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Glucose tolerance and the insulin response in recently drinking alcoholic patients: possible effects of withdrawal.

To investigate possible effects of withdrawal on carbohydrate metabolism in chronic alcoholic patients, intravenous glucose tolerance tests were performed in three periods in 11 alcoholic patients: early abstinence (less than three days), early abstinence plus ethanol (1 g/kg/BW IV), and late abstinence (three weeks later). According to liver biopsy results and laboratory tests, patients were classified as a group with liver damage (four cases) and a group without it (seven cases). In the group without damage, glucose tolerance expressed as K% and compared to a control group, was significantly decreased in early and late abstinence but not after the infusion of ethanol. Cases with damage also had glucose intolerance at admission. Plasma insulin levels after the glucose load were significantly lower at ten and 30 minutes in the group without damage, in early or late abstinence. They were normal in the presence of ethanol. Patients with liver damage presented higher basal and postglucose plasma insulin concentrations. It was concluded that glucose intolerance in alcoholic patients is a common finding that occurs in the presence or absence of liver damage. In cases with liver damage it seems to be due to peripheral insulin resistance. In those without damage it is related to low peripherovenous insulin levels.

Increased Blood Ethanol Elimination in Rats Treated with Halothane

The effect of chronic halothane inhalation and blood ethanol elimination was studied in the rat. Hepatic α-glycerophosphate, oxidase ADH and malic enzyme activities were determined. Malic enzyme activity was also assayed in adipose tissue. Halothane-treated rats showed an increased ethanol elimination (378 ± 13 vs. 292 ± 19; p

Lysosomal injury and hepatic necrosis: Effects of triton WR-1339 on liver cells in the rat

Abstract To investigate possible mechanisms of the aggravating effects of Triton adminstration upon CCl4-induced liver necrosis, serial chemical and ultrastructural studies on liver tissue during the first 24 hours after Triton injection were performed. Results indicate an early lysosomal damage, reflected in an increase of soluble acid phosphatase in liver homogenates and in an augmented number of lysosome vacuoles in liver cells. Increase in serum sorbitol dehydrogenase, reflecting a liver cell membrane injury, occurred at later periods. No other cell organelles or enzyme distribution were altered. The possible relationship between the lysosomal injury and the elevation of serum sorbitol dehydrogenase is discussed. Thioacetamide-induced liver necrosis was also aggravated by Triton injection, suggesting that Triton effects are nonspecific and could be mediated by a lysosomal injury.