title: Osmotic diarrhoea and skeletal muscle protein synthesis in vivo.
abstract: The pathogenic nature of the wasting seen in diarrhoea is unknown. This study measured protein synthesis in an established model of diarrhoea using lactose for seven days. Comparisons were also made with data obtained from rats fed an identical diet in which lactose was replaced by isocaloric glucose ad libitum (that is, the control diet). To account for diarrhoea induced anorexia, a third group of rats were included, which were fed identical amounts of the control diet as the rats with diarrhoea inducing diet. Comparisons of the diarrhoea induced group with rats fed the control diet ad libitum showed that diarrhoea caused a significant reduction in body weights. Type I and type II muscles showed significant reductions in protein, RNA, and DNA contents, as well as a fall in the derived parameters, RNA/DNA, protein/DNA, and RNA/protein. Fractional rates of protein synthesis (ks) were also reduced. However, synthesis rates of type I and II muscles relative to RNA (kRNA) were unchanged in these muscles in diarrhoea induced rats compared with ad libitum fed controls. In the jejunum there was an increase in the RNA/DNA ratio, and reductions in ks and kRNA. Comparisons were also made between rats with diarrhoea and rats pair fed the control diet. There were no changes in total muscle protein, RNA or DNA contents. This suggests that an important feature of body wasting in diarrhoea is the element of anorexia, which induces severe metabolic changes. The comparison between rats with diarrhoea and the pair fed group showed that histological features of the plantaris were not overtly changed, though diarrhoea caused significant reductions in RNA/DNA, protein/DNA, ks, and kRNA. Similar changes were seen for the soleus; though the reduction in ks failed to attain statistical significance. In the jejunum a comparison of diarrhoea induced rats with pair fed controls, showed increases in the ratios of RNA/DNA and protein/DNA.
authors.affiliation: Department of Clinical Biochemistry, King's College School of Medicine and Dentistry, London.
authors.forename: H
authors.initials: H
authors.lastname: Ansell
authors.forename: J S
authors.initials: JS
authors.lastname: Marway
authors.forename: A B
authors.initials: AB
authors.lastname: Bonner
authors.forename: J R
authors.initials: JR
authors.lastname: Salisbury
authors.forename: D C
authors.initials: DC
authors.lastname: Candy
authors.forename: V R
authors.initials: VR
authors.lastname: Preedy
mesh_terms: D000818:Animals; D003967:Diarrhea / Q000139:chemically induced / Q000378:metabolism*; D007785:Lactose; D008297:Male; D009124:Muscle Proteins / Q000096:biosynthesis*; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology; D009133:Muscular Atrophy / Q000209:etiology* / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D009124:Muscle Proteins; D007785:Lactose