Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experiment was conducted to clarify the combined effect of simultaneous administrations of insulin (Ins, 4 units/100 g body weight/day) and testosterone propionate (TP, 2 mg/100 g body weight/day) and feeding a high-protein-high-fat (HPHF) diet (50% protein, 36% fat) on corticosterone (CTC, 10 mg/100 g body weight/day)-induced muscle proteolysis or growth retardation in young growing male rats. After 6 days prefeeding of the standard (STD) diet (25% protein, 9% fat) and the HPHF diet, hormones were injected subcutaneously for 4 days. Urine was collected every day for the 4-day experimental period to measure N tau-methylhistidine excretions. The results were as follows. The growth was markedly inhibited and muscle proteolysis was accelerated by the CTC treatment. Feeding HPHF diet reduced CTC-induced muscle proteolysis and the growth retardation, and administrations of Ins and TP further reduced the proteolysis and the growth retardation. From these results, it is thought that administrations of Ins and TP and feeding HPHF diet minimize the muscle protein wasting by counteracting insulin resistance caused by CTC, and masking the CTC receptor.
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PMID:Reduction of corticosterone-induced muscle proteolysis and growth retardation by a combined treatment with insulin, testosterone and high-protein-high-fat diet in rats. 162 88

Gitelman's syndrome is an autosomal recessive disorder marked by salt wasting and hypokalaemia resulting from loss of-function mutations in the SLC12A3 gene that codes for the thiazide sensitive Na -Cl cotransporter. Gitelman's syndrome is usually distinguished from Bartter's syndrome by the presence of both hypomagnesaemia and hypocalciuria. The human SLC12A3 gene, which is located on chromosome 16, consists of 26 exons and encodes a protein that contains 12 putative transmembrane domains with long intracellular amino and carboxy termini. In the present study, we developed a method of genetic diagnosis for Gitelman's syndrome using DNA sequencing. A patient was found to be a compound heterozygote with a single base substitution at nucleotide 2552 (CTC-to-CAC, L849H) and a substitution at nucleotide 2561 (CGC-to-CAC, R852H) in exon 22. Familial linkage analysis confirmed that 849H was the paternal allele and 852H was the maternal allele. The method can save time and costs, and it should be useful for genetic testing in clinical laboratory of every hospital.
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PMID:[Establishment of genetic testing for Gitelman's syndrome]. 2022 14