Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were conducted to determine if food intake and adrenalectomy influenced abnormal antioxidant defense mechanisms observed in obese mice. Paired male C57BL/6J mice of two genotypes, obese (ob/ob) and lean (+/?), were fed a nonpurified diet ad libitum or restricted (2.5 g/d) until 3 mo old. Obese mice had larger livers and kidneys but smaller brains than lean mice. Plasma ceruloplasmin activity of obese mice was 240% of that of lean mice. Restricting food intake but not adrenalectomy reduced this difference, but ceruloplasmin activity of obese mice was still 150% of that of restricted-fed lean mice. Glutathione peroxidase (GSH-Px) activity in liver of obese mice was 70% of that in control lean mice; however, in kidney GSH-Px activity was 135% of that in obese mice. Both liver and kidney GSH-Px differences were eliminated by food restriction but not by adrenalectomy. Blood and brain GSH-Px activity was not influenced by the mutation. Liver and kidney copper-zinc superoxide dismutase activity was lower in obese mice than in lean littermates, 30 and 20%, respectively. Food restriction eliminated this difference in liver but not in kidney. Glutathione S-transferase activity using 1-chloro-2,4-dinitrobenzene as substrate was 55% lower in liver (not kidney) of obese mice than in lean mice and this difference was not markedly influenced by food restriction. Obese mice have marked changes in the steady-state activities of a number of protective enzymes that are organ dependent and, in part, due to the hyperphagia associated with this mutation.
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PMID:Influence of genetic obesity, food intake and adrenalectomy in mice on selected trace element-dependent protective enzymes. 337 40