40
Ν. G. PON
figures are no doubt overestimated since dilution of the radioactive
compounds by a large unlabeled pool of compounds was not considered.
In spite of the difficulties encountered in the interpretation of the
variable results, some conclusions can still be salvaged from the results
of experiments with normal fed rats as compared with those of normal
fasted rats. Listed in Table IV are the effects of fasting on the metabTABLE IV
EFFECT OF STARVATION ON THE METABOLISM OF RAT LIVER
Effect of fasting as compared with normal
Metabolic parameter
fed rat liver
References
Lipogenesis
Decreased
C-l: C-6 of CO2 from glucose
Decreased
C-l: C-3 of C0 2 from lactate
Decreased
G-6-P DH level
Unaltered
Oxidation of acetyl CoA
Increased
Relative contribution of pentose
No change
phosphate cycle
(111, 292,
(HI, 294)
(107, 111)
(Ul)
(HI)
(HI)
olism in normal rat liver. Actually the G-6-P DH level does change, but
this depends on the number of days of starvation. After 24 hours of
fasting, the liver G-6-P DH specific activity rises to 150% the normal
level; however, after 48 and 72 hours the specific activity falls to 75 and
60% of the normal level, respectively (295). Six days of fasting causes
the level to drop to only 5% of the normal fed animal (296). Because
there is a depressed C-l:C-6 of C0 2 from labeled glucose in the fasted
rat liver, and because a decreased lipogenesis means a lower rate of
TPN
+ production, one might expect that the oxidative pentose phosphate
cycle would also decrease. That the latter remains unchanged and, if
anything, tends to be larger, suggests that the TCA cycle activity as
reflected by the increased oxidation of acetyl coenzyme A is stimulated.
Thus we have here a clear-cut example of a case where the C-l:C-6
ratio of C0 2 from labeled glucose decreases and yet the pentose phosphate cycle participation in the metabolism of glucose is relatively
unaltered.
The role of the oxidative pentose phosphate cycle in fatty acid
metabolism appears to be quite clear by now. A large segment of the
literature is devoted to this subject and the general consensus is that
TPNH is the limiting factor in those cases where lipogenesis is reduced
(292, 297). However, some investigators feel that this interpretation is
somewhat oversimplified (298), because under conditions where there
is enhanced lipid incorporation of C-l and C-6 from glucose, the
293)
Ν. G. PON
figures are no doubt overestimated since dilution of the radioactive
compounds by a large unlabeled pool of compounds was not considered.
In spite of the difficulties encountered in the interpretation of the
variable results, some conclusions can still be salvaged from the results
of experiments with normal fed rats as compared with those of normal
fasted rats. Listed in Table IV are the effects of fasting on the metabTABLE IV
EFFECT OF STARVATION ON THE METABOLISM OF RAT LIVER
Effect of fasting as compared with normal
Metabolic parameter
fed rat liver
References
Lipogenesis
Decreased
C-l: C-6 of CO2 from glucose
Decreased
C-l: C-3 of C0 2 from lactate
Decreased
G-6-P DH level
Unaltered
Oxidation of acetyl CoA
Increased
Relative contribution of pentose
No change
phosphate cycle
(111, 292,
(HI, 294)
(107, 111)
(Ul)
(HI)
(HI)
olism in normal rat liver. Actually the G-6-P DH level does change, but
this depends on the number of days of starvation. After 24 hours of
fasting, the liver G-6-P DH specific activity rises to 150% the normal
level; however, after 48 and 72 hours the specific activity falls to 75 and
60% of the normal level, respectively (295). Six days of fasting causes
the level to drop to only 5% of the normal fed animal (296). Because
there is a depressed C-l:C-6 of C0 2 from labeled glucose in the fasted
rat liver, and because a decreased lipogenesis means a lower rate of
TPN
+ production, one might expect that the oxidative pentose phosphate
cycle would also decrease. That the latter remains unchanged and, if
anything, tends to be larger, suggests that the TCA cycle activity as
reflected by the increased oxidation of acetyl coenzyme A is stimulated.
Thus we have here a clear-cut example of a case where the C-l:C-6
ratio of C0 2 from labeled glucose decreases and yet the pentose phosphate cycle participation in the metabolism of glucose is relatively
unaltered.
The role of the oxidative pentose phosphate cycle in fatty acid
metabolism appears to be quite clear by now. A large segment of the
literature is devoted to this subject and the general consensus is that
TPNH is the limiting factor in those cases where lipogenesis is reduced
(292, 297). However, some investigators feel that this interpretation is
somewhat oversimplified (298), because under conditions where there
is enhanced lipid incorporation of C-l and C-6 from glucose, the
293)