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

Insulin antagonism characterizes infection, but the mechanism is unknown. Previous studies have been performed during the acute catabolic stage of infection, and the resultant metabolic changes reflect this decreased food intake and weight loss. To delineate metabolic alterations due to infection itself, rats with pyelonephritis induced by tail-vein injection of 1 ml. of Streptococcus faecalis (10(9) bacteria per milliliter) were studied two weeks later during a period of near-normal weight gain and food intake. Fasting growth hormone concentrations (nanograms per milliliter) in the pyelonephritic rats were nearly five times normal (45.8 vs. 9.9). Intra-arterial glucose and insulin tolerance tests were impaired. Early glucose-induced insulin release was depressed. Fat pads from infected rats manifested higher basal lipolysis per cell. Glycerol-mediated gluconeogenesis by liver slices was decreased. This pathway was unaffected by insulin in infected rats but readily inhibited in control rats. The following metabolic parameters were similar in control and infected animals: (in vivo) fasting concentrations of plasma glucose, free fatty acids, triglycerides, total corticoids, creatinine, insulin, glucagon, molar ratios of insulin and glucagon, glucose and insulin responses to tolbutamide, and glucagon and free fatty acid suppression after glucose; (in vitro) glucose metabolism by muscle and fat, epinephrine- and theophylline-stimulated lipolysis and re-esterification by epididymal fat pads, fasting hepatic glycogen content, glucose production by liver slices with and without alanine. No plasma insulin antagonist was found in the infected rats. Metabolic alterations in infected rats can be demonstrated independently of the associated catabolism. Increased growth hormone secretion cannot explain all of these changes.
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PMID:Metabolic studies in the pyelonephritic rat. 117 60

We have studied the effects of subcutaneous administration of monosodium-L-glutamate (MSG) to neonatal rats on nitrogen metabolism and on general parameters at several intervals after MSG treatment. As MSG-treated rats were hypophagic, all experiments were performed both in control rats pair-fed with the MSG-treated rats and in control rats fed ad libitum. Lee index, total serum lipids and weight of the epididymal fat depots were higher in MSG-treated rats. Body and tissue weights and the amount of protein in several tissues were lower in adult MSG-obese rats than in control rats. Locomotor activity was decreased following MSG administration. Creatinine clearance was diminished by about 50% in rats treated with MSG. Urinary nitrogen and urea excretion were lower, except at four weeks, and serum urea was higher in MSG-obese rats. Considering liver size, urea synthesis by isolated hepatocytes and urea cycle enzyme activities were increased in weanling MSG obese rats and diminished in adult MSG-obese rats when compared with ad libitum controls but were not changed compared with their pair-fed controls. It is concluded that administration of monosodium-L-glutamate shortly after birth induced an increase in urea synthesis in weanling rats that was followed by a reduction in the amount of tissue proteins, suggesting that more amino acids were used for lipid synthesis and urea production in treated rats. The accelerated amino acid degradation slowed down in adult MSG-obese rats which showed an in vitro capacity to synthesise urea similar to that of their pair-fed controls.
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PMID:Nitrogen metabolism in obesity induced by monosodium-L-glutamate in rats. 132 85

We have shown earlier that the administration of cyclosporine impairs testicular function and causes a decrease in sperm counts, sperm motility and fertility. In order to determine whether or not the deleterious effects of CsA could be reversed by hormonal therapy, we injected sexually mature male Sprague Dawley rats with cremaphor + saline or CsA (40 mg./kg./d) alone or in combination with human chorionic gonadotropin (hCG; five micrograms./d/rat) and follicle stimulating hormone (FSH; five micrograms./d/rat). The injections were given subcutaneously for 14 days. As expected, CsA administration decreased the body and reproductive organ weights, testicular and epididymal sperm counts, sperm motility and fertilizing ability. Serum levels of LH were elevated and testosterone was decreased. The administration of FSH + hCG to the CsA treated rats restored the body and reproductive organ weights, sperm counts and motility. Seventy five percent of gonadotropin treated males were fertile as compared to 25% in the CsA treated group. In the hormone treated group, the blood levels of CsA were 50% of that of CsA treated group. In order to verify whether or not the decline in the blood levels of CsA was the cause for the amelioration of CsA-induced changes in the reproductive function, we compared the CsA + hormone treated group with another group treated with five mg./kg./d CsA which had blood levels of CsA comparable to the former group. In the five mg./kg./d group the reproductive functions were significantly lower than the CsA + hormone treated group suggesting, therefore, that the restoration of reproductive functions in the CsA + hormone treated group is a result of hormonal treatment. Administration of CsA (40 mg./kg./d) reduced the kidney weight and increased the levels of serum creatinine: these changes were also ameliorated by the administration of hCG + FSH.
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PMID:Reversal of the toxic effects of cyclosporine on male reproduction and kidney function of rats by simultaneous administration of hCG + FSH. 212 12

Administration of cyclosporine to rats has been shown to impair testicular function, resulting in a decrease in sperm counts and fertility. In order to determine whether or not the deleterious effects of CsA could be reversed by hormonal therapy, mature male Sprague Dawley rats were treated with CsA (40 mg/kg/day, s.c.) alone or in combination with human chorionic gonadotropin (hCG) (5 micrograms/day/r; s.c.) for 14 days. Cyclosporine administration decreased the body weight (290 +/- 5.30 vs. 339 +/- 8.7 g; P less than 0.05) and reproductive organ weights (testis 1.49 +/- 0.42 vs. 1.60 +/- 0.03 g; epididymis 0.41 +/- 0.02 vs. 0.49 +/- 0.002 g; seminal vesicle 0.61 +/- 0.09 vs. 1.60 +/- 0.05 g; prostate 0.28 +/- 0.04 vs. 0.60 +/- 0.06 g; P less than 0.05) testicular sperm counts (5.80 +/- 0.42 vs. 8.49 +/- 0.48 x 10(7)/100 mg tissue; P less than 0.05) and epididymal sperm counts, (28.2 +/- 0.95 vs. 51 51.62 +/- 2.17 x 10(7)/100 mg tissue; P less than 0.05) and fertility (25% vs. 100%). Serum levels of LH were elevated (101.98 +/- 21.48 vs. 25.6 +/- 5.18 ng/ml; P less than 0.05) and testosterone was decreased (0.48 +/- 0.07 vs. 2.06 +/- 0.56 ng/ml; P less than 0.05). The administration of hCG to the CsA-treated rats restored the reproductive organ weights (testis 1.56 +/- 0.043 g; seminal vesicle 1.04 +/- 0.05 g; prostate 0.70 +/- 0.06 g) and sperm counts (testicular 7.88 +/- 1.0 x 10(7)/100 mg tissue; epididymal 59.86 +/- 4.16 x 10(7)/100 mg tissue; P less than 0.05) Serum levels of testosterone (18.63 +/- 4.45 ng/ml) and LH (431.65 +/- 31.41 ng/ml) were significantly elevated, as compared with control and CsA-treated groups (P less than 0.05). All the rats in the gonadotropin-treated group were fertile, as compared with 25% in the CsA-treated group. CsA reduced the kidney weight (1.17 +/- 0.02 vs. 1.27 +/- 0.03 g; P less than 0.05) and increased the levels of serum creatinine (0.97 +/- 0.07 vs. 0.59 +/- 0.03 mg/dl; P less than 0.05): these changes were ameliorated by the administration of hCG (kidney weight 1.35 +/- 0.03 g; creatinine 0.76 +/- 0.09 mg/dl).
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PMID:Evaluation of the effect of experimental cyclosporine toxicity on male reproduction and renal function. Reversal by concomitant human chorionic gonadotropin administration. 230 Oct 8

The authors examined the effects of the immunosuppressive drug cyclosporine (CsA) on the male reproductive system in prepubertal rats. Twenty-one-day-old rats were subcutaneously injected with either cremaphorsaline vehicle or CsA (1 and 2 mg/kg/d). The animals were treated until they were 66 days old. Cyclosporine did not affect the weights of the body or testis but decreased the weights of all sex accessory organs. Quantitative analysis of the tubules in stage VII of spermatogenesis revealed a decline in the cell counts of pachytene spermatocytes and step VII spermatids. Testicular and epididymal sperm counts and motility were decreased by 50% and fertility by 60%. Cyclosporine lowered serum testosterone despite an elevation of LH, indicating that the drug directly inhibited testosterone synthesis. Serum creatinine levels were normal in the treated animals, precluding renal failure as the cause for this impairment. Intratesticular concentrations of pregnenolone and 17-hydroxy progesterone were significantly elevated, while those of progesterone, androstenedione, and testosterone were markedly reduced. Determination of steroidogenic enzyme activities indicated that the administration of CsA inhibited the activity of delta 5-3B-hydroxy steroid dehydrogenase-delta 5-4 isomerase (3 beta-HSD). These results clearly indicate that CsA in the doses used is harmful to the male reproductive function in prepubertal rats.
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PMID:Cyclosporine: its effects on testicular function and fertility in the prepubertal rat. 231 96

Subcutaneous administration of the nematocide, 1,2-dibromo-3-chloropropane (DBCP), to adult, male, Fischer 344 rats transiently depleted hepatic and caput (head) epididymal nonprotein sulfhydryl (NPS) contents. NPS concentrations in the testis and kidney were not lowered by DBCP. Liver, kidney and testis all exhibited increases in tissue NPS concentrations 48 hr after treatment; the effects were most prominent in the outer medullary section of the kidney 24 hr after treatment with 80 mg/kg of DBCP. The glutathione-depleting agent diethyl maleate transiently lowered hepatic, renal and caput epididymal NPS concentrations in a dose- and time-dependent manner. Renal and caput epididymal NPS contents were increased relative to control 24 hr after diethyl maleate treatment. Single s.c. injections of DBCP produced dose-dependent lesions in the kidney, testis, caput epididymis and liver. Diethyl maleate treatment 90 min before DBCP treatment enhanced the nephrotoxic potency of DBCP as indicated by greater elevations of blood urea nitrogen and serum creatinine concentrations and by more severe renal tubular necrosis in diethyl maleate-pretreated animals than in vehicle controls, as determined 48 hr after DBCP exposure. Seminiferous tubular degeneration, as determined 48 hr post-DBCP treatment, was greater in rats pretreated with 600 mg/kg of diethyl maleate than in nonpretreated controls. When examined 16 days after DBCP treatment, however, the severity of testicular atrophy was virtually the same in rats pretreated with a lower dose of diethyl maleate (400 mg/kg) as in nonpretreated rats. These results indicate that DBCP is a depletor of hepatic and caput epididymal NPS in the acutely toxic dose range. Inasmuch as NPS concentrations were not lowered in two of the major target organs, kidney and testis, acute DBCP injury would not appear to be dependent on local glutathione depletion. However, the greater susceptibility of kidney and testis to DBCP injury after diethyl maleate pretreatment suggests an important role for NPS, particularly those in the liver, in modulating DBCP toxicities.
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PMID:Relationship of tissue nonprotein/sulfhydryls to the acute toxic effects of 1,2-dibromo-3-chloropropane. 705 99

We evaluated the effects of chronic renal failure (CRF) on the sperm fertilizing potential of rats. CRF was induced in 20 male 8-week-old Wistar rats (group A) by performing 5/6 nephrectomy in two stages. An additional 10 rats underwent a two-stage sham operation and served as a control group (group B). Seven weeks after the second operation, serum urea and creatinine concentrations were evaluated. Caudal epididymal spermatozoa from rats with CRF but not from controls had been filtrated via Sperm Prep tubes to isolate the sperm fraction showing strong forward progressions. Spermatozoa were processed for insemination of ten mature oocytes. After 18 and 36 h of insemination, the percentage of oocytes with two pronuclei and cleaved oocytes were evaluated, respectively. Serum urea and creatinine concentrations were significantly higher in group A than in group B. There was no significant difference between groups A and B in the percent sperm motility in final suspensions. The percentage of oocytes with two pronuclei and cleaved oocytes were significantly lower in group A than in group B . The present study suggests that CRF has adverse effects on the overall sperm fertilizing capacity.
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PMID:Effects of chronic renal failure on the sperm fertilizing capacity. 909 72

We evaluated the effects of chronic renal failure (CRF) on testicular function and semen physiology. A CRF model was created in 48 male rats by performance of five-sixths nephrectomies in two-stage procedures, and a control (group A) by two-stage sham operation on six male rats. Seven weeks later, serum urea and creatinine concentrations were assessed, and the nephrectomized rats were then equally divided into four groups, B, C, D and E, and treated with saline, erythropoietin, bromocryptine and hydralazine, respectively. Seventeen weeks after the first surgical procedure, the number of fertile rats, the mean values of epididymal sperm content and motility, the outcome of in vitro fertilization, and peripheral serum testosterone concentrations and responses to human chorionic gonadotropin were significantly higher (P < 0.05) in groups A, C and D than in groups B and E. Serum prolactin concentration was significantly higher (P < 0.05) in all groups of nephrectomized rats than in group A. Our results indicate that bromocryptine and erythropoetin improve Leydig cell function, spermatogenesis epididymal sperm maturation, and sperm fertilizing capacity in rats with CRF.
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PMID:Effects of erythropoietin, bromocryptine and hydralazine on testicular function in rats with chronic renal failure. 919 18

1,3-Diphenylguanidine (DPG) has been used as a primary and secondary accelerator in the vulcanization of rubber. Exposure to 1,3-diphenylguanidine may occur as a result of dermal contact during rubber manufacture or from contact with the finished products. DPG is poorly absorbed through skin. Therefore, to evaluate the toxicity associated with systemic exposure, 2-week and 13-week toxicology studies were conducted by administering DPG in feed to groups of male and female F344/N rats and B6C3F1 mice. Genetic toxicity was also evaluated in Salmonella typhimurium and in the micronucleus erythrocyte assay in peripheral blood from male and female mice. During 2-week studies, rats and mice received feed containing 0, 250, 500, 750, 1,500, or 3,000 ppm 1,3-diphenylguanidine. All rats and mice survived to the end of the study. Feed consumption and mean body weights of groups of rats that received 750, 1,500, or 3,000 ppm were lower than controls. No compound-related gross lesions were observed at the end of the study. The final mean body weight of female mice that received 3,000 ppm was 6% lower than the controls at the end of the study; however, no other effects attributable to chemical exposure were observed in mice. Based on these results the same exposure concentrations (0, 250, 500, 750, 1,500, and 3,000 ppm) were selected for the 13-week study; because of the poor palatability of the 750 ppm or higher dosed feed in rats, concentrations greater than 3,000 ppm were not considered appropriate. Six male rats and all female rats that received feed containing 3,000 ppm died or were killed moribund before the end of the 13-week study. Final mean body weights and feed consumption of male and female rats that received 1,500 or 3,000 ppm were lower than controls throughout the study. The values of several hematologic parameters were significantly different from the controls in groups of rats that received 1,500 or 3,000 ppm; however, these differences were attributable to reduced nutrient intake as a result of reduced feed consumption. Lower total serum protein, cholesterol, triglyceride, and creatinine concentrations were also considered to be the consequence of reduced nutrient intake. Alkaline phosphatase activity and bile acid concentrations were greater than the controls in most groups exposed to DPG and were considered to be an indication of cholestasis. Secretory depletion of the seminal vesicles and prostate gland, epididymal hypospermia, spermatogenic arrest, and significant reductions in the absolute weights of the prostate gland, seminal vesicles, and testis were observed in male rats in the 3,000 ppm group. Uterine hypoplasia characterized by a reduction in uterine size due to thinner and less developed endometrium was observed in female rats that received diets containing 750 ppm or greater. The mean length of the estrous cycle was greater in female rats that received 750 or 1,500 ppm feed than in the controls. All mice survived to the end of the 13-week study. Mean body weights of males and females that received feed containing 750, 1,500, or 3,000 ppm were lower than the controls. Reduced organ weights relative to control for mice that received 1,500 or 3,000 ppm were related to low body weights of these groups. In mice that received 3,000 ppm sperm motility was reduced and the number of spermatid heads was greater than for control males, and the estrous cycle length in females was longer than that of the controls. 1,3-Diphenylguanidine was tested for mutagenicity in Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537 with and without S9 metabolic activation enzymes. No mutagenic activity was observed in the absence of S9. With S9, positive responses were observed in strains TA98 and TA100, and an equivocal response was observed in strain TA1537. Results of a peripheral blood micronucleus test in B6C3F1 mice were concluded to be negative in males and equivocal in females. In summary, consumption of feed containing 1,3-diphenylguanidine for 2 weeks or 13 weeks was not associated with any histologic response which could be attributed to chemical exposure. Instead the observed changes were indicative of reduced nutrient intake and are consistent with similar changes observed in other studies of feed restricted rats and mice.
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PMID:Toxicity Studies of 1,3-Diphenylguanidine (CAS No. 102-06-7) Administered in Feed to F344/N Rats and B6C3F1 Mice. 1196 41

Ligation of the uterine arteries (LIG) in rats serves as a model of intrauterine growth restriction and subsequent developmental programming of impaired glucose tolerance, hyperinsulinemia, and adiposity in the offspring. Its impact on lipid metabolism has been less well investigated. We compared parameters of glucose and lipid metabolism and glucocorticoid levels in the offspring of dams that underwent either LIG or sham operation (SOP) with those of untreated controls. Blood parameters including insulin, leptin, and visfatin as well as body weight, food intake, and creatinine clearance were recorded up to an age of 30 wk. Glucose tolerance tests were performed, and both leptin and visfatin expression in liver, muscle, and epididymal and mesenteric fat was quantified by RT-PCR. After catch-up growth, weight gain of all groups was similar, despite lower food intake of the LIG rats. LIG offspring showed impaired glucose tolerance from the age of 15 wk as well as elevated glycosylated hemoglobin and corticosterone levels. However, the body fat content of both LIG and SOP animals increased relative to controls, and both showed elevated triglyceride, total cholesterol, and leptin levels as well as a reduced proportion of high-density lipoprotein cholesterol. Thus, use of the LIG model requires both SOP and untreated controls. Although only LIG is associated with impaired glucose tolerance, pathogenic programming of the lipid metabolism can also be induced by SOP. Visfatin does not appear to be involved in the disturbed glucose metabolism after intrauterine growth restriction and may represent only a marker of fat accumulation.
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PMID:Uteroplacental insufficiency after bilateral uterine artery ligation in the rat: impact on postnatal glucose and lipid metabolism and evidence for metabolic programming of the offspring by sham operation. 1806 78


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