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)

After i.m. injection of [3H]butyrobetaine into rats, the accumulation of carnitine into the epididymis, prostate gland, seminal vesicles, testis and heart was studied. The concentration of radiolabeled carnitine into the cauda epididymis increased linearly with time up to 72 h after the injection of the precursor, while its level in the prostate and seminal vesicles decreased rapidly. Very low levels of carnitine were found in the testis. Castration reduced the carnitine accumulation by cauda epididymis to 6% of the control levels while treatment of castrated animals with testosterone propionate (500 mug/day) partly restored the carnitine uptake. Similar treatment with 17beta-oestradiol valerate or 17alpha-hydroxyprogesterone had no effect. Surprisingly, cyproterone acetate (5 mg/day) also significantly stimulated carnitine accumulation by the epididymis to a level above that of the castrated controls. Simultaneous injection of both cyproterone acetate and testosterone propionate to castrated animals caused an additive effect of these steroids. This indicated that cyproterone acetate in this system is working as a weak androgen. Treatment of rats with 17beta-oestradiol valerate also reduced carnitine accumulation by the cauda epididymis. This is due to suppression of pituiatry gonadotrophin secretion, since concommitant treatment with testosterone propionate (500 mug/day) caused a normalization of the carnitine uptake. Treatment of intact rats with cyproterone acetate significantly reduced the epididymal weight, but not the carnitine accumulation. 17alpha-Hydroxyprogesterone treatment had no effect either on the epididymal weight or the accumulation of the carnitine. Unilateral orchiectomy reduced the carnitine accumulation by the cauda epididymis to about 40% of that occurring in the non-operated control side. This indicates that the luminal contact between the testis and epididymis or the luminal content of the epididymis itself is of importance for the androgen-dependent metabolic process occurring in the cauda epididymis. Castration or hormone treatment did not change the conversion of butyrobetaine to carnitine, or the carnitine uptake by heart. Carnitine uptake by the testis after [3H]butyrobetaine injection was rather low and this would exclude the possibility of synthesis of carnitine in the testis as a source of epididymal carnitine. Carnitine only accumulated in the cauda epididymis in vivo 4 to 96 h after injection of [3H]butyrobetaine. The presence of radioactively labeled butyrobetaine or methylcholine was not detected.
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PMID:Androgen-dependent accumulation of carnitine by rat epididymis after injection of [3H]butyrobetaine in vivo. 17 Jan 50

Luminal fluid was collected by micropuncture techniques from the testis and epididymis of the rat, hamster, rabbit, boar and ram and the concentration of free L-carnitine in the fluid was estimated using enzymic methods. Carnitine was present in the testicular fluid of the rat in concentrations less than 1 mM but increased down the epididymis to reach 53 mM in luminal fluid from the cauda epididymidis, approximately 2000 times higher than in blood plasma. A high concentration was first found in the luminal fluid from the distal caput epididymidis, at about the point where the spermatozoa become motile. Carnitine was also present in the epididymal luminal fluid of the other species studied; the amounts were not as high as those in the rat but were still higher than those in blood plasma.
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PMID:The concentration of carnitine in the luminal fluid of the testis and epididymis of the rat and some other mammals. 46 29

The uptake of radiolabeled L-carnitine has been studied in isolated epididymal tubules from the rat. The uptake of 3H-L-carnitine increases with a temperature coefficient KT of 0.22 nmol carnitine.mg protein-1 in the intermal 22--31 degrees and with a low uptake at 4 degrees C. The uptake of radiolabeled carnitine (as percent) is reduced at high concentrations of L-carnitine, by deoxycarnitine but not by D-carnitine. This uptake mechanism is especially active in the distal caput and corpus segments of the epididymis. Thus, an uptake mechanism for carnitine is present in the epididymal cells which besides the carnitine uptake in spermatozoa is responsible for the dramatic increase in carnitine concentration in cauda epididymis.
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PMID:Uptake of 3H-L-carnitine by isolated rat epididymal tubules. 48 33

After i.m. injection of [3H]butyrobetaine into intact and castrated rats, the specific activity of plasma carnitine remained nearly constant over 24--96 h and epididymal uptake of carnitine was constant per unit time up to 72 h. The uptake ratio of intact to castrated rats was high at 48, 72 and 96 h after injection. Administration of estradiol valerate over 20 days reduced carnitine uptake in epididymis. This reduction was dose-dependent when estrogen was administered i.m. at 0.33--10 microgram/day levels. A maximum reduction of 90% was obtained with the 10 microgram dose. A dose increase from 33 to 100 microgram/day caused no further reduction. Norspiroxenone (2--10 mg/day) and SK 7670 (1.5 and 7.5 mg/day) were less effective than estradiol valerate (10 microgram/day) in suppressing carnitine uptake in epididymis. Epididymal carnitine uptake in estradiol valerate treated rats (33 microgram/day for 20 days) increased in a time- and dose-dependent manner under testosterone propionate treatment (50, 250, 1250 microgram/day). Carnitine uptake increased to 80% of the nonsuppressed levels when testosterone propionate was adminsitered over a 6-day period at 1250 microgram/day. Dihydrotestosterone increased epididymal carnitine uptake to the same extent as testosterone propionate. delta4-androstene-3,17-dione and 5alpha-androstane-3alpha,17beta-diol (50 microgram/day) were less effective, stimulating uptake to only 15% and 40% respectively of the testosterone propionate (250 microgram/day) stimulated levels. Changes in epididymal carnitine uptake evoked by various experimental procedures were closely paralleled by weight changes in the ventral prostate. This response resemblance indicates a similarity between the androgen sensitivity of the prostate gland and that of the carnitine uptake system in epididymis. The dose-dependent effect of estrogen on the accumulation of epididymal carnitine, together with the marked responses induced in this system by manipulation of its androgen status, support a possible use for the system as an assay for androgen or antiandrogen potency in vivo.
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PMID:Accumulation of carnitine in rat epididymis after injection of [3H]butyrobetaine in vivo: quantitative aspects, and the effects of androgens and antiandrogens. 68 Mar 41

Diabetes, starvation and various hormonal treatments are known to alter drastically carnitine concentrations in the body. Before the mechanisms controlling carnitine metabolism could be determined, it was necessary to establish normal carnitine concentrations in both sexes at different ages. Carnitine was assayed in plasma, liver, heart and skeletal muscle of rats from birth to weaning. The plasma carnitine increased rapidly during the first 2 days after birth. Carnitine in both heart and skeletal muscle increased, whereas liver concentrations declined during the first week of life. A carnitine-free diet containing sufficient precursors for carnitine biosynthesis was fed to weanling rats. Groups of ten male and ten female rats were killed each week for 10 consecutive weeks. Carnitine was determined in plasma, liver, heart, skeletal muscle, urine and epididymis in the male. There was no difference in carnitine concentrations between the sexes at weaning. Plasma, heart and muscle concentrations were higher in adult male rats than in adult females. However, liver carnitine and urinary carnitine concentrations were higher in adult female than in adult male rats. The epididymal carnitine concentration increased very rapidly during 50 to 70 days of age and the differences in carnitine concentrations between the sexes also became apparent during this time. Thus both the age and the sex of the human subject or experimental animal must be considered when investigating carnitine metabolism.
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PMID:Variation in tissue carnitine concentrations with age and sex in the rat. 74 45

Carnitine determinations in human seminal fluid were shown to be useful in assessing epididymal and seminal vesicle function and in locating blockages in the male reproductive tract. The carnitine concentrations in 50 samples of seminal fluid ranged from 15 to 530 mug/ml (as carnitine-HCl). The patients could be divided into four classes. Patients with normal seminal vesicle and epididymal function had values of 250 mug/ml or above. Those with a defective epididymis and a functional seminal vesicle had intermediate carnitine levels (100 to 200 mug/ml) and normal fructose values in the seminal fluid. Patients with a defective seminal vesicle but a functional epididymis had intermediate carnitine concentrations and low fructose levels. Extremely low carnitine values (less than 100 mug/ml) were found in seminal fluid from patients whose epididymis and seminal vesicle both were defective. The possible role of carnitine in sperm maturation was discussed.
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PMID:Epididymis and seminal vesicle as sources of carnitine in human seminal fluid: the clinical significance of the carnitine concentration in human seminal fluid. 124 48

The authors report a review on the L-carnitine effects on the male genital tract. L-carnitine represents a cofactor in the transport of long chain fatty acids inside mitochondria and their subsequent oxidation. Therefore, its main role is that of intramitochondrial vehicle of acyl groups. In particular, the effects of L-carnitine on the male genital function seem connected mainly with the high concentration of L-carnitine in the epididymis; the uptake of the L-carnitine from the blood is an active, in part androgen-dependent, mechanism. Moreover, epididymal spermatozoa are able to concentrate L-carnitine (while they become progressively more impermeable to such a substance) during their passage from the caput to the cauda epididymis. The main function of the L-carnitine in the epididymis is to give to the spermatozoa an energetic substrate. In fact, this function should be of great importance since the epididymal spermatozoa employ fatty acid oxidation for their energy metabolism; on the contrary, the ejaculated sperm employ glycolytic process. As a consequence of the above-mentioned effects of L-carnitine the dosage of this substance in the evaluation of the integrity of the processes of maturation of the spermatozoa was proposed. Finally, there is growing interest in the use of L-carnitine as a therapeutic tool in some forms of male infertility.
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PMID:[Metabolism and action of L-carnitine: its possible role in sperm tail function]. 150 74

15 subjects with Hypogonadotropic Hypogonadism (HH) were treated with either gonadotropins (13 cases) or pulsatile subcutaneous Luteinizing Hormone Releasing Hormone (LHRH) (2 cases) for up to 42 months, to study the effects of therapy step by step. The following results were obtained: (A) In postpubertal HH (5 cases = Group A), therapy brought about onset of spermatogenesis within 3 months and its normalization within 6 months. In HH of prepubertal onset (10 cases = Group B), spermatogenesis started within 9 to 21 months and became normal in only 3 cases after at least 18 months. The best sperm counts were obtained in Group A in the third month of treatment (41.75 +/- 43.68 mil./ml) and in Group B in the 36th month (14.87 +/- 17.06 mil./ml). Sperm motility was normal in the majority of the cases in Group A from the beginning but did not become normal in Group B. (B) Seminal fructose and zinc were normal from the beginning of therapy in 66% of the cases in both groups. Zinc became normal in 100% within 3 months in Group A, in Group B within 18. Carnitine was normal in 50% of cases in both groups, contemporaneous with sperm appearance. Transferrin was normal in Group A after appearance of spermatozoa, but in Group B never became normal. (C) We hypothesize that the recovery of fertility passes through the following stages: (1) Functional recovery of Leydig cells, followed by seminal vesicles and prostate. (2) Recovery of epididymal function, which probably implies beginning of the tubular function. Recovery of Sertoli cell function occurs with more difficulty.
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PMID:Achievement of spermatogenesis and genital tract maturation in hypogonadotropic hypogonadic subjects during long term treatment with gonadotropins or LHRH. 177 42

Samples of sperm have been obtained from 95 who consulted us for infertility. In each case seminal plasma was examined for levels of alpha-1,4-glucosidase and L-carnitine. Our results have led us to fix the threshold value of 42.6 mlU per ejaculate for alpha-1,4-glucosidase and 960 nanomoles of L-carnitine below those levels that we thought occur where the origin of the oligospermia is obstructive (series 1 patients). In series 2 patients the cause of the oligospermia purely being secretory, there is normal epididymal function and therefore the excretory doubts are proven. It is not impossible to have both pathologies because we have found this in men of the intermediate groups C and D. We have found that there is a correlation between the presence of epididymal pathology and a drop in epididymal markers which can be found in severe oligospermia (which can be epididymal in origin and not testicular). Also when there is non abnormalities in the spermogram. This last situation can occur in "invisible" abnormalities of spermaturation in the epidymus.
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PMID:[The value of the level of alpha-1,4-glucosidase and seminal l-carnitine in patients with oligoasthenospermia]. 182 86

Biochemical analysis was made of specific accessory gland products in the ejaculates of 362 men suffering from various acute inflammatory diseases of the reproductive tract and 33 normozoospermic patients acting as controls. The ejaculate content of the epididymal markers alpha-glucosidase and L-carnitine, but not glycerophosphocholine, was significantly reduced in ejaculates from men with epididymitis; citric acid was reduced in men suffering from prostatitis; both citric acid and alpha-glucosidase were reduced in men suffering from adnexitis. The ejaculate content of epididymal and prostatic markers in prostato-urethritis (adnexitis), where the exact localization of the inflammation was unclear, was not as low as in epididymitis or prostatitis. Seminal vesicle function, as judged from semen volumes and seminal fructose, was not different in these groups of patients. The results, although strongly related to the clinical diagnosis, were unrelated to the microbiological flora of the semen and indicate that both the epididymis and the prostate glands are involved in some forms of adnexitis.
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PMID:The influence of inflammation of the human male genital tract on secretion of the seminal markers alpha-glucosidase, glycerophosphocholine, carnitine, fructose and citric acid. 228 78


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