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)

In epididymal adipose tissue from rats, human serum antagonizes inhibition of basal lipolysis by nicotinic acid in vitro. Under similar conditions caffeine-stimulated lipolysis was unaffected by the presence of human serum. Very low density (VLDL), low density (LDL) and high density (HDL) lipoproteins were all found to antagonize the action of nicotinic acid on basal lipolysis. VLDL also antagonized prostaglandin E1 (PGE1)-inhibition of basal lipolysis in vitro. The fat cell membrane was suggested as the site at which human serum lipoproteins antagonize nicotinic acid or PGE1 antilipolytic action on basal lipolysis in vitro.
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PMID:Modification of nicotinic acid and prostaglandin E1 antilipolytic action in vitro. 18 78

The effects of forskolin and the antilipolytic agents nicotinic acid and insulin on cAMP accumulation in rat epididymal adipocytes were evaluated. Forskolin markedly stimulated cAMP accumulation in adipocytes of the rat. Addition of epinephrine to cells treated with forskolin acted synergistically to increase the cAMP accumulation 4-fold when compared with cells treated with forskolin alone. Analysis of the forskolin dose-response kinetics indicated a dose-dependent increase in the accumulation of cAMP. The presence of 1-methyl-3-isobutylxanthine caused a shift in the forskolin dose-response to lower concentrations. In contrast, addition of nicotinic acid to cells treated with 1-methyl-3-isobutylxanthine caused a shift in the forskolin dose-response to higher concentrations. Preincubation of cells with adenosine deaminase did not alter the forskolin dose-response curve but potentiated its effect. Forskolin stimulation of cAMP accumulation in adipocytes was inhibited by the antilipolytic agents nicotinic acid and insulin.
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PMID:Evaluation of the effects of forskolin and the antilipolytic agents insulin and nicotinic acid on cyclic AMP levels in rat epididymal adipocytes. 242 74

An earlier report from this laboratory showed that feeding rats a high fat diet decreased epinephrine-stimulated lipolysis in their adipose tissue. Experiments were designed to explore further the effects of such diets on adipocyte response to epinephrine and to several other lipolytic and antilipolytic agents. Rats were fed diets with 67% of energy consisting of glucose or lard for 5 to 7 d. Adipocytes were prepared from epididymal fat pads and lipolysis measured by the release of glycerol into the medium during 1-h incubations. The cells from the rats fed the high fat diet showed lower lipolytic responses to stimulation by epinephrine, forskolin and dibutyryl cyclic AMP than those from rats fed the high glucose diet. The lard diet effect on the lipolytic response to isobutylmethylxanthine varied among experiments, but it also decreased it in some of them. However, the high fat diet did not induce decreased sensitivity or responsiveness to the antilipolytic effect of insulin, although previous reports have demonstrated resistance to other actions of insulin in rats fed a high fat diet. The antilipolytic effect of nicotinic acid was also similar in cells from rats fed a high fat diet to that found for cells from rats fed the high glucose diet.
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PMID:Effect of a high fat diet on rat adipocyte lipolysis: responses to epinephrine, forskolin, methylisobutylxanthine, dibutyryl cyclic AMP, insulin and nicotinic acid. 243 78

A biologically active, low-molecular-weight, chromium-binding substance present in milk (M-LMCr) was isolated from bovine colostrum and purified more than 2000 times by means of ethanol precipitation and successive ion-exchange and Sephadex gel chromatographies. The purified M-LMCr appeared to be an anionic organic Cr compound with a molecular weight of 1500, as determined by gel permeation chromatography. It contained aspartic acid, glutamic acid, glycine and cysteine in a ratio of 5:4:2:1 and no detectable carbohydrate. Although we were unable to detect nicotinic acid, some ultraviolet-absorbing (lambda max 260 nm) chemical structure was shown to be a constituent. Purified M-LMCr stimulated the rates of both [U-14C]glucose oxidation and [3-3H]glucose conversion into lipid in rat epididymal adipocytes at Cr concentrations greater than 1.5 ng/mL in relation to insulin action. This substance appears to have properties similar to those of glucose tolerance factor in yeast and the low-molecular-weight, chromium-binding substance present in mammalian liver. The role of M-LMCr in Cr nutrition and detoxication is discussed.
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PMID:Purification and properties of biologically active chromium complex from bovine colostrum. 327 60

Using an isolated rat epididymal adipocyte system we have studied the development of tolerance to and cross-tolerance between nicotinic acid, 5-methylpyrazole-3-carboxylic acid and pyridyl-3-tetrazole. Preincubating isolated adipocytes with any one of these compounds results in a reduction of the antilipolytic activity of that compound when the cells are exposed to a subsequent challenge dose. Furthermore, preincubation with nicotinic acid, 5-methylpyrazole-3-carboxylic acid or pyridyl-3-tetrazole results in a reduction of the antilipolytic response to challenge with either of the other two compounds. Preincubation of isolated adipocytes with nicotinic acid does not affect the subsequent antilipolytic activity of the PGE2 analogue, sulprostone. Preincubation with sulprostone does not lead to the development of tolerance to its own antilipolytic actions. The results obtained from these studies suggest that nicotinic acid, 5-methylpyrazole-3-carboxylic acid and pyridyl-3-tetrazole exert their antilipolytic activity via a common biochemical pathway which is distinct from that mediating the antilipolytic activity of prostaglandins. These findings also indicate that the development of tolerance occurs prior to the involvement of adenylate cyclase in lipolysis.
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PMID:The development of tolerance to antilipolytic agents by isolated rat adipocytes. 396 29

The antilipolytic activity of a series of N aryl-nicotinamides and of alpha picolinic acid, has been tested in vitro. Lipolysis was stimulated by epinephrine (20 micrograms/ml of incubation medium) using rat's epididymal adipose tissue slices. Only N(2-carboxy methyl phenyl) nicotinamide showed antilipolytic effect comparable to that of nicotinic acid at similar concentrations (2 X 10(-5) M). Picolinic acid (10(-4) M) showed no antilipolytic effect. These results, together with those of the literature, are discussed in regard to the relations between structure and antilipolytic activity.
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PMID:[Antilipolytic activity in vitro of various analogs of nicotinic acid. Structure-activity relationship]. 623 96

The effect of AY-25,712 [2-methyl-2-phenyl-3(2H)-furanone-5-carboxylic acid] on various aspects of free fatty acid (FFA) and triglyceride metabolism was studied in male rats. Serum triglycerides were lowered by a single oral dose of AY-25,712 or nicotinic acid, but not of clofibrate. Unlike with clofibrate, when AY-25,712 or nicotinic acid was given in the diet, serum triglycerides were not affected. In vitro, both AY-25,712 and nicotinic acid suppressed the theophylline-induced FFA release by epididymal fat pads, but had no effect on lipolysis induced by norepinephrine. Both AY-25,712 and nicotinic acid enhanced the activity of adipose tissue lipoprotein lipase. The initial decrease in plasma FFA and triglycerides, and in liver triglycerides after a single oral dose of nicotinic acid was followed by a rebound to levels which, at later time intervals, wee significantly higher than in controls. AY-25,712 was more potent than nicotinic acid in lowering plasma FFA and triglycerides as well as liver triglycerides, but produced no such rebound effect. The data show that, except for the absence of this rebound effect, the mode of action of AY-25,712 in rats resembles that of nicotinic acid and differs from that of clofibrate.
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PMID:Effect of AY-25,712 on fatty acid metabolism in rats. 715 99

To contribute to the understanding of the hypolipidemic action of etofibrate, which is the 1,2-ethandiol ester of clofibric acid and nicotinic acid, 300 mg of this drug/kg body weight or of the medium were administered daily by a stomach tube to normolipidemic rats. Some animals were decapitated at the 10th day of daily treatment (prolonged treatment), whereas others were studied at different times after one single administration (acute treatment). In animals on prolonged treatment etofibrate decreased plasma levels of cholesterol, triacylglycerols, free fatty acids (FFA) and glycerol, as well as the total and unesterified cholesterol concentrations, in liver microsomes. In these rats, etofibrate increased the activity of liver cytosolic glycerol-3-P dehydrogenase, whereas it decreased the activity of both microsomal HMG-CoA reductase and cholesterol 7 alpha-hydroxylase and did not affect acyl-CoA: cholesterol acyltransferase (ACAT). At 3, 5 and 7 h after acute treatment, etofibrate decreased plasma levels of triacylglycerols, glycerol and FFA, and this effect disappeared at 24 h, whereas plasma cholesterol did not change 3 h after etofibrate but decreased at 5 and 7 h and remained low after 24 h, and a similar change was found in the liver microsomes free cholesterol concentration. However, with the exception of a significant reduction in cytosolic glycerol-3-P dehydrogenase at 7 h and in ACAT at 5 h, acute etofibrate treatment did not affect the activity of the liver enzymes studied. At low concentrations (10(-5) M) in the incubation medium, etofibrate decreased the release of both FFA and glycerol by epididymal fat pad pieces incubated in vitro. These findings together with those previously reported by us in rats using a similar etofibrate treatment protocol [6] indicate that etofibrate decreases the availability of lipolytic products in the liver by acting on their release from adipose tissue and on their intrinsic hepatic metabolism. Consequently, this drug would decrease liver VLDL triacylglycerol synthesis and secretion, which together with facilitating the clearance of circulating triacylglycerols causes its hypotriglyceridemic effect. The hypocholesterolemic effect of etofibrate after acute treatment may be a secondary consequence of the reduced liver VLDL production caused by decreased adipose tissue lipolysis, but after prolonged treatment, this effect also seems to be influenced by the inhibition of HMG-CoA reductase activity which would reduce cholesterol synthesis.
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PMID:Studies with etofibrate in the rat. Part II: A comparison of the effects of prolonged and acute administration on plasma lipids, liver enzymes and adipose tissue lipolysis. 832 74

The synthesis of NAD and NADP by rat adipose tissue was measured in vitro. Nicotinamide-7-(14)C and NaH(2)(32)PO(4) were incorporated together into NAD with a (32)P/(14)C ratio of 1.82 and nicotinic-7-(14)C acid and NaH(2)(32)PO(4) with a ratio of 1.94. Nicotinic acid stimulated, by 90%, lipogenesis from glucose-U-(14)C by rat adipose tissue in vitro. Glucose plus insulin and refeeding for 48 hr after a 48 hr fast markedly increased the incorporation of nicotinic-7-(14)C into NAD in rat epididymal fat pads in vitro, but neither fructose, L-glutamine, nor insulin alone increased the synthesis of NAD in this tissue. Glucose-1-(14)C, ribose-1-(14)C, and to a greater extent glucose-6-(14)C are incorporated into the NAD of rat adipose tissue. Fasting followed by refeeding sharply increased the radioactivity of NAD-(14)C formed from glucose-1-(14)C and glucose-6-(14)C but not from ribose-1-(14)C. Increasing the ribose concentration from 2 mM to 10 mM increased its incorporation into adipose tissue NAD twofold. The nicotinic-7-(14)C acid incorporation into NAD increased over the 1st hr of incubation and remained constant for the next 3 hr. The concentration of NAD in the fat pads showed a similar response to the time of incubation. NADP concentrations increased over the entire 4 hr incubation period as did the incorporation of nicotinic-7-(14)C acid into NADP. The results of this study suggest that NAD is synthesized de novo by rat adipose tissue in vitro and that this synthesis is increased by factors which stimulate lipogenesis.
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PMID:Pyridine nucleotide synthesis by rat adipose tissue in vitro. 1456 2

Factors which regulate expression of the haptoglobin (acute phase reactant) gene in adipocytes have been examined using 3T3-L1 cells. Haptoglobin expression was observed by Northern blotting in each of the major white adipose tissue depots of mice (epididymal, subcutaneous, mesenteric, and perirenal) and in interscapular brown fat. Expression occurred in mature adipocytes, but not in the stromal-vascular fraction. In 3T3-L1 cells, haptoglobin mRNA was detected from day 4 after the induction of differentiation into adipocytes. Lipopolysaccharide and the cytokines, TNFalpha and interleukin-6, resulted in substantial increases in haptoglobin mRNA in 3T3-L1 adipocytes; the increase (7-fold) was highest with TNFalpha. Increases in haptoglobin mRNA level were also induced by dexamethasone, noradrenaline, isoprenaline, and a beta3-adrenoceptor agonist. In contrast, haptoglobin mRNA was reduced by nicotinic acid and the PPARgamma agonist, rosiglitazone. RT-PCR showed that the haptoglobin gene was expressed in human adipose tissue (subcutaneous, omental). It is concluded that haptoglobin gene expression in adipocytes is stimulated by inflammatory cytokines, glucocorticoids, and the sympathetic system, while activation of the PPARgamma nuclear receptor is strongly inhibitory.
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PMID:Regulation of haptoglobin gene expression in 3T3-L1 adipocytes by cytokines, catecholamines, and PPARgamma. 1469 47


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