1. PENTOSE PHOSPHATE CYCLE
47
in lactating rat mammary glands, such as interstitial cell-stimulating hormone, follicle-stimulating hormone, and thyroid-stimulating hormone; all
these hormones fail to exhibit any effect on glucose oxidation (320).
Mammary glands of hypophysectomized rats in midpregnancy can be
induced to undergo lactation by hormonal means (322). The hormones
required for this lactation are either a mixture of prolactin, hydrocortisone, and growth hormone or a mixture of prolactin and hydrocortisone,
all administered in vivo; any other combination is ineffective. As compared with normal lactating mammary glands, the metabolism of the
induced-lactating mammary glands is similar on the basis of the incorporation of C
14 into C0 2 and fatty acids from specifically labeled glucose
and on the basis of the stimulatory effect of glucose on the conversion
of acetate to fatty acid. In those cases where lactation was not established, the metabolic pattern resembles that of the mammary glands of
the normal nonlactating rat. A major portion of the fatty acids formed
from glucose is via the hexose monophosphate shunt in the mammary
glands of the lactating hypophysectomized rat whereas in the nonlactating mammary glands, little glucose is utilized and the fatty acids are
formed almost exclusively via the EMP pathway.
Oxytocin (315, 323) and vasopressin (315), both posterior pituitary
hormones having milk-ejecting activity, increase the oxidation of glucosel-C
14
to C
14 0 2 in lactating rat mammary glands. These hormones also
stimulate the oxidation of glucose-6-C
14 to C
14 0 2 , but to a lesser degree
than that of the C-l of glucose (315). However, the effect of these hormones on the activity of the oxidative pentose phosphate cycle is still
obscure because the oxytocin effect on the C-l oxidation of glucose is
found in mammary slices from pregnant rats and rabbits as well as from
lactating rabbits and mice. Acetylcholine, a substance involved in the
transmittance of nerve stimuli, also influences similarly the glucose
metabolism of lactating mammary glands (315, 323). Puromycin, a
known inhibitor of protein synthesis, inhibits the stimulatory effect of
both oxytocin and acetylcholine (323), but mammary tissues incubated
with this inhibitor show no change in levels of both G-6-P DH and
6-PG DH relative to the uninhibited system.
Nonhormonal substances also have an influence on the glucose
metabolism of lactating mammary glands. Thus bicarbonate gives a
marked stimulation of the incorporation of glucose carbon into fatty
acids along with a parallel enhancement of the oxidation of the glucose
C-l (18). In the presence of a suitable concentration of iodoacetate, fatty
acid synthesis via the malonyl CoA pathway is inhibited while the oxidation of glucose via G-6-P DH and 6-PG DH is not. Under these conditions, iodoacetate reduces lipid synthesis and concomitantly decreases
47
in lactating rat mammary glands, such as interstitial cell-stimulating hormone, follicle-stimulating hormone, and thyroid-stimulating hormone; all
these hormones fail to exhibit any effect on glucose oxidation (320).
Mammary glands of hypophysectomized rats in midpregnancy can be
induced to undergo lactation by hormonal means (322). The hormones
required for this lactation are either a mixture of prolactin, hydrocortisone, and growth hormone or a mixture of prolactin and hydrocortisone,
all administered in vivo; any other combination is ineffective. As compared with normal lactating mammary glands, the metabolism of the
induced-lactating mammary glands is similar on the basis of the incorporation of C
14 into C0 2 and fatty acids from specifically labeled glucose
and on the basis of the stimulatory effect of glucose on the conversion
of acetate to fatty acid. In those cases where lactation was not established, the metabolic pattern resembles that of the mammary glands of
the normal nonlactating rat. A major portion of the fatty acids formed
from glucose is via the hexose monophosphate shunt in the mammary
glands of the lactating hypophysectomized rat whereas in the nonlactating mammary glands, little glucose is utilized and the fatty acids are
formed almost exclusively via the EMP pathway.
Oxytocin (315, 323) and vasopressin (315), both posterior pituitary
hormones having milk-ejecting activity, increase the oxidation of glucosel-C
14
to C
14 0 2 in lactating rat mammary glands. These hormones also
stimulate the oxidation of glucose-6-C
14 to C
14 0 2 , but to a lesser degree
than that of the C-l of glucose (315). However, the effect of these hormones on the activity of the oxidative pentose phosphate cycle is still
obscure because the oxytocin effect on the C-l oxidation of glucose is
found in mammary slices from pregnant rats and rabbits as well as from
lactating rabbits and mice. Acetylcholine, a substance involved in the
transmittance of nerve stimuli, also influences similarly the glucose
metabolism of lactating mammary glands (315, 323). Puromycin, a
known inhibitor of protein synthesis, inhibits the stimulatory effect of
both oxytocin and acetylcholine (323), but mammary tissues incubated
with this inhibitor show no change in levels of both G-6-P DH and
6-PG DH relative to the uninhibited system.
Nonhormonal substances also have an influence on the glucose
metabolism of lactating mammary glands. Thus bicarbonate gives a
marked stimulation of the incorporation of glucose carbon into fatty
acids along with a parallel enhancement of the oxidation of the glucose
C-l (18). In the presence of a suitable concentration of iodoacetate, fatty
acid synthesis via the malonyl CoA pathway is inhibited while the oxidation of glucose via G-6-P DH and 6-PG DH is not. Under these conditions, iodoacetate reduces lipid synthesis and concomitantly decreases