Abstract:
:This study was undertaken to determine the pathogenesis of muscle atrophy that frequently accompanies liver disease. Hepatic injury was induced in rats by giving weekly intragastric doses of carbon tetrachloride (CCl4) in combination with phenobarbital in the drinking water. Muscle protein catabolism was assessed during three stages of liver injury and compared with pair-fed controls: group A had hepatic necrosis and inflammation without significant fibrosis; group B had cirrhosis as well as necrosis and inflammation; and group C had cirrhosis with minimal necrosis and inflammation. In group A, vastus lateralis white muscle, which contained predominantly fast glycolytic fibers, showed a significant increase in protein catabolic rates compared with pair fed controls (0.95 +/- 0.05 nmol tyrosine released.mg-1.2 h-1 vs. 0.86 +/- 0.04; P less than 0.05). In group B, protein catabolic rates were significantly increased in vastus lateralis white muscles, as well as two muscles that have a mixed fiber composition, diaphragm, and triceps. Protein catabolic rates were not increased in soleus muscle that predominantly contained slow oxidative fibers in either group A or B. In group C rats there was no increase in catabolic rates in diaphragm or vastus lateralis white muscle. None of the muscles from group B had any impairment in protein synthesis. In diaphragms from group B animals, there was a selective reduction in the cross-sectional areas of fast glycolytic fibers (3725 +/- 224 mm2 control vs. 2926 +/- 208 mm2 experimental; P less than 0.01). This study indicated that liver injury characterized by inflammation and hepatocyte necrosis, with or without cirrhosis, was associated with muscle atrophy that selectively affected fast glycolytic fibers. This muscle atrophy was caused by an increase in protein catabolism and was not the result of an inhibition of protein synthesis.
journal_name
Gastroenterologyjournal_title
Gastroenterologyauthors
Weber FL Jr,Macechko PT,Kelson SR,Karajiannis E,Hassan MOdoi
10.1016/0016-5085(92)91733-kkeywords:
subject
Has Abstractpub_date
1992-05-01 00:00:00pages
1700-6issue
5eissn
0016-5085issn
1528-0012pii
0016-5085(92)91733-Kjournal_volume
102pub_type
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