Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

[3-H]Epinephrine binding to isolated purified rat liver plasma membranes is a reversible process. An initial peak in binding occurs at about 15 min and a plateau occurs by 50 min. Optimal binding occurred at a membrane protein concentration of 125mug. Rat liver plasma membranes stored at-70 degrees C up to 4 weeks showed no difference in epinephrine binding capacity as compared to control fresh membranes. Epinephrine binding to liver plasma membranes was decreased by 79% by phospholipase A2 (phosphatide acylhydrolase EC 3.1.1.4), 81% by phospholipase C (phosphatidylcholine choline phosphohydrolase EC 3.1.4.3) and 59% by phospholipase D (phosphatidylcholine phosphatidohydrolase EC 3.1.4.4). Trypsin and pronase digestion of the membrane decreased epinephrine binding by 97 and 47% respectively. In the presence of 10-3M Mg-2+ ions, increasing concentrations of QTP decreased epinephrine binding to liver plasma membranes. A maximal effect was demonstrated with 10-5M GTP, representing an inhibition of 52% of the control. In a Mg-2+ -free system, epinephrine binding was unaffected by GTP. However, in a Mg-2+ -free system, increasing concentrations of ATP cause increasing inhibition of hormone binding. ATP at 10-3 M reduced epinephrine binding to 28% of the control. GRP (10-5 M) was shown to inhibit epinephrine uptake rather than epinephrine release from the membrane. [3-H]Epinephrine binding to isolated rat epididymal fat cells shows an initial peak within 5 min followed by a gradual rise which plateaus after 60 min. Epinephrine binding increased nearly linearly with increasing fat cell protein concentration (40-200 mug protein). GTP (10-5 M) and ATP (10-4 M) decreased epinephrine binding to rat epididymal fat cells by 41%. Nearly complete inhibition of binding was demonstrated with 10-2-10-3M ATP. Epinephrine analogs that contain two hydroxyl groups in the 3 and 4 position on the benzene ring act as inhibitors of [3-H]epinephrine binding to rat adipocytes. Alteration of the epinephrine side chain has relatively little influence on binding. Analogs in which one of the ring hydroxyl groups is missing or methylated are poor inhibitors of [3-H]epinephrine binding. Alpha-(phentolamine and phenoxybenzamine) and beta-(propranolol and dichorisoproterenol) adrenergic blocking agents were tested with respect to their ability to influence [3-H]epinephrine binding and their influence on epinephrine-stimulated lipolysis. Only dichloroisoproterenol significantly inhibited epinephrine binding (by 25%). The two beta-adrenergic blocking agents caused an inhibition of epinephrine-stimulated glycerol release, with propranolol being most effective. Phentolamine and phenoxybenzamine had no significant effect on the epinephrine stimulation of glycerol release by fat cells.
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PMID:Hormone action at the membrane level. IV. Epinephrine binding to rat liver plasma membranes and rat epididymal fat cells. 16 9

Insulin has been shown to lower cyclic AMP (cAMP) levels in hormonally sensitive tissue. The mechanism by which this lowering occurs has not yet been fully defined. We studied the effects of insulin on rat adipose tissue cyclic nucleotide phosphodiestrase (PDE) in an incubation system. The adipose tissue used was from both normal animals and animals rendered diabetic by intravenous injections of streptozotocin. Rat epididymal fat pads were incubated in a Krebs-Ringer bicarbonate-4% albumin system with O, 100, 1,000 or 10,000 PU/ml insulin (INS); epinephrine (EPI) or glucagon (GLU) at several different concentrations. After 15 min of incubation, each tissue was homogenized, centrifugated, and the supernatant assayed for cAMP PDE activity using the breakdown of (3-H)cAMP. The data was used to characterize cAMP PDE into apparent high and low K-m PDE components. In the normal animals, INS increased Vmax of the low Km PDE components; 100 pU/ml INS, 30%, 1000 p1/ML INS, 40; and 10,000 pU/ml INS, 20%. In contrast, streptoxotocin diabetes lowered this Vmax by 30%. In the diabetic animals, INS also increased Vmax by 30%. In the diabetic animals, INS also increased Vmax of the low Km PDE component; 100 pU/ml INS, 30%; 1000 pU/ml INS, 50% and 10,000 pU/ml INS, 100%. Epinephrine at 1, 10, and 100 pg/ml stimulated low Km cAMP PDE activity by 67%, 73% and 44% respectively. The stimulatory effect of EPI on both the low and high Km cAMP PDE activity was neutralized by propranolol or adenosine. In comparison to EPI, GLU at very low concentrations, 10-9M, stimulated low Km cAMP PDE. These studies suggest that some of the biologic actions of insulin, an antilipolytic substance, are mediated through activation of low Km PDE. Furthermore, this enzymatic activity is lower in experimental diabetes. The stimulation of low Km PDE by lipolytic hormones may reflect a long-range protective action of these agents.
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PMID:Effect of insulin and lipolytic hormones on cyclic AMP phosphodieterase activity in normal and diabetic rat adipose tissue. 16 58

Starvation did not cause increase of hormone-sensitive lipase in rat epididymal adipose tissue. Adrenaline did not activate lipase in the fat cells, although it accelerated the release of free fatty acids from the cells. The results suggest that the mechanism of the stimulation of lipolysis by adrenaline is different from that in the cyclic AMP theory. Adrenaline-sensitive fat globules were prepared by hypotonic treatment of fat cells. Lipolysis in the fat globules was stimulated by adrenaline. It was shown that adrenaline-induced lipolysis in the fat globules was not due to activation of lipase but to initiation of a reaction between lipase and triglyceride. It is well known that calcium ions are essential for ACTH-induced lipolysis and that the hormone stimulates calcium uptake into adipose tissue. It was demonstrated that calcium ions accelerated formation of a complex between fat and lipase. The mechanism of the actions of adrenaline and ACTH are discussed on the basis of these results.
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PMID:Mechanism of actions of adrenaline and ACTH in fat mobilization. 17 4

A perfusion system was used to investigate the lipolytic response to epinephrine of minced epididymal fat pads from fed and 24-hr fasted rats. Epinephrine was infused at a final concentration of 1 X 10(-6) M for 60-min periods. Basal glycerol release from tissue and cells of fed animals was 3 mumoles/min/ml of sample. Epinephrine stimulated lipolysis 20-fold in tissue pieces. There was an additional two-fold increase during a repeated epinephrine infusion after 30 min with buffer alone. In contrast, tissue from fasted rats showed no difference upon successive infusions of epinephrine. Isolated cells of fed and fasted animals also produced peaks of equal magnitude on both exposures to epinephrine. Preincubation of fed tissue with anti-insulin serum did not abolish the augmented response to the hormone. Preincubation of the fed tissue for 90 min with omission of the first epinephrine exposure did not produce an augmented response. It is concluded that exposure of adipose tissue to 1 X 10(-6)M epinephrine will produce augmented stimulation of lipolysis on a second exposure. Fasting and isolation of cells abolishes the augmented response by a mechanism which does not involve removal of insulin from the fat cell.
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PMID:Augmented lipolysis in rat adipose tissue upon repeated exposure to epinephrine. 49 63

Incubation of isolated rat epididymal fat cells is associated with the accumulation of adenosine in the incubation medium. To more clearly define the effect of adenosine on lipolysis, isolated rat epididymal adipocytes were studied with the perifusion system. Various combinations of epinephrine, adenosine, and adenosine deaminase were perifused through the adipocytes. Exogenous adenosine, 0.001-10.0 muM, had no discernible influence upon unstimulated lipolysis; but exogenous adenosine inhibited epinephrine-sensitive lipolysis in a concentration-dependent manner. Cells perifused with 0.3 muM epinephrine plus 0.001 muM adenosine did not show any impairment of the lipolytic response to 0.3 muM epinephrine alone. Adenosine, 0.01 muM, inhibited the response to epinephrine by 50%; response to 0.3 muM epinephrine plus 0.1 muM adenosine was similar to the basal rate. Perifusion with adenosine deaminase significantly increased basal lipolysis to 30% of the epinephrine response. Adenosine deaminase and epinephrine were synergistic in stimulating lipolysis to 180% of the response to epinephrine alone. Isolated fat cells were incubated for 30 min, and the cell-free used medium was perifused through fresh fat cells. Epinephrine in used medium was less effective in promoting lipolysis than epinephrine in fresh buffer. High-pressure liquid chromatography identified adenosine in the used medium. Bovine serum albumin possessed adenosine deaminase activity but accounted for negligible conversion of adenosine to inosine. Adenosine is shown to have a modulating effect upon basal and hormone-stimulated lipolysis in the perifusion system. Sufficient endogenous adenosine (<0.01 muM) is present to maximally affect basal lipolysis. Hormone-stimulated lipolysis, although inhibited somewhat by endogenous adenosine, requires the addition of exogenous adenosine for complete inhibition.
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PMID:Perifusion of isolated rat adipose cells. Modulation of lipolysis by adenosine. 87 2

This experiment was designed to determine if the adaptive increase in adipose tissue epinephrine-stimulated lipolysis (ESL) observed in exercise trained rats is related to decreased adipocyte size or a direct response to exercise. Two levels of treadmill exercise and three levels of food restriction were imposed on male rats over a 12 week experimental period to create a distribution of adipose tissue cell sizes. Epinephrine-stimulated lipolysis was subsequently measured in the isolated adipocytes from rats trained at two different exercise levels and in untrained rats fed either ad libitum or 16%, 27%, or 35% dietary restriction. Energy restriction was effective in reducing body weight and to some extent epididymal fat pad weight; however, adipocyte size and number were not significantly affected. Exercise in both groups of trained rats was effective in reducing adipocyte size; however, cell size did not differ between training groups. The group receiving the greatest amount of daily exercise had significantly greater ESL indicating that the adaptive increase in lipolytic potential seen in adipose tissue of exercise trained rats is a true metabolic adaptation not secondary to reduced cell size.
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PMID:Adipose tissue cell size and lipolysis in the rat: response to exercise intensity and food restriction. 95 16

The uptake and utilization of [1-14C]glycerol was determined in pieces of rat epididymal fat-pads incubated in Krebs--Ringer bicarbonate buffer containing albumin. Insulin (200 muunits/ml), adrenaline (epinephrine; 0.5 mug/ml) and glucose (0, 5, 15 and 20 mM) were added to the medium. Changes in the specific radioactivity of the tracer during the incubation were taken into account in calculating the rate of glycerol utilization. Adrenaline decreased glycerol uptake, whereas insulin plus adrenaline increased it. The rate of incorporation of glycerol into glycerides was decreased by adrenaline and insulin, singly or together. Insulin increased the rate of formation of CO2 and fatty acids from glycerol. The formation of CO2 and fatty acids was further enhanced by insulin plus adrenaline. The decrease in glycerol uptake induced by adrenaline, the decrease in incorporation of glycerol into glycerides induced by insulin and insulin plus adrenaline and the synthesis of fatty acids were dependent on the presence of glucose in the medium. Thus insulin and adrenaline act on glycerol utilization in adipose tissue and some of their effects are mediated by action on glucose metabolism, but others are independent of this.
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PMID:The effect of glucose, insulin and adrenaline on glycerol metabolism in vitro in rat adipose tissue. 98 22

In order to study the effect of epinephrine on the rate of esterification of fatty acids in adipose tissue, pieces of epididymal fat pad were incubated in KRB in the presence of purified albumin, glucose and either 1-14C-glycerol, 1-14C-glucose or 6-14C-glucose. Epinephrine enhances the production of glycerol but reduces the uptake of 1-14C-glycerol by the tissue and its conversion to 14CO2, 14C-fatty acids and 14C-glyceride glycerol. When the change in specific activity of the tracer is taken into account the effect of epinephrine on the utilization of glycerol by the tissue is only observed in the reduction of glyceride glycerol synthesis. When 14C-labelled glucose was used as tracer, epinephrine enhances both the production of 14CO2 from 6-14C-glucose and the synthesis of 14C-glyceride glycerol from 1-14C and 6-14C-glucose. The contrasting effects of epinephrine on the glyceride glycerol formation from glycerol and from glucose can explain the difficulties found in observing any change in the net rate of esterification of fatty acids by adipose tissue.
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PMID:Effect of epinephrine on the synthesis of glyceride glycerol in adipose tissue in vitro. 121 23

1. Primary monolayer cultures from adult human epididymis were grown on Petri dishes and previous supports. The epithelia so formed were used for whole-cell patch clamp recording and short-circuit current (ISC) measurement. 2. After 50 days of culture, the cells formed a tight epithelium with transepithelial potential of 5.5 +/- 1.3 mV (mean +/- S.E.M.., n = 16), apical side negative, and a basal ISC of 6.9 +/- 0.9 microA cm-2 (mean +/- S.E.M., n = 16). 3. Adrenaline, when added to the basolateral side, at a concentration of 0.23 mumol l-1 increased the ISC by 3.0 +/- 1.2 microA cm-2 (mean +/- S.E.M., n = 4). This increase was blockable by diphenylamine-2-carboxylate (DPC, 1 mmol l-1). Forskolin (10 mumol l-1) also evoked a similar response to adrenaline. 4. In whole-cell patch clamp experiment, the resting membrane potential of the cells after dialysis with pipette solution containing 135 mmol l-1 KCl was found to be -30 +/- 14 mV (mean +/- S.E.M., n = 15). 5. About 90% of the cells successfully forming patches responded to 1 mumol l-1 adrenaline by an increase in inward current at -70 mV holding potential (delta I = -1600 +/- 900 pA, mean +/- S.E.M., n = 15). This increase in current was accompanied by a shift in reversal potential to -2 +/- 1 mV (mean +/- S.E.M., n = 15). 6. The adrenaline-induced inward current was found to be blockable by the Cl- channel blocker, DPC (0.25 mmol l-1). Ion substitution experiments showed that the adrenaline-evoked current was carried mainly by Cl-. 7. The effect of adrenaline on the whole-cell current was found to be mimicked by forskolin and could be abolished by including GDP beta S or a protein kinase A inhibitor in the pipette solution. Propranolol, but not phentolamine, completely abolished the effect of adrenaline. 8. Inclusion of 20 mmol l-1 EGTA or 2 mmol l-1 BAPTA + 100 mumol l-1 TMB-8 (to inhibit intracellular Ca2+ release) in the pipette did not seem to have any marked effect on adrenaline-evoked whole-cell current. Lowering the pipette Ca2+ concentration to 1 nmol l-1 or raising it to 10 mumol l-1 had no effect on the whole-cell current response to adrenaline. 9. This study shows that adrenaline stimulates Cl- secretion in cultured human epididymal cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Electrophysiological studies of anion secretion in cultured human epididymal cells. 136 44

Primary monolayer cultures of rat epididymal cells have been shown to secrete chloride and bicarbonate when stimulated with beta-adrenergic agents, humoral agents and vasoactive peptides. The intracellular messengers mediating the secretory response are unknown. In this study intracellular AMP, Ca2+ and inositol phosphates were measured in epididymal monolayers at rest and upon stimulation with various secretory agonists. Adrenaline, forskolin, lysylbradykinin, prostaglandin, endothelin, angiotensin II, antidiuretic hormone and vasoactive intestinal peptide at concentrations that stimulate anion secretion caused a rise in intracellular cyclic AMP. The increase in cyclic AMP by adrenaline was blocked by propranolol but not by phentolamine. Studies of the concentration-effect relationships showed that for adrenaline and endothelin the EC50 for stimulation of cyclic AMP was higher than that for stimulation of anion secretion. None of these agonists affects intracellular Ca2+ concentration and inositol phosphate contents in epididymal monolayers. Ca2+ ionophores A21387, ionomycin and erythrosin B (with irradiation with white light), at concentrations that stimulate anion secretion, also stimulated a rise in intracellular cyclic AMP and concomitantly increased intracellular Ca2+. The increase in cyclic AMP was dependent on extracellular Ca2+. It is not known whether the secretory response to Ca2+ ionophores was mediated by an increase in cell Ca2+ per se, or cyclic AMP. However, it can be concluded that cyclic AMP is the second messenger which mediates the secretory responses to physiological stimuli.
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PMID:Secretory agonists stimulate a rise in intracellular cyclic AMP but not Ca2+ and inositol phosphates in cultured rat epididymal epithelium. 197 25


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