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

1. The concentrations of glucose, pyruvate, lactate, citrate, glutamate, malate and aspartate were measured in epididymal adipose tissue from starved, fed and starved-re-fed rats. 2. To measure these intermediates it was necessary to correct for their concentration in the extracellular tissue space, which was considered to be most satisfactorily equated with the glucose space. This space in vivo was 7.42, 4.90 and 7.54ml./100g. wet wt. of tissue in adipose tissue taken from starved, fed and starved-re-fed rats respectively. After correction for the glucose space, the concentrations of metabolites (nmoles/g. of cells) in epididymal adipose tissue of fed rats were: pyruvate, 8.5; lactate, 50.3; citrate, 18.5; glutamate, 100.0; malate, 6.4; aspartate, 34.2. 3. Starvation for 72hr. resulted in a fall in pyruvate and aspartate concentrations to 3.57 and 25.1nmoles/g.; starvation for 72hr. followed by re-feeding for 72hr. caused an increase in glutamate and aspartate concentrations to 140 and 67.6nmoles/g. 4. These changes are interpreted with regard to the simultaneous alteration in lipogenesis that occurs during the starvation-re-feeding cycle.
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PMID:Measurement of adipose-tissue metabolites in vivo. 580 Dec 95

Protein synthesis and degradation were measured simultaneously in epididymal fat pads of rats by use of the incorporation of [14C]phenylalanine into protein and the sum of net protein breakdown and protein synthesis, respectively. Neither glucose nor insulin altered protein synthesis, but together they promoted this process; pyruvate could be substituted for glucose. Separately, glucose or insulin diminished proteolysis, and these effects were additive. In the presence of glucose and insulin, leucine, alanine, glutamine, glutamate, and aspartate lowered protein degradation to varying degrees but did not alter protein synthesis. Glutamate, but not leucine or alanine, was inhibitory without glucose and insulin present. When aminooxyacetic acid was provided to decrease the rate of transamination of amino acids, the inhibitory effects of leucine, alanine, and aspartate, but not of glutamate, appeared to be diminished. alpha-Ketoglutarate, but neither alpha-ketoisocaproate nor pyruvate, could diminish proteolysis. Inhibition of proteolysis was associated with a higher tissue content of glutamate and a greater production of glutamate and glutamine. These results suggest that glutamate itself may inhibit proteolysis in adipose tissue and mediate, at least in part, the effects of other amino acids.
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PMID:Regulation of protein turnover by glucose, insulin, and amino acids in adipose tissue. 614 13

The binding of 1,25-dihydroxyvitamin D3-receptor complexes from chick intestinal cytosol to DNA-cellulose and isolated intestinal nuclei is inhibited by several dye-ligands in a dose-dependent manner. Concentrations of Cibacron blue F3GA, blue dextran, Procion red HE3B, and Green A dye causing 50% competition for receptor binding to DNA-cellulose ranged from 2.8 to 3.6 microM. A structural analogue of the anthraquinone moiety of Cibacron blue F3GA, bromaminic acid, was 111-fold less potent in inhibiting DNA-cellulose binding. Moreover, the inhibitory effects of these dye-ligands is not due to a simple electrostatic effect, since two other polyanions, heparin and poly-L-glutamate, are much less effective. Whereas dye-ligands can cause the release of receptors bound to DNA-cellulose, they do not alter the dissociation of 1,25-dihydroxyvitamin D3 from its receptor nor do they affect the apparent equilibrium binding constant of the receptor or the concentration of available sterol-binding sites. The inhibition of binding by dye-ligands is competitive with respect to DNA-cellulose binding, indicating that the effect of these dyes is at a domain common to polynucleotides.
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PMID:Specificity of dye-ligand interaction with the polynucleotide binding domain of 1,25-dihydroxyvitamin D3-receptor complexes of chicken intestinal cytosol. 632 54

Soft tissue injury to one hindlimb of rats was used to test the response to trauma of metabolism in epididymal fat pads. Degradation of [1-14)C]leucine was lower on day 2 after injury, but not on days 1 or 3, whether or not glucose or insulin were provided. Although trauma did not affect the basal rate of release of 14CO2, lactate or pyruvate from fat pads incubated with [U-14C] glucose, the stimulation by insulin of these processes was smaller in fat pads of 2 day traumatized than of normal animals. These results suggest that trauma due to injury may decrease the capacity for utilization of leucine and glucose by adipose tissue. Release of alanine, glutamine and glutamate by fat pads incubated with leucine was also lower on day 2. This decreased efflux could not be accounted for by changes in net protein breakdown or in pyruvate availability and probably reflected their reduced de novo synthesis due to the diminished release of nitrogen from leucine.
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PMID:Metabolism of amino acids, protein and glucose in fat pads of traumatized rats. 637 55

The reductive carboxylation of 2-oxoglutarate was found to proceed in mitochondria of rat epididymal fat pads and rabbit perirenal adipose tissue at a rate similar to that in liver mitochondria. In rat fat pads the incorporation of 14C from [5-14C]2-oxoglutarate into fatty acids via the carboxylation was suppressed by butylmalonate by 30%. 2-Oxoglutarate and glutamate stimulated the incorporation into fatty acids of 14C from [2-14C]acetate in rat fat pads with the simultaneous reduction of tissue NADP. These effects persisted after inhibition of succinate dehydrogenase by malonate. It is concluded that in adipose tissue 2-oxoglutarate carboxylation proceeds in both the cytoplasm and mitochondria. Therefore, it can supply carbon atoms as well as NADPH for fatty acid synthesis.
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PMID:Intramitochondrial reductive carboxylation of 2-oxoglutarate in adipose tissue and its contribution to fatty acid synthesis. 653 9

1. Activation of both anion and cation conductances was observed in primary cultured human epididymal cells during osmotic swelling under the patch-clamp whole-cell configuration. The swelling-induced anion conductance was 25.66 +/- 4.70 nS and the cation conductance was 7.35 +/- 1.40 nS. The permeability ratio of K+ to Cl- (PK/PCl) was calculated to be 0.40. Known anion or cation channel blockers could inhibit both conductances simultaneously. 2. When the major permeant ion species in the pipette and bath solution was Cl-, the mean conductance was found to be 17.06 +/- 1.8 nS, significantly smaller than that obtained in the presence of intracellular K+, 25.66 +/- 4.70 nS (P < 0.05). No significant current activation was observed when solutions containing only K+ as the permeant ion were used. 3. When the anionic amino acids glutamate and aspartate were used to replace extracellular Cl-, the permeability ratios were calculated to be PGlut/PCl = 0.20 and PAsp/PCl = 0.17. 4. The cation conductance was found to be non-selective since its permeability to other cations such as Na+ and choline, an organic compound highly concentrated in epididymal fluid, was similar to that of K+. 5. Regulatory volume decrease (RVD) was observed after initial osmotic swelling; this could be inhibited by either anion or cation channel blockers. 6. The results of this study suggest that both anion and cation conductances are activated during cellular swelling, and indicate the existence of an interdependent relationship between the swelling-induced cation and anion conductances. Both swelling-induced cation and anion conductances are involved in the volume regulatory process and may be responsible for transporting amino acids or organic compounds in human epididymal cells.
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PMID:Swelling-induced anion and cation conductances in human epididymal cells. 752 48

Glutamine synthetase (GS) activity was measured in the caput and cauda regions of rat epididymis. Specific GS activity in the caput was 27-fold higher than that in the cauda. To compare GS activity within the epididymis to that within other tissues, specific and total GS activities were measured in the brain, liver, testes, kidney, and striated muscle. Caput epididymal specific GS activity was from 4- to 38-fold higher than GS activity in any other tissue; caput total GS activity was equal to that in brain. Epididymal GS activity was rapidly and completely inhibited by preincubation with methionine sulfoximine, a known inhibitor of GS. These results suggest that the high concentrations of GS activity in the caput epididymis may have functional significance in maintaining an optimal microenvironment for sperm maturation, perhaps by restoring luminal acid-base balance, removing ammonium and/or glutamate from the lumen, or supplying glutamine for the production of nucleic acids.
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PMID:Glutamine synthetase activity in rat epididymis. 791 21

In male Wistar rats the influences of age and experimental obesity on the activity of malic enzyme (EC 1.1.1.40) in different organs were studied. Obesity was induced in newborn rats by injection of Na(+)-L-glutamate (2 mg/g b.w. daily) subcutaneously in the first 5 days. The enzyme activity was measured at the ages of 2, 6 and 18 months. In control animals the highest enzyme activities were found in the heart muscle, liver, epididymal fat pad and skeletal muscle after 6 months. After 18 months the activities in these organs are considerably reduced. In the kidneys the activity between the 2nd and the 18th months tends to decrease continuously and only the brain shows an opposite trend. In comparison with the control animals, in glutamate treated rats the enzyme activity doubles nearly in the lipogenic organs liver and fat tissue in all age groups. In liver and fat tissue of 6-month-old rats, previously treated with clonidine to stimulate growth hormone secretion, the activities are lower than in glutamate obese rats without clonidine, but still higher than in normal control animals. The qualification of glutamate obese rats as a model for the study of age-associated diseases like obesity or diabetes mellitus type II needs further investigation.
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PMID:[Obesity, malic enzyme and aging--an animal experiment study]. 908 41

The effect of fasting on hormonal and metabolic variables was evaluated in normal rats and in rats with obesity induced by neonatal treatment with monosodium glutamate (MSG). The hyperinsulinemia of the fed obese rats was reversed by fasting. Plasma corticosterone was also high in the fed obese and decreased to levels similar to fed controls, while it increased in the latter group during fasting. In contrast, thyroid hormone levels decreased in controls but increased in the obese rats in response to fasting. The fed obese group had lower carcass protein and higher carcass lipid contents than controls. In response to fasting, the decrements of the initial amount of both protein and fat were lower in MSG than in controls. Fasting induced a sustained increase in plasma free fatty acids only in the obese rats, although a single 100 mumol.l-1 dose of norepinephrine stimulated in vitro glycerol release more pronouncedly in epididymal adipocytes from control than obese rats. The results indicate that MSG-obese rats were able to mobilize fat stores during prolonged fasting. The high availability of lipid fuels and the sharp and sustained decrease in circulating corticosterone in the MSG group were probably important in diminishing body protein consumption during fasting.
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PMID:Hormonal and metabolic adaptations to fasting in monosodium glutamate-obese rats. 928 91

In the present work the effects of fasting and refeeding on fat pad weight and alkaline phosphatase activity in the brush border of individual duodenal enterocytes have been evaluated in male Wistar rats with obesity induced by monosodium glutamate (MSG) treatment during the early postnatal period. Neonatal rats were treated subcutaneously with MSG (2 mg/g b.w.) or saline (controls) for 4 days after birth. At 4 months of age, two types of experiments were performed. In the first experiment rats, were submitted to 3 or 6 days lasting food deprivation. In the second experiment the rats were refed for 3 or 6 days ad libitum or restrictedly (60% of pre-fasting intake) after a 6 day-fasting period. Fasting and refeeding influenced the body fat and function of the duodenum in MSG-treated rats differently as compared to the controls. However, alkaline phosphatase activity and the weight of epididymal and retroperitoneal fat depots were significantly increased in MSG obese rats (P<0.001) during all the periods examined. While 3 days of food deprivation resulted in both groups in a similar loss of adipose tissue weight and alkaline phosphatase activity, the decrements of these parameters after 6 days of fasting were lower in obese rats suggesting that their capacity to spare body fat stores was enhanced. After 3 days of ad libitum refeeding, a more marked adaptational increase of food consumption and also a significantly increased alkaline phosphatase activity above the pre-fasting level (P<0.01) was observed in the MSG-treated rats. Consequently, a more rapid body fat restoration was demonstrated in these animals. Refeeding of rats at 60% of the pre-fasting intake level resulted in a significant increase of alkaline phosphatase activity in both the MSG and control group; moreover, as food restriction continued, MSG-treated rats tended to further increase the enzyme activity. Our results revealed that MSG treatment of neonatal rats may significantly change the intestinal functions. Permanently increased alkaline phosphatase activity observed in MSG obese rats during all investigated periods suggests that this functional alteration is probably not a consequence of actual nutritional variation but could be a component of regulatory mechanisms maintaining their obesity at critical values.
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PMID:Effect of fasting and refeeding on duodenal alkaline phosphatase activity in monosodium glutamate obese rats. 1155 Nov 42


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