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)

myo-Inositol deficiency in rats produced an overaccumulation of triacylglycerols in the liver due to stimulated lipolysis in the adipose tissue (Hayashi, E., Maeda, T. and Tomita, T. (1974) Biochim. Biophys. Acta 360, 134--155). The mechanism of the enhancement in lipolysis has now been investigated. The lipolytic response to adrenalin, corticotropin and insulin of the epididymal adipose tissue did not change due to the deficiency, but hormone-sensitive lipase activity, plasma adrenalin level and blood pressure were higher in the deficient rats. Adrenalectomy had no influence, but administration of sympathetic nervous blockers (reserpine, hexamethonium and bupranolol) inhibited the liver lipid deposition and an increase of serum free fatty acids in the deficient rats. These results indicate that the enhancement in lipolysis is mediated by an excitation of sympathetic nerve terminals innervating in the adipose tissues.
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PMID:The effect of myo-inositol deficiency on lipid metabolism in rats. III. The mechanism of an enhancement in lipolysis due to myo-inositol deficiency in rats. 21 37

Inositol was detected by gas-liquid chromatography in fluid perfused at 1.3 microliter/min through the lumen of the distal cauda epididymidis of anaesthetized rats. The concentration (247 microM) exceeded that in blood (48 microM) and the secretion rate was constant for 5 h. D-[3H]Myo-inositol infused for 3 h into the general circulation of rats (1 muCi/min) also appeared in fluid perfusing the lumen, whether or not 50 mM-inositol was present in the perfusing solution. No plateau of radioactivity was reached during infusion, and by the end of 3 h perfusate activity was 26% of that in blood. Calculation of the specific activity of inositol in perfusates and blood plasma suggested that blood was not the immediate source of luminal inositol, and that any endogenous pool of cyclitol has a turnover time of greater than 3 h. [3H]Myo-inositol perfused through the lumen was not absorbed by the tissue. These data suggest that the high concentration of inositol in epididymal fluid (49 mM) is derived in part by epididymal secretion from a pool that is only slowly replenished from blood, and maintained by the impermeability of the epithelium. Glucose also appeared in fluid perfused through the epididymal lumen, but its concentration (461 microM) was much less than in blood (8.5 mM), so this sugar may diffuse down a concentration gradient.
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PMID:Secretion of inositol and glucose by the perfused rat cauda epididymidis. 706 56

The origin of glycerylphosphorylcholine (GPC), N-acetylaminosugar, inositol, and prostaglandins in human seminal plasma was investigated by correlating the concentration of these components in split ejaculates with known marker constituents. Fructose and acid phosphatase were selected as markers of the secretory activity of the seminal vesicles and prostate gland, respectively, and spermatozoa indicated epididymal origin. The concentration of fructose was lowest in the first fraction of the semen and increased to a maximum in the final portion. Prostaglandins E and F and N-acetylaminosugar values closely followed this pattern, indicating that these components originate in the seminal vesicles. The concentration of spermatozoa was high in the first two fractions, decreasing to a minimum in the final fraction. The distribution of GPC was similar to that of the spermatozoa, indicating that the epididymis secretes this compound. Inositol levels were similar in all fractions, indicating that it is probably present in epididymal, vesicular, and prostatic fluid. Human spermatozoa were unable to utilize N-acetylglucosamine or inositol. High concentrations of some prostaglandins (100 micrograms/ml of PGF1 alpha, 15S 15 met. F2 alpha, PGA1, and PGA2) depressed the endogenous oxygen uptake of human spermatozoa.
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PMID:Origin of glycerylphosphorylcholine, inositol, N-acetylaminosugar, and prostaglandins in human seminal plasma and their effects on sperm metabolism. 736 41

Adipose tissue plays a pivotal role in ageing and longevity; many studies, both human and animal, have focussed on the effects of food limitation. Here we present a new model based on striking differences between two 'normal' inbred strains of albino Wistar rats the Charles River (CR) and Harlan Olac (HO) that have marked differences in age-related accumulation of fat and insulin-stimulated rates of glucose incorporation into lipid in the epididymal fat pads (EFP). The incorporation [U-(14)C]glucose into lipid by adipocytes showed that the CR group had a twofold higher basal rate of lipogenesis and a greater response to insulin in vitro, exceptionally, adipocytes from CR group maintained the high response to insulin to late adulthood while retaining the lower EFP weight/100 g body weight. Inositol phosphoglycan A-type (IPG-A), a putative insulin second messenger, was 3.5-fold higher and cAMP significantly lower per EFP in the CR versus HO groups. Plasma insulin levels were similar and plasma leptin higher in CR versus HO groups. The anomaly of a higher rate of lipogenesis and response to insulin and lower EFP weight in the CR group is interpreted as the resultant effect of a faster turnover of lipid and stimulating effect of leptin in raising fatty acid oxidation by muscle, potentially key to the lower accumulation of visceral fat. The metabolic profile of the CR strain provides a template that could be central to therapies that may lead to the lowering of both adipose and non-adipocyte lipid accumulation in humans in ageing.
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PMID:Age-related changes in the response of rat adipocytes to insulin: evidence for a critical role for inositol phosphoglycans and cAMP. 2033 70