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Query: UNIPROT:P56851 (
epididymal
)
11,273
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In this work the kinetics of activation of the cyclic AMP-dependent protein kinase by several catecholamines and ACTH, have been studied in rat
epididymal
fat pads and isolated fat cells. The method of Soderling and co-workers which permits the measurement of the state of activation of the protein kinase after hormonal stimulation in adipose tissue, has been used. Kinetics experiments where norepinephrine was used showed that the results obtained with isolated cells conform to the models of Sutherland and Brostrom and co-workers. Wtih intact tissue, norepinephrine not only stimulates the protein kinase activity measured without exogenous cyclic
AMP
but also the total activity measured in the presence of cyclic
AMP
(5 X 10(-6) M); thus the effect of norepinephrine, obtained during incubation of the tissue, and that of cyclic
AMP
, added to the soluble fraction after incubation, were additive. This effect seems to be of the beta type because it is blocked completely by propranolol. A weak, additive but significant effect was also obtained with epinephrine and isoproterenol but not with ACTH. Neither cyclic GMP nor cyclic IMP seems implicated in this effect. It was shown that stroma vascular cells which are present in the fat pads are not involved. These results suggest that the effects of norepinephrine on the protein kinase of the fat pads cannot be completely explained by the model of Brostrom and colleagues.
...
PMID:Additive effects of norepinephrine and cyclic AMP on the activation of the protein kinase from adipose tissue. 18 9
Normal male rats were made chronically diabetic by injection of alloxan or acutely diabetic by injection of anti-insulin serum. The concentration of cyclic
AMP
in
epididymal
adipose tissue was increased approximately 2 1/2-fold 24 h after alloxan administration and up to 7-fold 72 h post-alloxan. Treatment of alloxan-diabetic rats with insulin for 4 h completely suppressed lipolysis but only partially suppressed cyclic
AMP
levels; 6 h following insulin treatment cyclic
AMP
levels were normal. When segments of the
epididymal
fat bodies were incubated in vitro the high cyclic
AMP
levels were not maintained but instead decreased spontaneously. Addition of insulin to the incubation media decreased lipolysis in tissues of diabetic rats to levels measured in tissues of normal rats and accelerated the decline in cyclic
AMP
levels but did not return cyclic
AMP
levels to normal. Rats rendered acutely insulin deficient by injection of anti-insulin serum showed increased plasma glucose and free fatty acid levels and increased adipose tissue free fatty acid, and cyclic
AMP
levels 30 min following injection of the antiserum. Plasma glucagon levels increased but not until 2 h following anti-insulin serum, thereby excluding the possibility that an increment in plasma glucagon is the primary stimulus for the acceleration of lipolysis in diabetes. These data are consistent with the view that control of adipose tissue cyclic
AMP
levels in situ is an important physiologic action of insulin.
...
PMID:Adenosine 3',5'cyclic monophosphate in adipose tissue of diabetic rats. 18 24
The effect of elevated body temperatures on the concentrations of
epididymal
cyclic
AMP
levels in non-diabetic, diabetic and hypophysectomized rats was studied. Cyclic AMP levels were increased during hyperthermia in all animals examined. This increase in
epididymal
cyclic
AMP
concentration was not seen in animals that had been supplemented with exogenous insulin prior to the experiment. The effect of pituitary lipolytic hormones on
epididymal
cyclic
AMP
levels was also investigated. Significant elevations of
epididymal
cyclic
AMP
levels were observed in hypophysectomized rats during hyperthermia indicating that pituitary hormones are not essential in causing these increases. Extrapituitary hormones, such as glucagon, might be responsible for
epididymal
cyclic
AMP
increases. Increases in
epididymal
cyclic
AMP
levels may therefore be the result of the reduction of blood insulin and concomitant increases of lipolytic hormones of both pituitary and extrapituitary origins.
...
PMID:Effect of hyperthermia on epididymal cyclic AMP levels in diabetic non-diabetic and hypophysectomized rats. 19 89
Two compounds, theophylline and 8-aza-9-furfuryl-adenine (SQ 4665), were found to maximally stimulate lipolysis in preparations of rat
epididymal
fat cells in the absence of exogenous hormones. Cyclic AMP levels in lipocytes maximally stimulated by either agent alone were unchanged from control levels. In contrast, lipolysis stimulated by either epinephrine alone or in combination with several cyclic nucleotide phosphodiesterase inhibitors correlated well with increases in the levels of cyclic
AMP
observed. These results suggest the presence of a non-cyclic
AMP
dependent pathway for the stimulation of lipolysis in rat
epididymal
fat cells.
...
PMID:Dissociation of lipolysis from the levels of cyclic AMP in rat epididymal fat cells. 19 20
Glycerol release from
epididymal
fat fragments of young adult (3-month old) ob/ob mice was three times lower than normal, on a tissue weight basis. Dose-response curves in response to isoproterenol and ACTH-(1--24) indicated that the capacity of the lipolytic process was reduced. However, the sensitivity to both hormones was normal, i.e. greater for ACTH than for isoproterenol. The burst of cyclic
AMP
observed at 7 minutes was affected even more than the lipolytic capacity in adipose tissue from obese mice. This was already observed in 1-month old animals, i.e. at a time when total body weight was still normal. It is concluded that the adenylate cyclase system is defective in adipose tissue of ob/ob mice. Besides, glucagon, vasoactive intestinal polypeptide, and secretin failed to stimulate glycerol release and cyclic
AMP
accumulation in both ob/ob, ob+/ob+, and HA-ICR mice, suggesting that mouse adipose tissue does not possess receptors for this group of hormones.
...
PMID:Lipolysis and cyclic AMP levels in epididymal adipose tissue of obese-hyperglycaemic mice. 20 30
Cyclic AMP phosphodiesterase activity was examined in particulate (30,000 X g for 30 min sediment) and supernatant subcellular fractions of
epididymal
fat cells isolated from obese-hyperglycemic (ob/ob) mice and their lean (+/?) LITTERMATES. The activity of the enzyme(s) was measured during both the early onset phase (5-6 weeks of age) and the static (5 months of age) of the obese-hyperglycemia syndrome. Fat cell particulate and supernate cyclic AMP phosphodiesterase activity of obese-hyperglycemic mice and their lean littermates at both ages displayed nonlinear Lineweaver-Burk kinetic plots. The maximum velocities of the fat cell particulate cyclic AMP phosphodiesterase activity of the obese mice were 67% and 84% lower than those of their lean littermates at 5-6 weeks and 5 months of age, respectively. Incubating fat cells obtained from either lean or obese mice of both age groups with 30 to 240 microunits of insulin per ml for 15 min increased the activity of the particulate, low Km cyclic AMP phosphodiesterase. This increase in activity was manifest as an increase in the maximum velocity of the enzyme(s) with no significant alteration of the affinity of the enzyme(s) for cyclic
AMP
.
...
PMID:Insulin stimulation of particulate, low Km adenosine 3',5'-monophosphate phosphodiesterase activity in fat cells of the obese-hyperglycemic (ob/ob) mouse. 20 79
The activity of the lipolytic system of the obese hyperglycemic mouse was assessed after treatment with physiological doses of thyroxin (T4). The treatment significantly increased fatty acid mobilization in response to adrenaline over the levels observed in the control mice under all conditions studied. The activities of the high- and low-Km phosphodiesterases and of adenylate cyclase were also studied. Treatment of the ob/ob mice with T4 had little effect on the activities of the cyclic
AMP
phosphodiesterases (high and low Km) but it partially restored the activity of adenylate cyclase, which is deficient in these animals. A correlation was found in the T4-treated obese animals between the ability of the
epididymal
adipose tissue to mobilize fatty acids, its ability to increase the intracellular levels of cyclic
AMP
, and the activity of adenylate cyclase in response to adrenaline stimulation.
...
PMID:Increased response of adipose tissue of the ob/ob mouse to the action of adrenaline after treatment with thyroxin. 20 80
The present study reports the effects on lipolysis occurring in isolated rat
epididymal
adipocytes of several agents which have each been found to interfere with membrane calcium transport in a variety of tissues. As reported by other workers, the local tetracaine was a strong inhibitor of hormone accelerated but not of basal lipolysis. The bivalent cations Mn2+ and Co2+ were similarly found to inhibit lipolysis stimulated with either epinephrine, ACTH, theophylline or dibutyryl cyclic
AMP
, whereas basal lipolysis was not markedly altered. This effect of Mn2+ and Co2+ was not mimicked by either Sr2+, Ba2+, Mg2+ or Ca2+. Cyclic AMP levels in adipocytes stimulated with epinephrine or ACTH tended to be higher in the presence of Mn2+ and Co2+. It is concluded, therefore, that Mn2+ and Co2+ inhibit lipolysis by uncoupling cyclic
AMP
accumulation from activation of triglyceride lipase. In contrast to Mn2+ and Co2+, the calcium antagonists La3+ and D600 were without effect on lipolysis. The antilipolytic effect of tetracaine, Mn2+ and Co2+ was found to persist in the absence of extracellular calcium, suggesting therefore that the antilipolytic effect of these drugs is unrelated to inhibition of calcium influx into adipocytes. The possibility is discussed that lipolytic agents cause an intracellular redistribution of calcium ion and that local anesthetics, Mn2+ and Co2+ interfere with lipolysis by preventing this intracellular redistribution of calcium.
...
PMID:Calcium antagonists and lipolysis in isolated rat epididymal adipocytes: effects of tetracaine, manganese, cobaltous and lanthanum ions and D600. 20 97
Spermatozoa acquire the capacity for motility as they traverse the mammalian epididymis. The biochemical basis for this induction of motility is still largely unknown. Current theories are discussed and recent studies from the authors' laboratory are described which indicate that two separate processes are involved and that these act synergistically. These processes are an increase in the intrasperm content of cyclic
AMP
during
epididymal
transit combined with the binding of a specific forward-motility protein. A second increase in cyclic
AMP
and stimulation by calcium ion is likely involved in the expression of the acquired potential for motility at the time of ejaculation.
...
PMID:Initiation of sperm motility in the mammalian epididymis. 21 Oct 50
Cyclic AMP metabolism in
epididymal
adipose tissue of exercise-trained rats was examined to determine if training induced changes in cyclic
AMP
production or inactivation. Beginning at 7 weeks of age, male rats were physically trained by 12 weeks of treadmill running. Pair-fed control rats remained sedentary in their cages for the duration of the experiment. Tissue levels of cyclic
AMP
were measured in
epididymal
adipose tissue slices incubated with norepinephrine. Adenyl cyclase was assayed in adipocyte ghost cell prepartions and low-Km phosphodiesterase was assayed in homogenates of adipose tissue. In response to norepinephrine stimulation, tissue cyclic
AMP
levels were reduced in trained compared to untrained rats. Training increased the ratio of activity of phosphodiesterase relative to adenyl cyclase. The results of this study indicate that cyclic
AMP
production in response to norepinephrine stimulation is not increased by training and may even be reduced, implying that adipose tissue cyclic
AMP
levels may be under a greater degree of control in trained rats. Modulation of adipose tissue cyclic
AMP
levels may function to regulate more closely the duration of lipolysis in exercise-trained rats.
...
PMID:Cyclic AMP metabolism in adipose tissue of exercise-trained rats. 21 Nov 72
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