2. The metabolic flow following a postfeeding fast. Blood glucose
levels begin to decrease, triggering homeostatic mechanisms to prevent it from
decreasing dramatically.
CoA (Figure 36-3). This occurs only in liver mitochondria because of its crit-
ical role in gluconeogenesis. The ketone bodies are transported out of the liver
mitochondria and the liver into the bloodstream for transport to other tissues
where they reenter metabolism by being converted to acetoacetyl-CoA at the
expense of succinyl-CoA and then cleaved by ß-ketothiolase to produce two
molecules of acetyl-CoA for metabolism in the TCA cycle.
The ß-oxidation of fatty acids that occurs in the mitochondrial matrix
provides the energy for gluconeogenesis in the liver. Fatty acids transported
from adipose tissues by blood albumin cross the hepatic plasma membrane and
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