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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brown adipose tissue (Na+-K+)-ATPase activity, in vitro glucose and 2-aminoisobutyric acid uptake, as well as mitochondrial GDP-binding and succinate dehydrogenase activity were determined in order to study the relationship between these parameters and the thermogenic status. Analysis were carried out on control animal, pregnant rats, dams and pups during lactation, GDP-binding, (Na+-K+)-ATPase and glucose uptake were found to be decreased in brown adipose tissue from pregnant rats and dams, and increased in pups, 2-aminoisobutyric acid uptake was only increased in pups, but no changes were observed in the other experimental groups tested. GDP-binding and (Na+-K+)-ATPase activity showed a parallelism which suggests that the enzyme is a good index of thermogenic status of the animal.
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PMID:Brown adipose tissue (Na+-K+)-ATPase activity and substrate uptake during the breeding cycle of rats. 255 Dec 96

Milk yield, feed intake, physiology, health, and reproduction of cows supplemented with somatotropin are like those of genetically superior cows. Lactation curves are shifted upward and are more persistent. Holsteins, Jerseys, Brown Swiss, and Ayrshires respond. In most cases, responses in primiparous and multiparous animals are similar. Milk composition, ration digestibility, maintenance requirements, and the partial efficiency of lactation are not affected by somatotropin. More nutrients are directed to milk synthesis. Initially, body stores of fat, protein, and glycogen provide these nutrients, but after a few weeks, feed intake increases. Cows supplemented with somatotropin should be fed like high producing cows. When ration energy density is increased by feeding grain, buffers such as sodium bicarbonate should be included to prevent alterations of hydrogen balance in the rumen and tissues. Ration energy density can also be increased with ruminally inert fat like calcium salts of fatty acids. Rations should be balanced for rumen degradable and undegradable protein. Rations for high milk yields are expensive, but income over feed costs are greater. Cows should be moved to rations with lower nutrient densities on the basis of body condition and milk yield. Current feeding recommendations can be used for cows supplemented with somatotropin.
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PMID:Nutritional implications of somatotropin for lactating cows. 260 Feb 19

Cadmium exposure is known to induce hypertension, but development of hypertension is not universal in exposed animals. However, the cellular uptake of cadmium could also exert renal cytotoxic effects which have been, until now, essentially only studied at the proximal tubule level. Kallikrein is an enzyme synthetized in renal cortex and excreted in the urine in the distal tubule. Therefore, to evaluate the distal renal effect of cadmium, we studied the daily urinary kallikrein excretion (UKE) in conscious unrestrained female Brown Norway rats during long-term chronic exposure to 2 dosages of cadmium given subcutaneously 3 times a week, a low dose (LD): 0.25 mg/kg and a high dose (HD): 1 mg/kg. Neither dose of cadmium was able to induce significant hypertension in the treated animals. HD administration for 24 weeks resulted in a decreased UKE associated with an increase in plasma renin activity and sodium and potassium excretions. LD administration had no significant effect on UKE. Twenty weeks after stopping cadmium administration, a persistent reduction in UKE was still observed; furthermore, the group which had been previously administered a LD of cadmium, now also exhibited a reduced UKE. During this re-examination period in both groups, the UKE reductions were associated with normal systolic blood pressure, glycosuria, natriuresis. Our data show that cadmium administration can influence UKE, plasma renin activity, plasma aldosterone concentration and electrolyte excretion without inducing any variation of blood pressure. This may reflect a nephrotoxic, non-hypertensive effect. Since this effect persisted after stopping cadmium administration, it may indicate a prolonged irreversible nephrotoxic effect at the distal nephron level. Thus, UKE may be a useful non-invasive index to evaluate distal nephrotoxicity.
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PMID:Renal kallikrein excretion as a distal nephrotoxicity marker during cadmium exposure in rats. 265 77

We reported previously the purification of a 165-kDa muscle-specific protein identified by virtue of its ability to bind 125I-labeled low density lipoprotein with high affinity after sodium dodecyl sulfate-polyacrylamide gel electrophoresis (Hoffmann, S. L., Brown, M. S., Lee, E., Pathak, R. K., Anderson, R. G. W., and Goldstein, J. J. (1989) J. Biol. Chem. 264, 8260-8270). The protein is located in the lumen of the sarcoplasmic reticulum, where it has no access to plasma lipoproteins. It binds to 45Ca2+ on nitrocellulose blots and stains metachromatically blue with Stains-all, a cationic dye that stains Ca2+-binding proteins. In the current paper, we have isolated a full-length rabbit cDNA clone for the 165-kDa protein. The deduced amino acid sequence reveals a 852-amino acid protein with the following structural features: 1) an NH2-terminal 27-residue putative signal sequence; 2) a highly repetitive region containing nine nearly identical tandem repeats of 29 residues, each consisting of a histidine-rich sequence HRHRGH, a stretch of 10-11 acidic amino acids, and a sequence containing 2 serines and a threonine in a negatively charged context; 3) a 13-residue stretch of polyglutamic acid; and 4) a COOH-terminal cluster of 14 closely spaced cysteine residues with the repeating pattern of Cys-X-X-Cys suggestive of a heavy metal binding domain. Histidine, aspartic acid, and glutamic acid accounted, respectively, for 13, 12, and 19% of the amino acids. The protein does not share any significant sequence homology with the cell surface low density lipoprotein receptor. Stretches of acidic amino acids are a feature of two other luminal sarcoplasmic reticulum proteins, suggesting that these may be a general feature of luminal sarcoplasmic reticulum proteins. We suggest that the histidine-rich Ca2+-binding protein described in the current study be designated HCP. The role of HCP in Ca2+ homeostasis in the sarcoplasmic reticulum of skeletal and cardiac muscle remains to be determined.
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PMID:Molecular cloning of a histidine-rich Ca2+-binding protein of sarcoplasmic reticulum that contains highly conserved repeated elements. 280 65

The beta-adrenergic receptor of rodent brown fat plays a key role in the control of energy dissipation by this tissue. The aim of the present study was to further characterize the biochemical properties of this receptor. The beta-receptor of rat interscapular brown adipose tissue plasma membranes was found to bind the beta-adrenergic antagonist [125I]cyanopindolol with a high affinity (KD 67 pM). The [125I]cyanopindolol receptor complex could be solubilized by digitonin and the isoelectric point of the solubilized receptor was found to be 5.8. Brown adipose tissue plasma membranes were labeled with the photoaffinity ligand [125I] cyanopindolol diazirine and labeled membrane proteins were separated by sodium dodecylsulfate polyacrylamide gel electrophoresis and analyzed by autoradiography. Autoradiograms revealed a peptide of 62 kDa whose labeling was stereoselectively displaced by alprenolol and isoproterenol. The beta 1-selective antagonist betaxolol was about 100 times more potent in displacing the labeling of this 62 kDa peptide than the beta 2-selective antagonist ICI 118,551. Based upon these data, it appears that the beta-receptor in brown adipose tissue is a beta 1 subtype with molecular weight of 62 kDa.
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PMID:Biochemical characterization of brown adipose tissue beta-adrenergic receptor. 283 80

Brown trouts, Salmo trutta, were exposed to water containing 0.1 or 10 micrograms/l of 63Ni2+, alone or with potassium ethylxanthate or sodium diethyldithiocarbamate. After one and three weeks the accumulation and disposition of the 63Ni2+ in the fish were examined by liquid scintillation spectrometry and whole-body autoradiography. The sodium diethyldithiocarbamate was found to greatly enhance the uptake of 63Ni2+ in several tissues of the trouts. Potassium ethylxanthate was without effect. Diethyldithiocarbamate is known to form lipophilic complexes with metals, including nickel, and a facilitated penetration of the complexed nickel over the cellular membranes of the gills and other tissues is a likely mechanism underlying our results. The ethylxanthate is also able to form a lipophilic nickel-chelate, although of a lower lipophilicity than the nickel-diethyldithiocarbamate-complex. This variance in lipophilicity may explain why the disposition of the 63Ni2+ was affected by the diethyldithiocarbamate, but not by the ethylxanthate.
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PMID:Effect of potassium ethylxanthate and sodium diethyldithiocarbamate on the accumulation and disposition of nickel in the brown trout (Salmo trutta). 284 Jun 49

Brown trout, Salmo trutta, were exposed to water containing 0.1 microgram/l 203Hg2+, alone or with potassium ethylxanthate (PEX), sodium isopropylxanthate (SIX), sodium diethyldithiophosphate (SEP), sodium diisopropyldithiophosphate (SIP), sodium dimethyldithiocarbamate (SMC), sodium diethyldithiocarbamate (SEC) or sodium pyridinethione (SPyr), respectively. After 1 week the uptake and distribution of the 203Hg2+ in the fish were examined by gamma spectrometry. SIX, SIP, SMC, SEC and SPyr induced 2-3 times higher 203Hg2+ concentrations in most tissues in comparison with trout exposed to 203Hg2+ only. In the trout exposed to PEX slightly enhanced 203Hg2+ levels were found only in some tissues, and after exposure to SEP a few tissues showed decreased 203Hg2+ concentrations. Determinations of chloroform/water partition coefficients showed that lipophilic chelates are formed between all the examined substances and the 203Hg2+. However, SIX, SIP, SMC, SEC and SPyr, which induced markedly increased tissue levels of the metal, formed 203Hg2+ complexes with higher lipophilicities than SEX and SEP. A facilitated penetration of the lipophilic 203Hg2+ complexes over the gill membranes may underly the increment in the tissue levels of the metal, and the relative lipophilicity of the complexes may be of importance for this effect. In some instances, as with SEP, the 203Hg2+ chelated in complexes with low lipophilicity may even be less able to acumulate in some tissues than the non-complexed metal.
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PMID:Effects of some chelating agents on the uptake and distribution of 203Hg2+ in the brown trout (Salmo trutta): studies on ethyl- and isopropylxanthate, diethyl- and diisopropyldithiophosphate, dimethyl- and diethyldithiocarbamate and pyridinethione. 285 39

A high rate of lipogenesis in obese mice plays a major role in their excessive deposition of body lipid. Inhibition of lipogenesis may decrease their obesity. Therefore, we have investigated the effects of sodium 2-n-pentadecyl-benzimidazole-5-carboxylate (M & B 35347B), an inhibitor of acetyl-CoA carboxylase, on in-vivo lipogenesis in obese and lean mice. It significantly inhibited hepatic cholesterol and fatty acid synthesis, measured using 3H2O, in both lean and obese mice, with or without a glucose load. Brown adipose tissue (scapular) lipogenesis was decreased by M & B 35347B in obese mice but not in lean mice. In white adipose tissue, M & B 35347B did not affect the rates of lipogenesis in either scapular white, inguinal or epididymal depots of obese mice, or the inguinal and scapular white depot of lean mice. However, it doubled lipogenesis in the epididymal fat pad of lean mice. After a glucose load, lipogenesis in the lean epididymal fat pad was not inhibited but that in the inguinal depot was. M & B 35347B inhibited acetyl CoA carboxylase of adipose tissue in vitro but only a small inhibition was detected after in-vivo treatment. These different responses according to type of mouse, treatment and tissue site appear to stem from differences in inhibitor concentration and the importance of acetyl CoA carboxylase as the rate-limiting enzyme of lipogenesis. The weight gain of obese mice dosed orally (200 mg M & B 35347B/kg daily) for 60 days was unaffected and they continued to deposit excess body fat. This presumably occurred because of the lack of inhibition of fatty acid synthesis in white adipose tissue.
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PMID:Effect of sodium 2-n-pentadecyl-benzimidazole-5-carboxylate (M & B 35347B), an inhibitor of acetyl-CoA carboxylase, on lipogenesis and fat deposition in obese hyperglycaemic (ob/ob) and lean mice. 289 66

Depletion of intracellular K+ has been reported to result in an arrest of the formation of coated pits in human fibroblasts (Larkin, J.M., M.S. Brown, J.L. Goldstein, and R.G.W. Anderson, 1983, Cell, 33:273-285). We have studied the effects of K+ depletion on the cytotoxicities of ricin, Pseudomonas exotoxin A, and diphtheria toxin in Chinese hamster ovary (CHO) cells. The cytotoxicities of ricin and Pseudomonas toxin were enhanced in K+-depleted CHO cells whereas the cytotoxicity of diphtheria toxin was reduced by K+ depletion. The effects of NH4Cl on the cytotoxicities of ricin, Pseudomonas toxin, and diphtheria toxin were found to be similar to those of K+ depletion, and there were no additive or synergistic effects on ricin cytotoxicity by NH4Cl in K+-depleted medium. The enhancement of ricin cytotoxicity by K+ depletion could be completely reversed by the addition of K+, Rb+, and partially by the addition of Cs+, before the ricin treatment, whereas Li+ was ineffective. These protective effects of K+ or Rb+ requires a functional Na+/K+ ATPase. CHO cells grown in K+-depleted media were found to contain 6.3-fold increase in intracellular Na+ level, concomitant with a 10-fold reduction in intracellular K+ level. The enhanced cytotoxicity of ricin in K+-free medium and the increased uptake of Na+ could be abolished by amiloride or amiloride analogues, which are known to be potent inhibitors of the Na+/H+ antiport system. Our results suggest that a depletion of intracellular K+ results in an influx of Na+, which is accompanied by the extrusion of H+. Consequently, there is an alkalinization of the cytosol and the ricin-containing endosomes. As a result, ricin is more efficiently released from the endosomes in-K+-depleted cells. Results from the studies of the binding, internalization, and degradation of 125I-ricin, and the kinetics of inhibition of protein synthesis by ricin in K+-depleted cells are consistent with this working hypothesis.
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PMID:Enhancement of ricin cytotoxicity in Chinese hamster ovary cells by depletion of intracellular K+: evidence for an Na+/H+ exchange system in Chinese hamster ovary cells. 299 Dec 97

Brown Norway rats were injected without adjuvant with the soluble products liberated in a 16-hour culture by schistosomula (schistosomula-released products, SRP-A). A strong cytotoxic and protective IgE response was elicited, mainly directed against 22- and 26-kilodalton (kDa) SRP-A molecules. In the present study, we have attempted to characterize further those molecules. Metaperiodate denaturing treatment of the SRP-A glycans before injection into rats did not modify the immunogenicity of the SRP-A antigens. Results obtained by lectin affinity suggested that the 22- and 26-kDa molecules were glycoconjugates binding to ConA. Preparative sodium dodecylsulfate electrophoresis has allowed the separation of enriched fractions of 22- and 26-kDa molecules which have been injected separately into rats. The corresponding sera were tested in antibody-dependent cell cytotoxicity and displayed a significant cytotoxic IgE response (65 and 53%, respectively) towards the larvae. These results lend further support to the view that the 22- and 26-kDa antigens are the major targets of the protective IgE response and thus appear as potentially protective antigens.
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PMID:Induction of a protective immune IgE response in rats by injection of defined antigens of schistosomulum-released products: immunochemical properties of the target antigens. 300 74


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