Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were conducted from 1968 to 1974 to investigate reproductive complications and mortality in mink fed Great Lakes coho salmon and to ascertain the effects of polychlorinated biphenyls (PCB's) on this fur bearer. The results of mink feeding trials indicated that coho salmon, as such, were not responsible for the loss of reproduction in the adult, or the kit mortality. Mink diets that contained other species of Great Lakes fish caused similar reproductive complications, but to a lesser degree. Rancidity, mercury poisoning and chlorinated hydrocarbon pesticide contamination of the fish were all discounted as being responsible for the problem. The clinical signs and lesions noted in mink that died while receiving diets that contained Lake Michigan coho salmon were very similar to those observed in mink fed on rations that contained supplemental PCB's. These included anorexia, blood stools, fatty liver, kidney degeneration, and hemorrhagic gastric ulcers. Analyses of tissues from mink that died when fed 30% Lake Michigan coho salmon or 30 ppm supplemental PCB diets showed similar PCB residues. PCB toxicity experiments revealed that mink are very sensitive to these compounds and that the lethal dose varied inversely with the chlorine content of the PCB's although only Aroclor 1254 exerted a detrimental effect on reproduction when fed at a low level (2 ppm) for 8 months. The reproductive failure encountered in feeding mink Lake Michigan coho salmon and Aroclor 1254 was shown to be of a non-permanent nature.
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PMID:Current status of PCB toxicity to mink, and effect on their reproduction. 40 55

Biotin deficiency can be induced readily in monogastric animals and is accompanied by characteristic abnormalities. These include dermal lesions involving hyper- and parakeratosis and, in fur-bearing animals, alopecia and achromatricia. Biochemical changes include depressions in the activities of biotin-dependent enzymes and the metabolic pathways in which they are involved. However, it has been shown in chickens that the relative changes in the activities of these enzymes and the resultant manifestations of the deficiency can be markedly influenced by the dietary content of other nutrients such as protein or fat. Biochemical criteria are required for the diagnosis of subclinical deficiency and these are best-established for poultry. Blood pyruvate carboxylase activity is a good criterion in young birds. Biotin-responsive disorders have been identified in several species. The etiology of fatty liver and kidney syndrome in chickens is now largely understood and is an interesting example of how a combination of nutritional and environmental factors can result in sudden death in, until then, apparently healthy animals.
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PMID:Assessment of biotin deficiency in animals. 286 81

Groups of normal and heterozygote sparse-fur (spf) mutant mice were studied at various stages of gestation, to assess the effects of normal pregnancy on orotate excretion, hepatic mitochondrial urea cycle enzymes and any predisposition to the development of fatty liver. Results show a higher total daily excretion of urinary orotate by normal pregnant mice on the 8th and 15th days of gestation, which came to within the usual basal range of excretion of non-pregnant mutant heterozygotes with hereditary ornithine transcarbamylase deficiency. Liver ornithine transcarbamylase and carbamyl phosphate synthetase-I activities were reduced in pregnant mice on the 16th day of gestation (P less than 0.05). No fatty change, bile stasis or glycogen depletion was discernible on optical microscopy in normal or mutant mice. Nonspecific changes were seen on ultrastructural examination. Orotic aciduria seen in pregnant mice may be directly related to a physiological deficiency of liver ornithine transcarbamylase. However, the depletion of both the mitochondrial urea cycle enzymes, seen on the 16th day of pregnancy, may be indicative of a metabolic stress at the mitochondrial level.
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PMID:The role of hepatic ornithine transcarbamylase deficiency in the orotic aciduria of pregnant mice. 373 88