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)

A six-months out-patient study of chronic alcoholics with undecompensated liver disease has shown a statistically significant inverse correlation between the change in mean corpuscular volume and the change in body weight (r = -0.4, P less than 0.01). A fall in body weight over this period was the best clinical indicator of apparently continuing alcohol abuse. Previous anthropometric studies have indicated that reduced adipose tissue is one cause of lower body weights in such patients. To determine whether this is due to the effects of alcohol or of poor nutrition, the epididymal fat pad weights of rats following 28 days administration of alcohol (36% of total calories) as part of a nutritionally adequate liquid diet were compared with those of pair-fed controls initially matched for body weight. At the end of the experiment, body weight gain was the same in both groups but the mean weight of the fat pads of alcohol-fed animals (371.7 mg +/- 60.0 mg SD) all of which developed hepatic steatosis was 29% greater than that of pair-fed controls (288.7 mg +/- 42.4 mg). This difference was statistically significant (P less than 0.025). This study shows that alcohol intake per se does not prevent an increase in body weight or fat even if hepatic steatosis is induced and that loss of adipose tissue in chronic alcoholics who continue to drink is probably due to simultaneous inadequate nutritional intake.
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PMID:Differential effect of chronic alcohol intake and poor nutrition on body weight and fat stores. 653 64

Alcohol abuse is considered as one of the problems associated with poor semen production and sperm quality. Both acute and chronic alcohol consumption may affect spermatozoal chromatin disorders through apoptosis. Therefore, for the first time, this experimental study was performed to evaluate the effect of ethanol consumption on sperm parameters and chromatin integrity of spermatozoa aspirated from cauda epididymis of rats. Twenty adult Wistar rats were divided into ethanol consumption and control groups. Access to ethanol and water was provided ad libitum for experimental and control animals, respectively. The cauda epididymal spermatozoa were aspirated for analysis of sperm parameters and sperm chromatin integrity with aniline blue (AB), chromomycin A3 (CMA3), toluidine blue (TB), and acridine orange (AO) assays. Sperm progressive and nonprogressive motility of ethanol-consuming rats were significantly decreased compared with control animals (P < .05). In addition, the rates of AB-reacted spermatozoa were similar in both groups (P > .05). However, with regard to CMA3, AO, and TB stainings, there was a significant increase in ethanol group when compared with the controls (P < .05). The majority of TB+ and AO+ spermatozoa were higher than "cut-off" value in ethanol group, whereas the mean rates of CMA3+ spermatozoa was below the "cut-off" value in both groups. The results showed that ethanol consumption disturbs sperm motility, nuclear maturity and DNA integrity of spermatozoa in rat. Therefore, ethanol abuse results in the production of spermatozoa with less condensed chromatin, and this may be one possible cause of infertility following ethanol consumption.
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PMID:Effects of ethanol consumption on chromatin condensation and DNA integrity of epididymal spermatozoa in rat. 2114 92

While the risks of maternal alcohol abuse during pregnancy are well-established, several preclinical studies suggest that chronic preconception alcohol consumption by either parent may also have significance consequences for offspring health and development. Notably, since isogenic male mice used in these studies are not involved in gestation or rearing of offspring, the cross-generational effects of paternal alcohol exposure suggest a germline-based epigenetic mechanism. Many recent studies have demonstrated that the effects of paternal environmental exposures such as stress or malnutrition can be transmitted to the next generation via alterations to small noncoding RNAs in sperm. Therefore, we used high throughput sequencing to examine the effect of preconception ethanol on small noncoding RNAs in sperm. We found that chronic intermittent ethanol exposure altered several small noncoding RNAs from three of the major small RNA classes in sperm, tRNA-derived small RNA (tDR), mitochondrial small RNA, and microRNA. Six of the ethanol-responsive small noncoding RNAs were evaluated with RT-qPCR on a separate cohort of mice and five of the six were confirmed to be altered by chronic ethanol exposure, supporting the validity of the sequencing results. In addition to altered sperm RNA abundance, chronic ethanol exposure affected post-transcriptional modifications to sperm small noncoding RNAs, increasing two nucleoside modifications previously identified in mitochondrial tRNA. Furthermore, we found that chronic ethanol reduced epididymal expression of a tRNA methyltransferase, Nsun2, known to directly regulate tDR biogenesis. Finally, ethanol-responsive sperm tDR are similarly altered in extracellular vesicles of the epididymis (i.e., epididymosomes), supporting the hypothesis that alterations to sperm tDR emerge in the epididymis and that epididymosomes are the primary source of small noncoding RNAs in sperm. These results add chronic ethanol to the growing list of paternal exposures that can affect small noncoding RNA abundance and nucleoside modifications in sperm. As small noncoding RNAs in sperm have been shown to causally induce heritable phenotypes in offspring, additional research is warranted to understand the potential effects of ethanol-responsive sperm small noncoding RNAs on offspring health and development.
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PMID:Heavy Chronic Intermittent Ethanol Exposure Alters Small Noncoding RNAs in Mouse Sperm and Epididymosomes. 2947 46