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 order to elucidate the mechanism(s) of hyperlipidemia following glucocorticoid administration, dexamethasone (0.125 mg/Kg) was administered daily intramuscularly for 2 wk to male Sprague-Dawley rats and the effects on plasma triglyceride (TG) and cholesterol (Chol), lipoprotein neutral lipids, hepatic triglyceride secretion rates (TGSR; Triton), and epididymal fat lipoprotein lipase (LPL) were determined. Special measures were taken to maintain positive caloric balance and keep the weights of control and dexamethasone-treated animals comparable. Significant increases (p less than 0.001) in TG and very-low density lipoprotein (VLDL) triglyceride associated with no change in Chol and actual reduction in both triglyceride and cholesterol in low density lipoprotein (ldl) were observed in the steroid-treated animals. Dexamethasone treatment was associated with increased basal insulin and glucose levels, an insignificant increment in TGSR, and a highly significant reduction (p less than 0.001) in LPL. These findings suggest that glucocorticoid treatment increases splanchnic triglyceride production rates, but the resulting hypertriglyceridemia is primarily a consequence of impaired VLDL removal due to low adipose tissue LPL activity.
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PMID:Glucocorticoids and triglyceride transport: effects on triglyceride secretion rates, lipoprotein lipase, and plasma lipoproteins in the rat. 17 40

Dexamethasone acetate (100 microgram IP) protected male Holtzman rats (300-330 gm) against endotoxin shock due to Salmonella enteritidis lipopoly-saccharide B IV. Endotoxin (5.0 mg/rat) produced hypoglycemia within 180 minutes, ie, plasma glucose fell from 87 to 24 mg/dl; dexamethasone prevented the hypoglycemia, ie, plasma glucose levels were 129 mg/dl at 180 minutes after endotoxin. Dexamethasone antagonized both endotoxin-induced depression of hepatic gluconeogenesis and enhanced glucose oxidation as evaluated in vivo. Epididymal fat pads from endotoxic rats (100-110 gm) had increased rates of glucose oxidation as evaluated by the in vitro conversion of 14C-D-glucose to 14CO2. Dexamethasone both in vivo and in vitro antagonized endotoxin glucose hypercatabolism by isolated epididymal fat pads following administrated of endotoxin. Glucocorticoid protection against endotoxin shock is related to antagonism of glucose dyshomeostasis.
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PMID:Dexamethasone antagonism of glucose dyshomeostasis in endotoxin shock. 28 Apr 23

Glucocorticoids administration presumably affects the vascular system and causes avascular necrosis of the femoral head. However, the mechanism by which this occurs is still unknown. In order to clarify the action of glucocorticoids on the vascular system, we investigated the effects of dexamethasone on an angiogenesis model in vitro. The angiogenesis model was obtained by co-culturing vessel fragments and myofibroblastic cells from rat epididymal fat pads. In this model, myofibroblastic cells induce capillary formation by producing an endothelial cell growth factor and collagen. Dexamethasone at physiological doses inhibited significantly capillary growth by suppressing the collagen synthesis by myofibroblastic cells. However, dexamethasone had no effect on endothelial cells. These results indicate that glucocorticoids are related to the pathogenesis of avascular necrosis of the femoral head by inhibiting the repair of the vascular system in vivo.
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PMID:[The effects of glucocorticoids on angiogenesis in vitro]. 138 Sep 69

Lipoprotein lipase (LPL) is an enzyme found in adipose tissue that is important in the hydrolysis of triglyceride rich lipoproteins, and in the uptake of FFA lipid into the adipocyte. To examine the effects of glucocorticoids on adipose tissue LPL, male Sprague-Dawley rats were injected with dexamethasone (1 mg/kg) every other day for 10 days, followed by measurement of LPL in epididymal adipose tissue. Compared to sham-injected controls, heparin-releasable LPL activity and LPL mass in the dexamethasone-treated rats were 44% and 62% of those in control rats, respectively. Adipocytes were prepared from the fat pads and pulse labeled with [35S]methionine, demonstrating a decrease in the LPL synthetic rate in the treated rats to 57% of the rate in control rats. In addition, LPL mRNA was quantitated by Northern blotting, demonstrating a decrease in LPL mRNA in the dexamethasone-treated rats. A simultaneous decrease in the message for gamma-actin was also noted. To examine the effects of dexamethasone on LPL in vitro, adipocytes were prepared from normal rats and treated with dexamethasone for 24 h in vitro. Dexamethasone decreased heparin-releasable LPL activity in cultured adipocytes to 40 +/- 6% of the control value (P less than 0.01). This decrease in LPL activity was accompanied by a decrease in the LPL synthetic rate using [35S]methionine labeling, to 33% of the control value, and no specific change in LPL turnover or secretion. In addition, dexamethasone added to adipocytes decreased LPL mRNA levels. Because the combination of insulin plus dexamethasone has been shown to yield synergistic increases in LPL in adipose tissue pieces, insulin was added to isolated adipocytes in combination with dexamethasone. Whereas insulin and dexamethasone individually had opposite effects on LPL, the combination of insulin plus dexamethasone resulted in no change in any aspect of LPL gene expression. Thus, dexamethasone resulted in a decrease in adipocyte LPL mRNA levels both when added to cultured adipocytes in vitro as well as when injected into rats. This decreased LPL mRNA level yielded corresponding changes in the LPL synthetic rate and LPL activity.
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PMID:The regulation of lipoprotein lipase gene expression by dexamethasone in isolated rat adipocytes. 154 42

Rat epididymal fat cells were isolated and incubated with 25 microunits insulin/ml for 15 minutes. Insulin induced a significant shift in the saturated/unsaturated fatty acid ratio of the cerebroside fraction isolated from fat cell ghosts. This change was due to a decrease of saturated fatty acids and an increase of unsaturated fatty acids which were hydrolyzed from the isolated lipids. There were no significant changes in the amount of phospholipids isolated from the fat cell ghosts after this period of incubation with insulin or of fatty acids associated with them. Isolated adipocytes were also incubated with 8 x 10(-8) M dexamethasone for 2 1/2 hours. Insulin (25 microunits/ml) was then added, and the incubation continued for 15 minutes. Dexamethasone treated cells did not show a statistically significant insulin stimulated decrease in the saturated/unsaturated fatty acid ratio. These studies demonstrate an insulin induced change in membrane lipids which appeared to be partially blocked by previous exposure to dexamethasone.
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PMID:Insulin induced alterations of acyl groups of the cerebroside fraction isolated from fat cell ghosts. 701 90

Studies were undertaken to evaluate the direct insulin-like action of S enteritidis endotoxin on glucose oxidation in the rat epididymal fat pad and to assess antagonism by steroidal and nonsteroidal anti-inflammatory agents. In vitro administration of endotoxin at concentrations of 500, 100, 50, and 10 micrograms/ml significantly increased adipose tissue glucose oxidation by 115, 92, 55, and 32%, respectively. Exposure of the fat pads to endotoxin (100 microgram/ml) for timed incubations of 120 to 5 min, all produced significant increments in glucose oxidation. The insulin-like action of endotoxin was significantly less in Ca2+ free-KRB plus EGTA. Cotreatment of the fat pads with endotoxin and the steroidal anti-inflammatory agents, dexamethasone and methylprednisolone, as well as the nonsteroidal anti-inflammatory agent, indomethacin, significantly antagonized endotoxin-stimulated glucose oxidation. Dexamethasone antagonism was not significant if it was added after endotoxin treatment. Testosterone, a steroid with no anti-inflammatory activity, did not antagonize endotoxin's insulin-like action. The data provide further evidence of the direct insulin-like action of endotoxin and suggest that the protective effect of dexamethasone, methylprednisolone, and indomethacin may be due, in part, to a direct antagonism of endotoxin at the tissue level.
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PMID:Insulin-like action of endotoxin: antagonism by steroidal and nonsteroidal anti-inflammatory agents. 702 80

Adrenalectomy produces a significant fall in the sphingomyelin and cholesterol content of ghosts isolated from rat epididymal fat cells. Previous studies from this laboratory have demonstrated an effect of dexamethasone in vitro to increase the sphingomyelin content of fat cell ghosts obtained from adrenalectomized animals. The present study demonstrates that adrenalectomy influences the membrane lipid content. Dexamethasone, in vitro, was found to increase the sphingomyelin of epididymal fat cell ghosts isolated from intact animals, as it previously had been shown to affect epididymal fat cell ghosts obtained from adrenalectomized animals. Incubation with dexamethasone for 3 h had no effect on the cholesterol content of the ghosts. Adrenalectomy, on the other hand, resulted in a significant decrease in the cholesterol content of the fat cell ghosts.
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PMID:Adrenalectomy decreases the sphingomyelin and cholesterol content of fat cell ghosts. 709 79

Previous quantification of glucocorticoid receptor (GR) binding in adipose tissue has been performed in cytosol preparations, which did not allow the determination of the total number of GR in the cell. Therefore, GR binding was determined in intact adipocytes. Dexamethasone (dex) was used as a ligand in adipocytes isolated from epididymal (Epi), retroperitoneal (Ret), inguinal (Ing) and mesenteric (Mes) adipose tissue regions in male rats. The binding was saturable and specific with a Kd in the nanomolar range, not different from previously reported affinity of binding in cytosol preparations from adipocytes. Binding capacity rose after removal of endogenous glucocorticoids either by adrenalectomy (ADX) or culture in a glucocorticoid-free medium. Binding capacity of adipocytes was in general higher in Mes adipose cells than in adipocytes from Epi, Ing and Ret tissues from intact and ADX animals when expressed per unit of triglyceride weight of adipose tissues. This seemed to be largely explainable by a higher cellular density in Mes than in other adipose tissues. When comparisons were performed with binding per adipocyte, intraabdominal (Epi, Ret and Mes) cells bound more dex than adipocytes from subcutaneous (Ing) adipose tissue. It is suggested that in comparison with other adipose tissues Mes tissue has a higher density of the GR in situ, due mainly to a higher cellular density. Intraabdominal adipocytes in general seem to have a higher GR density than subcutaneous cells. This might explain the high activity of glucocorticoid-regulated metabolic pathways in intraabdominal particularly Mes adipose tissue.
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PMID:Glucocorticoid hormone binding to rat adipocytes. 794 39

The obese (ob) gene has been cloned recently and its protein product is called "leptin". Leptin is an adipocyte-derived satiety factor that regulates body weight homeostasis. Several hormonal factors have been reported to regulate ob mRNA expression. To determine which factors are most important for regulation of ob mRNA expression, we examined the effects of insulin, dexamethasone, a beta3-adrenergic agonist (CGP12177A), 8-bromo-cAMP, 8-bromo-cGMP and 1-methyl-3-isobutylxanthine (MIX) on primary cultured adipocytes. Rat adipocytes obtained from epididymal fat were cultured using the ceiling method. Total RNA was extracted and the expression of ob mRNA was measured by quantitative reverse transcription-polymerase chain reaction. After 24 h of incubation, 100 nmol/l insulin significantly increased the expression of ob mRNA (21.4-fold compared to control). Moreover, insulin increased ob mRNA expression in a dose-dependent manner over a range of 1-100 nmol/l. The effect of 100 nmol/l insulin was similar to that seen with 20% newborn calf serum. Dexamethasone (25-1000 nmol/l) also increased ob mRNA expression (2.5-2.9-fold). The effect of dexamethasone occurred more rapidly than insulin. CGP12177A (1-10 micromol/l) and 0.5 mmol/l 8-bromo-cAMP had no effects, whereas 0.5 mmol/l 8-bromo-cGMP and 0.5 mmol/l MIX had stimulatory effects (2.8- and 2.4-fold increase in ob mRNA, respectively). The combination of 250 nmol/l dexamethasone and 0.5 mmol/l MIX did not have an additive effect on ob mRNA levels. Our present data suggest that, of these agents, insulin is the most important factor regulating ob mRNA expression.
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PMID:Regulation of obese mRNA expression by hormonal factors in primary cultures of rat adipocytes. 898 Jan 66

The aim of this study was to investigate the effect of dexamethasone on acrosin activity of spermatozoa in Chios rams during autumn (breeding season for sheep in Greece), in correlation with possible changes in blood testosterone. Dexamethasone was administered in four equal consecutive intramuscular injections, one every four hours (total dose: 3 mg kg(-1)). Total acrosin activity was determined in semen samples collected 48 h before and on the 4th and 7th day and thereafter once every week until the 77th day after dexamethasone administration. Blood samples for testosterone radioimmunoassays were collected 24 h before, during dexamethasone administration and on the 4th, 7th, 14th and 21st day after administration. Total acrosin activity in spermatozoa was reduced between days 7-28 after dexamethasone administration. Dexamethasone also induced a reduction in mean value and basal level of blood testosterone and inhibited its episodic secretion between 1 and 4 days after administration. As the reduction of acrosin activity appeared relatively soon after dexamethasone administration (7th day), it is likely that the increased amount of dexamethasone did not influence the synthesis of proacrosin in the late spermatids. As glucocorticoid receptors exist in the epididymis and accessory glands in various species, dexamethasone may have a direct influence on the synthesis and/or release of acrosin inhibitors in epididymal fluid or seminal plasma. These changes in acrosin activity in ovine spermatozoa mediated by dexamethasone may be of importance regarding the role of stress in the reduction of sperm fertilizing ability.
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PMID:Dexamethasone reduces acrosin activity of ram spermatozoa. 1205 16


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