THE EFFECT OF GROWTH HORMONE ON THE UTILIZATION OF 1-C14OCTANOIC ACID BY RAT LIVER SLICES

1957 ◽  
Vol 35 (7) ◽  
pp. 497-502 ◽  
Author(s):  
W. F. Perry ◽  
H. G. Friesen

Young ([Formula: see text] months), adult (4–5 months), and old (2(+) years) rats were injected with growth hormone intraperitoneally in doses of 4 mg./100 g. at various intervals of time before removal of the liver. Slices of liver were incubated with radioactive octanoic acid and the production of CO2and acetoacetic acid measured.In adult rats fed ad libitum, growth hormone injected 4 hours before the rats were killed had no consistent effect on acetoacetic acid or carbon dioxide production by the liver slices. In adult rats fasted 24 hours before they were killed, growth hormone was likewise found to have no effect on ketogenesis and CO2production irrespective of whether it was injected 4, 12, or 24 hours before the rats were killed. Young rats that were fasted 24 hours and to which growth hormone was administered at the 20th hour of fasting showed a slight ketogenesis but the values for the specific activity of the acetoacetic acid suggested the increased ketogenesis was not derived from the labelled fatty acid. No effect on CO2production was noted. In old rats that were fasted 24 hours and to which growth hormone was given at the 20th hour of fasting, a slight decrease in acetoacetic acid formation by the liver slices was observed which appeared to be due to an over-all reduction in fatty acid utilization. There was again no alteration in CO2production. Treatment of adult rats for 5 days with growth hormone, followed by incubation of the liver slices with octanoate, was found to influence neither ketogenesis nor CO2production.

1957 ◽  
Vol 35 (1) ◽  
pp. 497-502
Author(s):  
W. F. Perry ◽  
H. G. Friesen

Young ([Formula: see text] months), adult (4–5 months), and old (2(+) years) rats were injected with growth hormone intraperitoneally in doses of 4 mg./100 g. at various intervals of time before removal of the liver. Slices of liver were incubated with radioactive octanoic acid and the production of CO2and acetoacetic acid measured.In adult rats fed ad libitum, growth hormone injected 4 hours before the rats were killed had no consistent effect on acetoacetic acid or carbon dioxide production by the liver slices. In adult rats fasted 24 hours before they were killed, growth hormone was likewise found to have no effect on ketogenesis and CO2production irrespective of whether it was injected 4, 12, or 24 hours before the rats were killed. Young rats that were fasted 24 hours and to which growth hormone was administered at the 20th hour of fasting showed a slight ketogenesis but the values for the specific activity of the acetoacetic acid suggested the increased ketogenesis was not derived from the labelled fatty acid. No effect on CO2production was noted. In old rats that were fasted 24 hours and to which growth hormone was given at the 20th hour of fasting, a slight decrease in acetoacetic acid formation by the liver slices was observed which appeared to be due to an over-all reduction in fatty acid utilization. There was again no alteration in CO2production. Treatment of adult rats for 5 days with growth hormone, followed by incubation of the liver slices with octanoate, was found to influence neither ketogenesis nor CO2production.


1956 ◽  
Vol 186 (2) ◽  
pp. 190-192 ◽  
Author(s):  
W. F. Perry ◽  
Helen F. Bowen

The production of radioactive CO2 by intact and adrenalectomized rats given 1 C14 octanoic acid and the production of radioactive CO2 and radioactive acetoacetic acid by surviving liver slices from adrenalectomized and unoperated rats using 1 C14 octanoic acid as substrate have been studied. It was found that the CO2 production and acetoacetic acid production in vitro and CO2 production in vivo did not differ in the two types of animals. These results suggest that the adrenalectomized rat does not utilize fatty acids at a higher than normal rate and that the previously reported decreased incorporation of acetate into fatty acids by the liver slices from adrenalectomized rats is a reflection of decreased hepatic lipogenesis.


1973 ◽  
Vol 134 (2) ◽  
pp. 545-555 ◽  
Author(s):  
John M. Land ◽  
John B. Clark

1. The activities of, and the effects of phenylpyruvate on, citrate synthase (EC 4.1.3.7), acetyl-CoA carboxylase (EC 6.4.1.2) and fatty acid synthetase derived from the brains of 14-day-old and adult rats were investigated. 2. The brain citrate synthase from 14-day-old rats had a Km for oxaloacetate of 2.38μm and for acetyl-CoA of 16.9μm, and a Vmax. of 838nmol of acetyl-CoA incorporation/min per mg of mitochondrial protein. From adult rat brain this enzyme had a Km for oxaloacetate of 2.5μm and for acetyl-CoA of 16.6μm and a Vmax. of 1070nmol of acetyl-CoA incorporated/min per mg of mitochondrial protein. Phenylpyruvate inhibited the enzyme from adult and young rat brains in a competitive fashion with respect to acetyl-CoA, with a Ki of 700μm. 3. The brain acetyl-CoA carboxylase from 14-day-old rats had a Km for acetyl-CoA of 21μm and a Vmax. of 0.248nmol/min per mg of protein, and from adult rats a Km for acetyl-CoA of 21μm and a Vmax. of 0.173nmol/min per mg of protein. The enzyme from young and adult rats required citrate (Ka=3mm) for activation and were inhibited non-competitively by phenylpyruvate, with a Ki of 10mm. 4. The brain fatty acid synthetase from 14-day-old rats had a Km for acetyl-CoA of 7.58μm and a Vmax. of 1.1 nmol of malonyl-CoA incorporated/min per mg of protein, and from adult rats a Km for acetyl-CoA of 4.9μm and a Vmax. of 0.48nmol of malonyl-CoA incorporated/min per mg of protein. Phenylpyruvate acted as a competitive inhibitor with respect to acetyl-CoA with a Ki of 250μm for the enzyme from 14-day-old rats. 5. These results are discussed with respect to phenylketonuria, and it is suggested that the inhibition of the brain fatty acid synthetase and possibly the citrate synthetase by phenylpyruvate could explain the defective myelination characteristic of this condition.


1955 ◽  
Vol 184 (1) ◽  
pp. 59-62 ◽  
Author(s):  
W. F. Perry ◽  
Helen F. Bowen

The incorporation of C14 acetate into fatty acids, cholesterol, acetoacetic acid and CO2 by liver slices of intact and adrenalectomized rats was studied, the slices being incubated in bicarbonate and phosphate buffers. It was found that in both buffer systems incorporation into fatty acids and cholesterol was depressed while incorporation into acetoacetic acid was unaffected by adrenalectomy. However, total acetoacetic acid formation by the slices tended to be higher in preparations from adrenalectomized animals. The amount of acetate carbon appearing as CO2 was similar with slices from both types of animals. Bicarbonate was found to be a more favorable medium than PO4 for fatty acid formation, while PO4 was the more favorable medium for cholesterogenesis, though the differences between adrenalectomized and intact animals persisted in either buffer. Forced feeding with glucose increased the incorporation of acetate into fat and cholesterol in both buffer systems in adrenalectomized as well as in intact animals. However, the adrenalectomized preparation still incorporated acetate to a lesser extent than the controls. It was concluded that while the depressed incorporation of acetate into fatty acid and cholesterol by adrenalectomized liver slices was consistent with a depressed synthesis of these lipids, there was also the possibility that it reflected an increased turnover of lipids in the liver of the adrenalectomized animal.


1963 ◽  
Vol 205 (4) ◽  
pp. 663-666 ◽  
Author(s):  
Lawrence M. Gartner ◽  
Irwin M. Arias

o-Aminophenol (OAP) glucuronide formation by liver slices from fetal and newborn Wistar rats up to 70 hr old is equivalent to or greater than OAP glucuronide formation by liver slices from adult rats. OAP glucuronide formation by homogenates of liver from 3-day-old rats, and slices or homogenates of liver from 3-day-old guinea pigs is substantially less than that observed in comparable preparations of adult liver. These observations suggest that glucuronidation is deficient in newborn guinea pigs but not in newborn rats. Although the mechanisms responsible for these differences are unknown, the possibility is discussed that disruption of rat liver cells reduces glucuronide formation by activation of an inhibitor.


1957 ◽  
Vol 35 (1) ◽  
pp. 759-766 ◽  
Author(s):  
W. F. Perry ◽  
Helen F. Bowen

The effect of growth hormone on the in vitro incorporation of C14 acetate into fatty acids, carbon dioxide, and cholesterol by liver and adipose tissue from young, adult, and old rats was studied.In all three age groups of animals, growth hormone was found to depress the incorporation of acetate into fatty acids by liver slices but the CO2 production was unaffected. In both young and old animals growth hormone did not significantly alter the incorporation of acetate into fatty acids and CO2 by preparations of adipose tissue, but did result in a decline in the fat content of the adipose tissue. It was noted that the CO2 production from acetate was much less with adipose tissue from old rats than with similar preparations from young rats.Incorporation of acetate into cholesterol was unaffected by growth hormone in young and old animals but was significantly increased in liver slices from adult animals.


1980 ◽  
Vol 84 (3) ◽  
pp. 692-704 ◽  
Author(s):  
M I Johnson ◽  
C D Ross ◽  
R P Bunge

Superior cervical ganglion (SCG) neurons taken from perinatal rats and dissociated in culture develop cholinergic properties. This report examines this "plasticity" of neurotransmitter function with regard to its dependence on the stage of neuronal development. Explants of SCG from rats ranging in age from 2 d to adult were cultured, and the number of neurons surviving after 6 wk in culture was evaluated. The activities of choline acetyltransferase (ChAc) and DOPA decarboxylase (DDC) were assayed for each age group over time in culture, and the cytochemistry of the synaptic vesicle population was studied after norepinephrine loading and KMnO4 fixation. The specific activity of ChAc in all explants fell during the first 3--4 d in culture (secondary to degeneration of presynaptic terminals), with an increase during the next 30 d in explants from all age groups except in those from the 22-d-old and adult rats. The highest activity found after 1 mo in culture was in explants from 2-d-old rats (62.5 mmol per kg dry wt per h); the lowest was in explants from adults (1.3 nmol per kg dry wt per h). After 1 mo in vitro, there were no significant differences in DDC activity among explants from animals of any age (similar to approximately 220 mmol per kg dry wt per h). Co-culture of the SCG explants with heart muscle increased even further the ChAc activity in explants from 2-d-old rats but not in explants from 16-d-old and 6.5-wk-old animals. The cytochemistry of the synaptic vesicle population in 1-mo-old cultures correlated well with the ChAc activity; when the ChAc activity was high, the proportion of synaptic vesicles with clear centers was 71--88%. In explants from adult animals, only 12% of the vesicles contained clear centers. From these data we conclude that the maturity of the SCG neuron influences the degree to which it is able to adjust its neurotransmitter mechanisms. That the axons of this neuron are interacting with target tissues during the time that neurotransmitter plasticity is retained suggests that interaction with the target may play a role in the determination of transmitter type.


1991 ◽  
Vol 131 (2) ◽  
pp. 251-257 ◽  
Author(s):  
M. Parenti ◽  
D. Cocchi ◽  
G. Ceresoli ◽  
C. Marcozzi ◽  
E. E. Müller

ABSTRACT The mechanisms underlying the age-related decrease and increase in somatotroph responsiveness to growth hormone-releasing factor (GHRF) and somatostatin respectively were studied in rat pituitary membranes in vitro. Basal adenylate cyclase (AC) activity was similar in pituitary membranes from rats of 8 days (either sex) and male rats of 3 months, but it was almost threefold higher in membranes from male rats of 21–23 months. GHRF induced a lower percentage stimulation of AC activity in membranes from infant and old than adult rats. Somatostatin inhibited stimulation of AC induced by forskolin more effectively in membranes from adult than infant and old rats. In parallel experiments, since the tissue we used is formed by a mixed population of pituitary cells, we evaluated, for comparison, the effect on AC of neurohormones, i.e. vasoactive intestinal polypeptide (VIP) and dopamine which act primarily on lactotrophs. VIP induced a lower fold-stimulation of AC activity in membranes from infant and old than adult rats. Dopamine inhibited forskolin-induced stimulation of AC in the following rank order of magnitude: old, adult and infant rats, and was also more effective in inhibiting basal AC activity in old than in adult rats. The stimulatory and inhibitory G proteins (Gs and Gi) coupled to AC were measured indirectly by evaluating stimulatory and inhibitory effects of different concentrations of GTP on AC. GTP, at stimulatory concentrations, increased AC activity in membranes from infant and adult rats similarly whereas its effect was significantly greater in membranes from old rats. Conversely, GTP, at inhibitory concentrations, decreased AC activity similarly in membranes from adult and infant rats, whereas in old rats inhibition was apparent at more than a tenfold lower concentration of GTP. These data suggest (1) that the greater somatotroph sensitivity to GHRF in terms of GH secretion of the early postnatal period is not due to supersensitive GHRF receptors but rather may be accounted for, at least partially, by the low function of somatostatinergic receptors; (2) that the inability of GHRF to stimulate GH release in aged rats probably results from an uncoupling between the GHRF receptor and the G protein; and (3) that in aged rats the decreased ability of somatostatin to inhibit AC activity, in spite of the high Gi activity, results from a reduced number of somatotroph cells and, hence, receptors. Journal of Endocrinology (1991) 131, 251–257


1957 ◽  
Vol 35 (9) ◽  
pp. 759-766 ◽  
Author(s):  
W. F. Perry ◽  
Helen F. Bowen

The effect of growth hormone on the in vitro incorporation of C14 acetate into fatty acids, carbon dioxide, and cholesterol by liver and adipose tissue from young, adult, and old rats was studied.In all three age groups of animals, growth hormone was found to depress the incorporation of acetate into fatty acids by liver slices but the CO2 production was unaffected. In both young and old animals growth hormone did not significantly alter the incorporation of acetate into fatty acids and CO2 by preparations of adipose tissue, but did result in a decline in the fat content of the adipose tissue. It was noted that the CO2 production from acetate was much less with adipose tissue from old rats than with similar preparations from young rats.Incorporation of acetate into cholesterol was unaffected by growth hormone in young and old animals but was significantly increased in liver slices from adult animals.


1969 ◽  
Vol 114 (2) ◽  
pp. 343-350 ◽  
Author(s):  
S. H. Danovitch ◽  
L. Laster

1. Arylsulphatase activity was measured in stomach, proximal and distal third of small intestine, colon, liver and kidney of foetal and neonatal Sprague–Dawley rats and Swiss mice, with nitrocatechol sulphate as substrate. 2. The specific activity in the distal small intestine, but not in the stomach, proximal small intestine or colon, increased about fourfold between 5 and 16 days after birth in both conventional and germ-free rats. 3. No comparable increase occurred in the distal small intestine of the mouse. 4. The specific activity of acid phosphatase in the distal small intestine of the rat rose only slightly when the arylsulphatase activity increased. 5. The pH optimum and Michaelis constant of arylsulphatase activity of the distal small intestine were similar for 1-day-old, 9-day-old and adult rats. 6. When extracts of distal small intestine of 1-day-old and 9-day-old rats were incubated together, the arylsulphatase activities were additive.


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