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

The relationship between histamine (Hi)-induced depolarization and the cyclic AMP system in adipocytes was studied in guinea pigs, which seem to be more sensitive than rats to Hi. Hi caused a dose-dependent depolarization in guinea pig mesenterial and epididymal adipocytes with EC50 values of 1.69 x 10(-7) M and 1.19 x 10(-7) M, respectively. Guinea pig adipocytes were 280-750 times more sensitive than rat adipocytes to Hi. Isoproterenol, forskolin and 3-isobutyl-1-methylxanthine (IBMX) also caused a depolarization, and the slopes of the concentration response lines for these drugs were almost the same as that for Hi. Furthermore, pretreatment with these drugs resulted in a potentiation of Hi-induced depolarization at lower concentrations which are not effective when each drug is used alone. In addition, Hi-induced depolarization was inhibited by pretreatment with prostaglandin E1 (PGE1) and insulin dose-dependently. The content of cyclic AMP in adipocytes was increased by Hi (10(-7) M) in association with a decrease in membrane potential. KT5720, a protein kinase A inhibitor, which provides no significant effect even at a concentration of 10(-6) M, showed an antagonistic effect on Hi-induced depolarization.
 ...
PMID:Histamine-induced depolarization and the cyclic AMP--protein kinase A system in isolated guinea pig adipocytes. 128 21

l-Isoproterenol has been proposed to stimulate lipolysis in rat epididymal adipocytes via atypical beta adrenergic receptors, whereas radioligand binding studies only revealed the presence of beta 1 adrenergic receptors on adipocyte membranes. We have made use of the unique properties of CGP12177 to evidence that both the beta 1 and the atypical beta adrenergic receptor subtypes are mediating the lipolytic response of rat epididymal adipocytes to l-isoproterenol. CGP12177, an antagonist with high affinity for beta 1 receptors, triggers lipolysis by specifically stimulating the atypical receptors. For this response, CGP12177 displays low potency (EC50 = 68 nM), but high intrinsic activity (94% relative to l-isoproterenol). At low concentrations (3 nM), CGP12177 inhibits the lipolytic response to 10 nM l-isoproterenol by 43%, indicating that at least this fraction of the response is beta 1 receptor-mediated. The response to BRL37344, which is a selective agonist for the atypical receptors, is not inhibited by CGP12177. The pA2 values of the beta adrenergic antagonists propranolol, metoprolol and atenolol were calculated from the rightward shifts that they impose on dose-response curves of both l-isoproterenol and CGP12177. With l-isoproterenol, these values (6.54, 5.83 and 5.07, respectively) are lower than those expected for beta 1 and beta 2 receptors, indicating that atypical receptors are also involved in the lipolytic response to this agonist. With CGP12177, the pA2 values of propranolol, metoprolol and atenolol are even lower (5.80, 5.03 and 4.06, respectively), and are likely to be a more accurate reflection of their affinities for the atypical receptors.
 ...
PMID:Multiple beta adrenergic receptor subclasses mediate the l-isoproterenol-induced lipolytic response in rat adipocytes. 132 52

Dietary fish oils, enriched with omega-3 fatty acids (e.g., MaxEPA fish oil), inhibit lipogenesis and have a marked hypotriglyceridemic effect in man and experimental animals. Dietary omega-3 fatty acids also reduce adipose tissue trophic growth in rats. To understand the metabolic basis for this, we measured the effect of fish oil feeding upon rat plasma triglyceride concentration, fat pad mass, fat cell size, fat cell lipolysis, as well as lipoprotein binding to adipocyte plasma membranes. In adolescent (250 g) male Wistar rats fed 20% (w/w) fish oil supplemented diets for 3 weeks, plasma triglyceride levels and epididymal and perirenal fat pad mass were significantly (P less than 0.005) reduced compared to pair-fed controls given 20% lard diets. These differences in fat pad mass between the diets were greater than differences in whole animal mass or in the mass of livers, testes, kidneys, spleens, or hearts. Isoproterenol-stimulated lipolysis was significantly (P less than 0.005) higher in fish oil fed rats than in pair-fed controls. In young (100 g) rats plasma triglyceride levels were 10 times lower in the fish oil fed group after 5 weeks as compared to the lard-fed controls. This was accompanied by a reduction in epididymal and perirenal fat pad mass as well as a 2-3-fold decrease in adipocyte volumes; there was no significant difference between the two groups in fat cell number in each region. Plasma membranes of epididymal adipocytes from fish oil fed rats bound significantly (P less than 0.001) less HDL1 than the lard-fed rats, possibly as a result of a reduction in fat cell size and/or alteration of plasma membrane structure. Thus in both young and old rats, the reduction in plasma triglyceride concentration in conjunction with increased hormone-stimulated lipolysis may explain in part the selective reduction in adipose tissue trophic growth accompanying fish oil consumption.
 ...
PMID:Dietary fish oils modify adipocyte structure and function. 165 18

We compared the ability of adipocytes isolated from the epididymal fat pads of Sprague-Dawley and Fischer 344 rats of different ages and weights to release glycerol in response to beta-adrenergic stimulation. Twelve-month-old Sprague-Dawley rats weighed approximately three times more than did 2-month-old rats of the same strain (761 +/- 61 g vs 223 +/- 8 g, p less than .001). Basal glycerol release was increased in the adipocytes of the 12-month-old rats (128 +/- 8 nmol/10(5) cells/L compared to the 2-month-old rats 51 +/- 3 nmol/10(5) cells/L). However, the ability of isoproterenol to stimulate glycerol release above basal was markedly decreased in the older and fatter Sprague-Dawley rats (178 +/- 15 nmol/10(5) cells/L vs 482 +/- 20 nmol/10(5) cells/L, p less than .001), and significant correlation coefficients between isoproterenol-stimulated glycerol release and both total body (r = .76, p less than .001) and fat pad (r = .83, p less than .001) weight were seen in Sprague-Dawley rats. Total body weights of 2-month (188 +/- 16 g), 12-month (393 +/- 15 g), and 27-month-old (402 +/- 36 g) Fischer 344 rats were less disparate. Isoproterenol-stimulated glycerol release was similar in the three groups of Fischer 344 rats, and there was no correlation between either total body or fat pad weight and lipolysis in these rats.
 ...
PMID:Age-associated differences in beta adrenergic-stimulated lipolysis in adipocytes from Sprague-Dawley and Fischer 344 rats. 207 26

1. Phosphate-dependent glutaminase activity in the epididymal fat-pad was 15.1 nmol/min per mg of protein. Glutaminase activity demonstrated differences with respect to adipose-tissue sites. Considerable variation was found in different sites of adipose tissue from lean control and Zucker obese animals. 2. Adipocytes incubated in the presence of 2 mM-glutamine utilized glutamine at a rate of 1.8 mumol/h per g dry wt., and glutamate, ammonia, lactate and alanine were produced. Addition of glucose plus insulin increased the rates of glutamine utilization and glutamate, ammonia, lactate and alanine production. Isoprenaline alone or plus glucose further stimulated the rate of glutamine utilization and formation of end products. 3. The rate of incorporation of 14C from glutamine into CO2 was similar to that of glucose, but the rate of incorporation into triacylglycerol was much less. Addition of unlabelled glucose or glucose plus insulin stimulated the rate of incorporation of [14C]glutamine into triacylglycerol, but had no effect on that of 14CO2 formation. Isoprenaline plus glucose increased the rate of incorporation of [14C]glutamine into CO2, but decreased the rate of incorporation into triacylglycerol. 4. In the absence of insulin, the rate of [14C]glutamine incorporation into triacylglycerol was related to the glucose concentration (0-10 mM). However, in the presence of insulin, the rate of incorporation of [14C]glutamine was maximal at 1 mM-glucose.
 ...
PMID:Glutamine metabolism in isolated incubated adipocytes of the rat. 289 33

Electrical field stimulation of ring preparations of the epididymal (Ve) and prostatic (Vp) parts of the human isolated vas deferens produced contractions with similar frequency-dependence and appearance. The contractions of Ve, but not of Vp preparations were abolished by tetrodotoxin (10(-6)M). Noradrenaline (NA), phenylephrine, and methoxamine, but not clonidine induced repetitive, phasic contractions in both Ve and Vp preparations, and increased the amplitude of electrically induced responses. Clonidine concentration-dependently decreased electrically induced contractions in Ve preparations, but had no significant effects in Vp preparations. Phentolamine and prazosin abolished electrically induced contractions in Ve but not in Vp preparations. In Ve rings the contractions were increased by rauwolscine; no such effect was observed in Vp preparations. Isoprenaline, propranolol, acetylcholine and carbachol had no effects in the Ve or Vp preparations. Scopolamine and atropine reduced electrically induced responses. Clonidine decreased and rauwolscine increased the electrically induced release of 3H in both Ve and Vp preparations pre-loaded with 3H-NA. Phenylephrine, prazosin, isoprenaline, propranolol, carbachol and scopolamine had minor or no effects on the 3H release. Radioligand receptor binding experiments using 3H-prazosin and 3H-rauwolscine as ligands revealed similar densities of alpha 1- and alpha 2-adrenoreceptors in the human vas deferens. There seemed to be no differences in their distribution between the epididymal, middle and prostatic part of the organ. It is concluded that the neurotransmission in the human vas deferens is noradrenergic and mediated via alpha 1-adrenoreceptors. The prazosin and tetrodotoxin resistant part of the electrically induced contraction in Vp preparations may be caused by direct smooth muscle stimulation.
 ...
PMID:Effect of drugs interacting with adrenoreceptors and muscarinic receptors in the epididymal and prostatic parts of the human isolated vas deferens. 299 31

Intravenous administration of methacholine (200 micrograms/kg) caused no changes in the seminiferous tubules of rats, but significantly increased intraluminal pressures and contractility of the caput, the corpus and the cauda epididymidis. The effect of methacholine was abolished by pretreatment with atropine (500 micrograms/kg), but not by phentolamine (400 micrograms/kg) or propranolol (400 micrograms/kg). Adrenaline (5-40 micrograms/kg), noradrenaline (5-40 micrograms/kg) and phenylephrine (100-400 micrograms/kg) had no effect on the seminiferous tubules, but dose-dependently elevated intraluminal pressures and enhanced the contractility of all regions of the epididymis. Isoproterenol (100-800 micrograms/kg) did not affect intraluminal pressures of the seminiferous tubules and the epididymal duct. The stimulatory effect of adrenergic agonists was specifically blocked by phentolamine, but not by propranolol or atropine. Cholinergic and adrenergic antagonists did not alter spontaneous contraction of the epididymis. The results suggest that the contractility of all segments of the rat epididymis, but not the seminiferous tubules, can be increased by autonomic drugs. The enhancing effect of adrenergic drugs is probably the result of activation through alpha-adrenergic receptors.
 ...
PMID:Effects of cholinergic and adrenergic drugs on intraluminal pressures and contractility of the rat testis and epididymis in vivo. 614 94

The interrelationships among cAMP-dependent protein kinase activity, lipolysis, and cellular concentrations of cAMP were investigated in hamster epididymal adipose tissue. Isoproterenol, norepinephrine, and theophylline increased the protein kinase activity assayed in tissue extracts with no added cAMP, but not in the presence of added cyclic nucleotide. The maximum rate of lipolysis was associated with a nearly three-fold increase in cAMP levels and a protein kinase activity ratio of 0.8 (the ratio of activity assayed without cAMP to that assayed with cAMP). Rates of lipolysis less than maximum were associated with lesser degrees of protein kinase activity and lower levels of cAMP. The relatively pure alpha-adrenergic agent phenylephrine partially suppressed the isoproterenol-stimulated protein kinase activity, lipolysis, and cAMP levels. Conversely, the alpha-adrenergic blocking agent phentolamine increased the activity of protein kinase and cAMP levels in adipose tissues exposed to norepinephrine. These data are consistent with the primary role for cAMP and its dependent protein kinase in control of lipolysis in adipose tissue. Moreover, our data are consistent with the view that the antilipolytic action of alpha-adrenergic agents is mediated by a decrease in activity of protein kinase, caused by a decrease in cellular cAMP concentrations.
 ...
PMID:Activation of adenosine 3',5'-monophosphate-dependent protein kinase and its relationship to cyclic AMP and lipolysis in hamster adipose tissue. 624 85

An inhibitor (inhibitor-1) of phosphorylase a phosphatase has been identified in rat epididymal fat pads. This heat-stable, acid-soluble protein only exhibits phosphatase inhibitory activity when it itself is phosphorylated. Inhibitor-1 in rat adipose tissue migrates at 32,000 Da on sodium dodecyl sulfate-polyacrylamide gels, and at 64,000 Da on gel filtration. Exposure of fat pads to insulin (1 milliunit/ml) resulted in a 50% decrease in inhibitor-1 activity, compared to control (p less than 0.001). Isoproterenol (10(-6) M) caused a 25% increase in inhibitor-1 activity (p less than 0.05). Electrophoresis of heat-stable proteins prepared from hormone-treated 32P-labeled fat cells showed that insulin caused a dephosphorylation of the 32,000 Da phosphoprotein by 30% (p less than 0.01), whereas isoproterenol stimulated 32P incorporation in this protein by 35% compared to control (p less than 0.05). Thus, insulin appears to dephosphorylate and inactivate inhibitor-1, and might thereby result in an increase of protein phosphatase activity. Insulin regulation of inhibitor-1 is a mechanism which may underlie other of insulin's effects in adipose tissue, such as the activation of glycogen synthase.
 ...
PMID:Hormonal regulation of protein dephosphorylation. Identification and hormonal regulation of protein phosphatase inhibitor-1 in rat adipose tissue. 634 43

The effect of catecholamines on the levels of S-100 protein and nervous system-specific enolase (NSE) in epididymal adipose tissue of Wistar rats in vivo was examined by sensitive enzyme immunoassay methods. Soluble S-100 protein levels in the adipose tissue of 9-12-week-old rats (1.46 +/- 0.19 microgram/mg protein) were decreased to less than 50% of those of controls by serial injection (for 4-7 days) of epinephrine (0.1 mg/day) or norepinephrine (0.15 mg) with, however, little effect on the levels of membrane-bound (pentanol-extractable) S-100 protein. A significant decrease in the soluble S-100 protein levels was observed at 2 h after a single injection of epinephrine (1.04 +/- 0.13 microgram/mg protein). On the other hand, levels of NSE subunit (gamma subunit or 14-3-2 protein) in adipose tissue (0.51 +/- 0.03 gamma gamma-equivalent pmol/mg protein) were increased to 170% of control by serial injection (for 7 days) of epinephrine or norepinephrine with little change of the level of enolase alpha subunit on a mg protein basis. Isoproterenol had no apparent effect on the levels of soluble S-100 protein and NSE subunit. These results suggest that the levels of S-100 protein and NSE in adipose tissue are regulated by catecholamines.
 ...
PMID:Regulation of nervous system-specific S-100 protein and enolase levels in adipose tissue by catecholamines. 635 12


1 2 Next >>