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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a first series of experiments, the effects of uridine and inosine on glucose metabolism in rat diaphragm muscle incubated in Krebs-bicarbonate buffer were studied. Uridine in concentrations of 10(-4) to 10(-6) M stimulated the uptake of glucose and increased the content of glycogen, but had no effect on the production of lactate. When diaphragm muscles were incubated in the buffer without glucose, uridine (10(-4)-10(-6) M) had no effects on the content of glycogen and on the production of lactate. On the other hand, inosine in concentrations of 10(-4) to 10(-6) M stimulated the uptake of glucose and the production of lactate, but had no effect on the content of glycogen in the muscle. In a second series of experiments, uridine (10(-4)-10(-5) M) and inosine (10(-4)-10(-7) M) inhibited the relase of glycerol from isolated rat epididymal adipose tissue in Krebs-bicarbonate buffer. Uridine and inosine in concentrations of 10(-4) M inhibited the epinephrine (10(-5) M)-, the norepinephrine (10(-5) M)- and the theophylline (10(-3) M)-stimulated lipolysis. Dibutyryl 3',5'-adenosine monophosphate-stimulated lipolysis was further activated in the presence of 10(-4) M uridine or inosine. Dose-response curves studies suggested that inosine, but not uridine, has a common receptor site with epinephrine in adipose tissue. These results demonstrated that both nucleosides stimulated the glucose uptake, but only uridine increased the synthesis of glycogen in the muscle. Both nucleosides also inhibited lipolysis in adipose tissue. The mechanism of antilipolytic action of these nucleosides is unknown, but one of the receptor sites for inosine might be adenylate cyclase.
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PMID:Effects of uridine and inosine on glucose metabolism in skeletal muscle and activated lipolysis in adipose tissue. 18 86

The reversible deactivation of chicken adipose tissue hormone-sensitive lipase alpha(previously activated with Mg2+ ATP and adenosine 3':5'-monophosphate) required Mg2+ and was inhibited by phosphate. These results are consistent with the assumption that deactivation of the protein kinase-activated enzyme is catalyzed by a lipase phosphatase. Cholesterol ester is catalyzed by a lipase phosphatase. Cholesterol ester hydrolase similarly was activated and reversibly deactivated. The activity of endogenous lipase phosphatase in pH 5.2 precipitate fractions was reduced, and in some cases eliminated, by incubation at 50 degrees for 20 min in buffer containing 20% glycerol. Heating at 50 degrees greatly increased the apparent percentage activation of triglyceride and cholesterol ester hydrolases but this was due to a selective decrease in basal (nonactivated) hydrolase activities. Essentially all endogenous lipase phosphatase could be removed by treatment of the pH 5.2 precipitate fraction with ATP-Sepharose affinity gel. The addition of a partially purified preparation of rat liver phosphorylase phosphatase deactivated triglyceride and cholesterol ester hydrolases. The deactivation process was concentration, 5 mM) and was inhibited by 5 mM phosphate and by phosphorylase alpha. Reversible deactivation of hormone-sensitive lipase alpha was also observed with crude prepa- and by phosphorylase alpha. Reversible deactivation of hormone-sensitive lipas alpha was also observed with crude preparations of phosphoprotein phosphatases from rat and turkey hearts, and from rat epididymal fat pads. Thus, hormone-sensitive lipase is deactivated by a variety of phosphoprotein phosphatases from different tissues and different species, implying a low degree of specificity for the deactivating system.
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PMID:Role of phosphoprotein phosphatases in reversible deactivation of chicken adipose tissue hormone-sensitive lipase. 19 Feb 35

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.
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PMID:Lipolysis and cyclic AMP levels in epididymal adipose tissue of obese-hyperglycaemic mice. 20 30

Early report by Kopp et al. have demonstrated that p-nitrophenyl-glycerol (PNPG) is an effective antiswarming agent in Proteus and that this inhibition may have been caused by PNPG interfering with the negative chemotaxis mechanism in the organism. With an inverted capillary assay, designed to test the motility response of rat epididymal spermatozoa to various suspending conditions including those exposed to chemical gradient, PNPG was shown in this study to exhibit an inhibitory effect at slightly higher than 10(-5) M. Moreover, this inhibitory effect appears to have stemmed from spermatozoa being repelled by PNPG as indicated by the observation that significantly less spermatozoa swim into a gradient of PNPG. The possibility of using spermatozoa repellents as contraceptives is discussed.
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PMID:Spermatozoa repellent as a contraceptive. 45 77

The effects of adrenaline (0.5 microM) and the combination of adrenaline and insulin (1.7nM) on [6-14C]glucose metabolism were assessed in epididymal fat-pads from rats fed either a low- or high-fat diet. The response of lipolysis to adrenaline was clearly diminished in fat-fed rats. Insulin added to adrenaline inhibited the lipolysis by 50% regardless of the diet. Glucose utilization in adipose tissue of fat-fed rats was markedly stimulated by adrenaline (glucose uptake was increased 3-fold and the production of CO2 and the glycerol moiety of acylglycerol was increased 4-fold). However, adipose tissue from fat-fed rats was resistant to the effect of insulin to produce a further increase in adrenaline-stimulated glucose uptake. The intracellular capacity of lipogenesis on the one hand, and the production of CO2 and the glycerol moiety of acylglycerol on the other, are of prime importance in the action of insulin and adrenaline on glucose utilization in this model.
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PMID:Adrenaline responsiveness of glucose metabolism in insulin-resistant adipose tissue of rats fed a high-fat diet. 48 19

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

It was demonstrated that Ledakrin, an antitumour drug, causes mobilization of free fatty acids and glycerol from the epididymal adipose tissue of rat in vitro. The disproportion observed in the release of glycerol and free fatty acids following Ledakrin administration suggested a biphasic effect of this drug, with initial stimulation and later inhibition of the processes of lipolysis and lipogenesis. Blockade of adrenergic membrane receptors (with propranolol or regitine) abolished the lipolytic effect of Ledakrin.
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PMID:Ledakrin effect on free fatty acid and glycerol mobilization from epididymal adipose tissue of rat in vitro. 53 74

Metabolic adaptations to cyclic patterns of food intake were studied in genetically lean and obese Zucker rats. Twenty-four lean and 24 obese rats were exposed to 12 hours of light and 12 hours of dark and allowed food ad libitum. Both groups of rats ate more during the dark period of the cycle. The obese consumed nearly twice as much food as the lean during the light period of the cycle. At 4-hour intervals, rats were killed and liver and epididymal fat pads were removed for metabolic studies. Adipose tissue from lean rats demonstrated marked changes in rates of lipogenesis during the 24-hour cycle whereas adipose tissue from obese rats maintained a relatively steady rate of lipogenesis. Glucose incorporation into the glycerol moiety of triacylglycerol was nearly 3-fold higher in adipose tissue from obese rats. Liver lipogenesis in lean and obese rats followed their food intake pattern. Liver lipogenic rate (expressed per organ) was 3- to 5-fold higher in obese than lean rats during most of the 24-hour cycle. These data support the concept that the excessive fatty acids produced in the liver of obese rats are being esterified by adipose cells. Lipolytic response to glucagon was found in adipose tissue from obese rats during the dark and light periods, but only during the dark period for lean rats. These data suggest, in comparison to lean rats, that obese rats do not enter a relative catabolic state during a 24-hour cycle. A constant anabolic state in the genetically prone individual may lead to excessive lipid deposition and obesity.
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PMID:Diurnal changes in adipose and liver tissue metabolism of lean and obese Zucker rats. 57 Oct 11

The effect of 10 mM fluoride on glycerol production in vitro from rat epididymal adipocytes was investigated. Fluoride had no effect on the basal glycerol production, irrespective of the presence or absence of Ca++ and Mg++ ions. When stimulating the glycerol production with 10 mM theophylline, fluoride reduced the stimulation in the absence of either Ca++ or Mg++ or both. In the presence of both ions, fluoride had no effect on the theophylline stimulation. Fluoride also reduced the stimulative effect of adrenaline on glycerol production, but not that of glucagon. Increased adrenaline concentration could not overcome the inhibitory effect of fluoride.
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PMID:Effect of fluoride on glycerol production in rat adipocytes in vitro. 57 58

Subfractionation of the fat free homogenate of rat adipose tissue showed that a high yield of triglyceride lipase was recovered reproducibly in the microsomal supernatant fraction (cytosol) when rat epididymal fat pads were homogenized in sucrose-EDTA-Tris medium. Triglyceride lipase was bound on heparin-Sepharose. Hydrolyzing activity towards triacylglycerol was eluted as a single, sharp peak in 0.7 M NaCl, 5 mM sodium barbital and 20% glycerol (pH 7.0). The triglyceride lipase was not inhibited by 1 M NaCl and not stimulated by the presence of fresh human serum. A lipoprotein-lipase activity was demonstrable in the cytosol when adipose tissue from fed rats were used. Fasting of the animals lowered this activity.
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PMID:Affinity chromatography on heparin-sepharose of rat adipose tissue triglyceride lipase from cytosol. 66 59


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