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Biomedical subjects

R Lester

Publications and source records attributed to R Lester.

At least 91 records · Page 5Linked to original sources
PubMed1975

Plasma estrone, prolactin, neurophysin, and sex steroid-binding globulin in chronic alcoholic men.

The feminization frequently observed in men with alcoholic liver disease has not been satisfactorily explained by existing reports. We have measured plasma estrone, prolactin, estrogen-stimulated neuorphysin, and sex steroid-binding globulin concentrations in 50 men with chronic alcoholism and varying degrees of alcoholic liver disease in an effort to further elucidate possible hormonal mechanisms responsible for the observed feminization. Plasma concentrations of each of these parameters were at least two-fold elevated (p smaller than or equal to 0.01) when compared to values obtained for the same steroid or protein in plasma obtained from normal men. The plasma concentrations of estrone and prolactin in men studied with synecomastia were significantly greater (p smaller than or equal to 0.01 and p smaller than or equal to 0.05, respectively) than were the concentrations of these two hormones in those without this physical sign. Similarly, those men with spider angiomata had significantly greater (p smaller than or equal to 0.01) plasma estrone levels than did the men without this cutaneous vascular abnormality. These significant hormone elevations may contribute to the pathogenesis of feminization so frequently observed in chronic alcoholic men.

Adult↗
PubMed1975

Bile salt metabolism in the human premature infant. Preliminary observations of pool size and synthesis rate following prenatal administration of dexamethasone and phenobarbital.

Bile salt synthesis and bile salt pool size were determined by isotope dilution in two groups of healthy premature infants, utilizing nonradioactive deuterium-labeled bile salts. All 9 infants were between 32 and 36 weeks of gestation; however, in one group (4 infants), the mothers had received either dexamethasone or phenobarbital prior to delivery. The total bile salt pool averaged 20 mg for the infants of untreated mothers and 79 mg for the infants of treated mothers; similarly, the bile salt synthesis of 8 mg per day in the untreated group was increased to 27 mg per day for the treated group. Expressed per sq m of body surface, the cholic acid pool for the treated group was 321 mg per sq m, and the cholic acid synthesis rate equaled 98 mg per sq m per day; values equal to those for full term infants and nearly 4 times those for the untreated prematures. The intraduodenal bile salt concentrations obtained during meals were also low in the untreated group, equaling 1.2 mM as compared to 5.3 mM for the treated group. The reductions of bile salt pool size, synthesis, and intestinal concentration establish that the functional maturity of the liver, and possibly the gastrointestinal tract, is reduced in premature infants. The results further suggest that this maturity may be dramatically influenced by medications administered to the mother prior to delivery.

Bile Acids and Salts↗
PubMed1975

Alcohol-induced testicular atrophy. An experimental model for hypogonadism occurring in chronic alcoholic men.

Elucidation of mechanisms involved in the hypogonadism and feminization observed in chronic alcoholic men requires the development of an experimental animals model system. Such an animal system should be inducible with ethanol feeding and should duplicate endocrine changes known to occur in chronic alcoholic men. We report such an animal model system. Animals fed a diet with ethanol accounting for 36% of total calories develop significant testicular, prostatic, and seminal vesicle atrophy (P less than 0.01) and greatly reduced plasma testosterone levels (P less than 0.01). Animals fed a similar diet with sucrose isocalorically substituted for ethanol do not. Testicular, prostatic, and seminal vesicular mass relative to body mass and plasma testosterone levels in these isocaloric control animals do not vary significantly from those obtained for age-matched control animals fed an ad libitum rat chow diet. These findings indicate that the caloric deprivation associated with chronic ethanol ingestion is not responsible for gonadal injury and atrophy of the sex steroid-sensitive tissues in the alcohol-fed animals. This animal model provides a useful means of directly examining perturbation in gonadal function that occurs in man as a consequence of chronic ethanol ingestion and confirms our previous data which suggest that ethanol is a primary testicular toxin.

Alcoholism↗
PubMed1975

Bile-salt metabolism in the primate fetus.

Fetal bile salt metabolism was assessed by the intravenous infusion of e114C]cholate into 6 monkey fetuses. The placental transfer, fetal plasma clearance, and fetal hepatic excretion of the administered radiolabeled bile salt were measured. Placental transfer averaged 30% of the injected dose, while biliary excretion averaged 36%. Of the amount excreted by the fetal liver, 78% was in the form of [14C]taurocholate. The findings suggest that bile salt metabolic and excretory mechanisms are undergoing developmental maturation at birth.

Animals↗
PubMed1974

Ethanol inhibition of vitamin A metabolism in the testes: possible mechanism for sterility in alcoholics.

Vitanin A (retinol) is essential for spermatogenesis. Alcohol dehydrogenase, the enzyme responsible for ethanol metabolism, is also required for the conversion of retinol to bioactive retinal at the end organ site. Ethanol inhibits the oxidation of retinol by testicular homogenates containing alcohol dehydrogenase. Thus, a possible biochemnical mechanism for the sterility of chronic alcoholics is identified.

Alcohol Oxidoreductases↗
PubMed1973

Foetal bile pigment handling after administration of (14C)haemin.

1. Advanced techniques for intra-uterine surgery were used to study haem degradation in foetal sheep prepared in utero with indwelling jugular, carotid and biliary cannulas. [(14)C]haemin was administered I.V. to the foetus, and plasma disappearance, biliary excretion, placental transfer and tissue distribution of radioactivity were measured over a 5-8 hr period.2. 8-30% of the (14)C-label was recovered in foetal bile, about 40% of this as bilirubin and the rest as unidentified [(14)C]haemin derivatives. 4-21% was transferred across the placenta, appearing in maternal bile almost exclusively as [(14)C]bilirubin. Excretion of (14)C-label totalled 18-33%.3. Six adult sheep infused with [(14)C]haemin excreted 19-49% of the dose in the bile over 8 hr, one third as bilirubin.4. The amount of endogenous bilirubin excreted per unit time/unit wt. of foetal liver increased with increasing foetal wt.5. It is concluded that near-term foetal sheep have a maturing mechanism for haem catabolism. Haem is partially excreted in foetal bile as bilirubin. Another fraction is transferred across the placenta, probably after prior conversion to bilirubin. The remainder is converted to un-identifiable end-products. Total excretion is approximately as effective as that in adults.

Animals↗