18
Ν. G. PON
transketolase-transaldolase sequence of reactions and partly by the oxidative pathway. A small contribution toward pentose formation is by
way of the glucuronate pathway (15, 114). Results from experiments
with lactating cows will be discussed under mammary glands (Section
VI,A,12). That any of the above conclusions can be reached is indeed
remarkable in view of the facts that the resultant expired C0 2 , the blood
glucose, and the urinary ribose may be a reflection of the over-all
metabolism of the intact animal. Furthermore, Katz (111) has repeatedly
emphasized that the ratios of C0 2 respired from feeding experiments
with labeled glucose may be a measure only of the metabolic fate of the
triose phosphate that is formed. Nevertheless he has recently conceded
that, under certain conditions, use can be made of the specific yields of
C
14 0 2 from glucose-l-C
14
and from glucose-6-C
14
(124) to estimate the
relative participation of the EMP and the pentose phosphate pathways.
2. Adipose Tissue
There is no doubt that the oxidative pentose phosphate cycle occurs
in the adipose tissue, as shown by experiments with variously labeled
glucose and by measuring the incorporation of the radioactive carbon
into the expired C0 2 , long-chain fatty acids, glyceride glycerol, and free
fatty acids (125). Moreover, Weber et al. have shown that both glucose6-phosphate and 6-phosphogluconate dehydrogenases are present in
extracts of rat fatty tissue (126). The question is, What is the relative contribution of this pathway toward the metabolism of glucose?
Using the data supplied by Cahill et al, Katz has recalculated this contribution and obtained a range of 10-15% for the relative contribution of
the pentose cycle to the triose pathway (111).
So far, only adipose tissue from rats and mice have been investigated;
therefore, the comparative biochemistry of pentose phosphate metabolism is reduced to a study of the in vivo and in vitro disturbances of
substances on these tissues. Because most of the synthesis and degradation of body fat takes place in the adipose tissue, one might expect that
hormones would regulate carbohydrate and lipid metabolism in these
tissues. Table I summarizes the effect of some hormones added in vitro
to epididymal fat pads of rats on the oxidative pentose phosphate pathway. Both insulin and prolactin stimulate the activity of the pentose
phosphate cycle, the former to an extent between 15 and 20% of the relative participation of the two major pathways of glucose metabolism
(III). Although both insulin and prolactin increase the C0 2 yield and
fatty acid synthesis, the resemblance ends here in that prolactin fails to
correct the defect in fatty acid synthesis found in adipose tissues of
alloxan-treated rats (127).
Ν. G. PON
transketolase-transaldolase sequence of reactions and partly by the oxidative pathway. A small contribution toward pentose formation is by
way of the glucuronate pathway (15, 114). Results from experiments
with lactating cows will be discussed under mammary glands (Section
VI,A,12). That any of the above conclusions can be reached is indeed
remarkable in view of the facts that the resultant expired C0 2 , the blood
glucose, and the urinary ribose may be a reflection of the over-all
metabolism of the intact animal. Furthermore, Katz (111) has repeatedly
emphasized that the ratios of C0 2 respired from feeding experiments
with labeled glucose may be a measure only of the metabolic fate of the
triose phosphate that is formed. Nevertheless he has recently conceded
that, under certain conditions, use can be made of the specific yields of
C
14 0 2 from glucose-l-C
14
and from glucose-6-C
14
(124) to estimate the
relative participation of the EMP and the pentose phosphate pathways.
2. Adipose Tissue
There is no doubt that the oxidative pentose phosphate cycle occurs
in the adipose tissue, as shown by experiments with variously labeled
glucose and by measuring the incorporation of the radioactive carbon
into the expired C0 2 , long-chain fatty acids, glyceride glycerol, and free
fatty acids (125). Moreover, Weber et al. have shown that both glucose6-phosphate and 6-phosphogluconate dehydrogenases are present in
extracts of rat fatty tissue (126). The question is, What is the relative contribution of this pathway toward the metabolism of glucose?
Using the data supplied by Cahill et al, Katz has recalculated this contribution and obtained a range of 10-15% for the relative contribution of
the pentose cycle to the triose pathway (111).
So far, only adipose tissue from rats and mice have been investigated;
therefore, the comparative biochemistry of pentose phosphate metabolism is reduced to a study of the in vivo and in vitro disturbances of
substances on these tissues. Because most of the synthesis and degradation of body fat takes place in the adipose tissue, one might expect that
hormones would regulate carbohydrate and lipid metabolism in these
tissues. Table I summarizes the effect of some hormones added in vitro
to epididymal fat pads of rats on the oxidative pentose phosphate pathway. Both insulin and prolactin stimulate the activity of the pentose
phosphate cycle, the former to an extent between 15 and 20% of the relative participation of the two major pathways of glucose metabolism
(III). Although both insulin and prolactin increase the C0 2 yield and
fatty acid synthesis, the resemblance ends here in that prolactin fails to
correct the defect in fatty acid synthesis found in adipose tissues of
alloxan-treated rats (127).