Carbohydrate intolerance associated with reduced hepatic glucose phosphorylating and releasing enzyme activities and peripheral insulin resistance in alcoholics with liver cirrhosis

Molecular Mechanisms of Alcoholic Fatty Liver

“…Consequently, insulin-mediated glucose/lipid metabolism should be altered in ethanol-exposed tissues. These results may provide one reason why ethanol-exposed animals or human alcoholics produce greater amounts of ROS from elevated CYP2E1 and thus may be more prone to develop type II diabetes with insulin resistance and fatty liver than non-drinkers (Beulens et al, 2005; Carlsson et al, 2003; Sotaniemi et al, 1985). Therefore, it is possible that ethanol-related ROS/RNS may activate stress-activated protein kinases including JNK, which is known to phopshorylate and inhibit IRS-1, as observed in multiple forms of insulin resistance (Houstis et al, 2006) or in obese mice (Diehl 2004; Solinas et al, 2006).…”

Effects of late evening snack on diurnal plasma glucose profile in patients with chronic viral liver disease

“…In patients with liver cirrhosis, hepatic parenchymal cells decrease, tissue fibrosis occurs, and the glucose absorbed to rebuild lobular structures is not taken up by hepatic cells. As a result, glucose not taken up in the liver is thought to be oxidized in peripheral skeletal muscle and brain by the action of insulin and used as an energy source, so hyperinsulinemia is expressed 15 . Thus, in patients with liver cirrhosis eating three meals/day, the glucose that is not processed in the liver is used in peripheral tissues through the actions of insulin, and this increases insulin secretory capacity.…”

“…As a result, glucose not taken up in the liver is thought to be oxidized in peripheral skeletal muscle and brain by the action of insulin and used as an energy source, so hyperinsulinemia is expressed. 15 Thus, in patients with liver cirrhosis eating three meals/day, the glucose that is not processed in the liver is used in peripheral tissues through the actions of insulin, and this increases insulin secretory capacity. With four meals including LES, plasma glucose is conjectured to decrease because glucose is processed adequately in the liver, so the amount of glucose transported to peripheral tissues is decreases, thereby decreasing insulin secretory capacity.…”

The Relationship Between Chronic Alcohol Use and Type 2 Diabetes Mellitus: New Insights into Mechanisms of Appetite-Regulating Peptides

“…Chronic, heavy alcohol consumption, an independent risk factor for T2DM [35][36][37], disrupts glucose homeostasis and is associated with development of insulin resistance [38][39][40].…”

“…In regards to the diabetogenic effects of chronic use of alcohol, development of pancreatic -cell dysfunction, insulin resistance, obesity, impairment of liver function in glucose metabolism have been noted [35]. Indeed, alcoholic patients with T2DM have repeatedly been found to have deregulation of the ghrelin and leptin systems, as indicated by impaired insulin secretion, increased hepatic glucose production and decreased peripheral glucose utilization [38][39][40]. Moreover, these peptides are regarded to have an influence on T2DM-mediated alcohol cravings and relapses in alcoholism during alcohol abstinace [91][92][93][94].…”