Metabolic effects of alcohol on skeletal muscle

Abstract

The purpose of this review is to summarize our current understanding of the acute and chronic interactions between alcohol and nutrient metabolism in skeletal muscle. Insulin is well known to play an important regulatory role in nutrient, especially glucose, uptake and utilization in skeletal muscle. Several studies have shown that alcohol can acutely reduce the normal metabolic responses of skeletal muscle to the action of insulin. The most obvious of these is an acute impairment in glucose metabolism associated with alcohol consumption. While the exact mechanism(s) underlying this acute insulin resistance is presently unclear, several possible factors are discussed in this review. In contrast to these short-term effects, the effects of alcohol on skeletal muscle insulin sensitivity in chronic alcohol abusers are not as well established. Chronic alcohol abuse is known to be associated with skeletal myopathies, believed to result from alcohol induced abnormalities in muscle protein synthesis. Finally, the alcohol-mediated impairments of many aspects of skeletal muscle metabolism are discussed in relation to the insulin resistance associated broad spectrum of common lifestyle-related disorders, including non-insulin dependent diabetes mellitus and obesity, the consequences of which may be important to the pathogenesis of alcohol-related diseases.

Ethanol stimulates glucose uptake and translocation of GLUT-4 in H9c2 myotubes via a Ca2+-dependent mechanism

“…Although ethanol exposure can have profound effects on whole body glucose homeostasis, the mechanisms for ethanol action are not well understood. Short-term ethanol exposure can have an impact on hepatic glucose production (2), insulin release and extraction (1,11,21,22), as well as peripheral utilization of glucose (27,37). Acute ethanol exposure results in peripheral insulin resistance in both rats and humans (27,37,40), but it is not clear whether this is a direct effect of ethanol on skeletal muscle to impair insulin signaling and/or glucose utilization or an indirect, systemic response (3).…”

“…These results suggest that impaired glucose disposal by acute ethanol exposure in vivo is most likely mediated by ethanol-induced changes in the hormonal regulation of glucose transport rather than by a direct inhibition of glucose transport by ethanol. Furthermore, because acute and chronic alcohol consumption results in the development of a variety of skeletal muscle abnormalities (37), the inability of H9c2 myotubes to maintain normal GLUT-4 localization after ethanol exposure suggests that disruption of intracellular Ca 2ϩ homeostasis by ethanol may also contribute to the development of skeletal muscle abnormalities.…”

“…Erwin and Towell (10) have suggested that ethanol-induced hyperglycemia may result from increased sympathetic output. Brief exposure of rats to ethanol results in insulin resistance (37). During hyperinsulinemic-euglycemic clamping, ethanol decreases insulin-stimulated glycogen synthesis and glucose oxidation in heart and skeletal muscle of overnight-fasted rats (36).…”

“…Ethanol treatment also decreases glucose-stimulated glycogen synthesis in oxidative muscles (38). Xu et al (37) proposed that, because ethanol decreases both glycogen synthesis and glucose oxidation, ethanol is likely acting at a metabolic step common to both pathways, such as insulin signaling or glucose transport.…”

Acute alcohol administration inhibits the refeeding response after starvation in rat skeletal muscle

“…THE CONSUMPTION OF ALCOHOL induces a variety of pathogenic responses in many different tissues, including skeletal muscle (7,29,39,40). Studies have shown that up to 60% of chronic alcoholics exhibit associated alcoholic myopathy (characterized by muscle weakness and wasting) (15,34,35).…”