Chronic Ethanol Ingestion Enhances Catabolism and Muscle Protease Activity in Acutely Uremic Rats

Abstract

Skeletal muscle wasting in men as well as enhanced urea production in animals due to ethanol consumption has been demonstrated by numerous authors. Furthermore, the outcome of acute renal failure is closely related to the extent of catabolism. The present study was performed to investigate whether chronic ethanol exposition prior to binephrectomy (BN) may represent a predisposing factor for enhanced protein breakdown. Rats underwent BN after exposure to ethanol or isocaloric substrate for 4 weeks. Blood chemistries and muscle samples were obtained 48 h after BN. Animals fed with ethanol revealed significantly higher levels of serum urea nitrogen (SUN) and urea nitrogen appearance (UNA) in comparison to controls. Preconditioning on ethanol-derived calories induced an accelerated fractional degradation rate of myofibrillar protein as demonstrated by a significantly enhanced serum N^t-methylhistidine/creatinine ratio. The increase in serum indicators of enhanced myofibrillar breakdown correlated with the stimulated activities of alkaline myofibrillar protease and cathepsin B. Finally, serum corticosterone levels were enhanced in the experimental group in comparison to controls, indicating an ethanol-related adrenocortical stimulation to be a possible mediating factor of enhanced catabolism in ARF. Thus, chronic ethanol intake prior to the onset of ARF seems to be a risk factor for enhanced catabolism in the course of acute uremia.

Chronic binge alcohol consumption alters myogenic gene expression and reduces in vitro myogenic differentiation potential of myoblasts from rhesus macaques

“…It occurs in almost 50% of alcoholics who can exhibit up to 30% reduction of skeletal muscle mass (33). Chronic alcoholic skeletal myopathy can result either from decreased muscle protein synthesis (29,34) or accelerated muscle protein degradation (40) or a combination of both. Little attention has been directed to the function of adult muscle stem cells, satellite cells (SCs), in alcohol-induced myopathies.…”

Chronic Alcohol Accentuates Simian Acquired Immunodeficiency Syndrome‐Associated Wasting

“…Muscle wasting remains an important determinant of the increased morbidity and mortality observed in AIDS (Grunfeld and Feingold, 1992; Tang et al., 2002; Van Loan et al., 1999; Wanke et al., 2000; Grinspoon and Mulligan, 2003). Chronic alcohol abuse is also associated with skeletal muscle myopathy (Preedy et al., 1994) resulting from decreased muscle protein synthesis (Lang et al., 1999a;Pacy et al., 1991; Reilly et al., 1997) and possibly accelerated muscle proteolysis (Teschner et al., 1988). In addition, indirect effects of alcohol such as alterations in nutritional state, micronutrient availability and growth factor expression have also been implicated in the etiology of the alcohol‐induced muscle wasting (Molina et al., 1996; Bergheim et al., 2003; Yeomans et al., 2003).…”

Chronic Alcohol Accentuates Nutritional, Metabolic, and Immune Alterations During Asymptomatic Simian Immunodeficiency Virus Infection

“…One of the hallmarks of chronic alcohol abuse is the negative nitrogen balance resulting from the net catabolism of skeletal muscle protein. Excess alcohol consumption is associated with an ∼50% incidence of skeletal muscle myopathy (Preedy et al, 1994) resulting from decreased muscle protein synthesis (Lang et al, 1999a; Pacy et al, 1991; Reilly et al, 1997) and possibly accelerated muscle proteolysis (Teschner et al, 1988). In addition, alcohol can alter the nutritional state of the individual either by decreasing food consumption and/or by producing malabsorption.…”