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This study was designed to measure the effect of chronic alcohol intake on leucine turnover in outpatients with stable alcoholic liver cirrhosis.Protein turnover rate was measured using L [1-14C] leucine in ten outpatients with proven alcoholic cirrhosis and in five healthy controls. After the performance of the turnover, the patients were divided in two groups depending on the evidence of alcohol ingestion in the previous month.Non-abstinent patients had a significantly higher leucine flux and non-oxidative disposal (73.8 +/− 25.4 and 65.9 +/− 21.6) than abstinent cirrhotic patients (48.9 +/− 9.5 and 43.7 +/− 9.0) and normal controls 37.3 +/− 8.9 and 31.1 +/− 7.6 mumol/m2/min (p < 0.01). Leucine oxidation and serum leucine levels were similar in the three groups.Alcohol intake in alcoholic cirrhotic patients has a catabolic effect that could be associated with the nutritional imbalances observed in alcoholic liver disease.

Protein digestion was studied in pair-fed rats receiving an adequate (protein 12% and alcohol 35% of calories) diet during 24 weeks. No differences in fecal nitrogen excretion were observed between the alcohol-treated and control rats. At the 24th week the rats were sacrificed and jejunal mucosa dipeptidase activity was studied. No differences were found either between controls and alcohol-treated animals.

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.

Chronic administration of epinephrine to adult male rats resulted in a significant increase in the rate of ethanol elimination, when given alone or together with the beta-adrenergic blocker alprenolol. This effect was observed concomitantly with an increased hepatic oxygen utilization and no changes in mitochondrial respiratory functions. Epinephrine given acutely did not modify the rate of ethanol metabolism. Blood glucose levels were enhanced in these conditions, but were unaffected in rats treated with epinephrine plus alprenolol. These results suggest that chronic epinephrine treatment induces an increased oxidative capacity in the liver characterized by enhanced rates of oxygen uptake and ethanol metabolism, which is not related to its beta-adrenergic actions.

1. The relationship between the content of hepatic reduced glutathione (GSH) and the length of abstinence was investigated in 45 chronic alcoholic patients. 2. Hepatic GSH levels were significantly correlated (r = 0.58; P 3. According to the period of abstinence patients were separated into two groups, with a short (≪ 5 days) and a prolonged (> 5 days) alcohol withdrawal. Patients with and without necrosis exhibited comparable mean levels of liver GSH (2.04 ± sem 0.21 and 1.74 ± 0.23 μmol/g respectively; P 4. Parameters assessing the nutritional status of patients with and without necrosis were not significantly different. Steatosis, histologically scored and irrespective of the period of abstinence, was higher in patients with liver necrosis and it did not correlate with hepatic GSH (r = −0.17; not significant). Fibrosis was observed in 20 cases and it did not modify the positive correlation between liver GSH content and the period of abstinence (with fibrosis: r = 0.57; P < 0.01; without fibrosis: r = 0.58;P < 0.01). 5. The changes observed in liver GSH content might be of pathogenic importance in alcoholic liver disease through alterations in lipoperoxidative processes in the hepatocyte.

The rate of ethanol metabolism (EMR) was determined in alcoholic patients with or without hepatic necrosis, steatosis, and/or cirrhosis. Fifty six cases were studied after 9-25 days of abstinence (mean 15 days). A significant increase in EMR (P less than 0.01) was found in alcoholics with hepatic necrosis (265 +/- 20.5 mg/kg/hr) compared with alcoholics with normal liver histology (154 +/- 17) and nonalcoholic controls (159 +/- 15). In alcoholics with liver steatosis but without necrosis a lesser increase in EMR (207 +/- 20, P less than 0.05 was also observed. Patients with slight fibrosis but without other abnormalities in their liver biopsies and cirrhotics with overt liver failure (jaundice, ascites) showed EMR similar to controls.

Differing rates of blood ethanol clearance among groups of alcoholics with varying lengths of abstinence suggest that there may be adaptive changes in alcohol metabolism in alcoholics.

Duodenal content from subjects without pancreatic disease and 3 patients with chronic pancreatitis were studied after Pentagastrin (I.C.I. 50, 123) administration. The output of lipase and trypsin in patients with pancreatitis was lower than that in control subjects. Cholecystokinetic activity of Pentagastrin was evidenced by an increase of bilirubin content in duodenal aspirate.

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

This study was performed to look for a possible relationship between the nutritional status and the presence of liver damage in alcoholic patients. One hundred chronic alcoholics admitted for treatment to the Alcoholism Ward, without clinical signs of liver failure, were studied. In 84, anthropometric nutritional indexes, liver function tests, and a liver biopsy were performed; in 69 patients a dietary survey was obtained. A dietary imbalance was observed in the total group; 65% of ingested calories were derived from ethanol. The intake of proteins, vitamins, and minerals was below the RDA, NAS/USA, and no differences were found between patients with and without liver damage. Neither were significant differences in daily alcohol calories or total ethanol dose found between both groups of patients. Mean anthropometric values were within 80 to 100% of commonly used standards. However, patients with alcoholic hepatitis and/or cirrhosis had a significantly higher percentage of ideal body weight, compared to alcoholics with normal livers or less severe histological alterations (109.7 +/- 20.3 versus 95.6 +/- 12.5, SD, p less than 0.005). A similar difference was observed in arm muscle areas. These findings show that overweight is associated with liver alterations in the alcoholic and should be investigated as a risk factor to develop liver damage.

This study analyzes whether increased body weight is related to histological liver damage in chronic alcoholic patients. Data from 152 recently abstinent alcoholics without evidences of liver failure were analyzed. Liver biopsies were scored for the presence of fat, necrosis, fibrosis, inflammation, and Mallory material. Total histological score correlated significantly with body weight (BW), length of alcoholism (L), and age (A) but not with the amount of ethanol ingested (E). Forward stepwise multiple regression analysis with histological score as the dependent variable gave significant F values for BW and L but not for A. Patients with severe damage had higher BW than patients with mild damage. The group with BW greater than 110% showed a higher histological score. These results confirm the association between increased BW and liver damage in asymptomatic alcoholic patients suggesting that overweight is a risk factor for alcoholic liver disease.

To determine whether hepatic hypoxia is associated with hepatocellular necrosis in alcoholics, oxygen tension in the hepatic vein and hepatic blood flow were determined in thirteen patients without overt clinical liver disease. Ethanol metabolic rate was also assayed as an index of liver metabolism. Hepatic blood flow and ethanol metabolic rate were also determined in six normal volunteers. According to liver histology patients were separated into two groups, with and without hepatocellular necrosis. Alcoholics with necrosis showed a higher (P less than 0.002) ethanol metabolic rate (4.05 +/- 0.23 mmol/kg/h) than those without necrosis (2.46 +/- 0.34). Hepatic blood flow in the total group of alcoholics was not significantly different from controls; in the group with necrosis it was lower (651.7 +/- 44.6 ml/min/m2) than in the group without necrosis (878.3 +/- 81.6; P less than 0.025). Hepatic vein pO2 was lower (P less than 0.01) in patients with hepatocellular necrosis (31.7 +/- 0.68 mmHg) than in patients without necrosis (35.7 +/- 0.99). In the whole group, a significant negative correlation (r = 0.76, P less than 0.003) was observed between hepatic vein pO2 and ethanol metabolic rate. Acute administration of ethanol (21.7 mmol/kg) did not alter hepatic blood flow in six normal individuals nor in five alcoholic patients, although an increase in hepatic vein pO2 was observed in the latter. The changes observed in hepatic vein pO2 functional hepatic blood flow, and ethanol metabolic rate which correlate with hepatocellular necrosis, may be of pathogenic importance in alcoholic liver disease.

Glucose intolerance is frequently found in alcoholic patients and an impaired insulin response has been documented in them. To look for alternative mechanisms that could explain this intolerance, a glucose turnover using tritiated glucose and an euglycemic glucose clamp were performed to measure the glucose production rate and peripheral insulin sensitivity, respectively. Two groups of recently abstinent chronic male alcoholic patients without evidence of liver damage were studied. The glucose turnover technique showed a higher basal glucose production rate in alcoholics, compared with normal volunteers (2.83 +/- 0.29 vs. 1.84 +/- 0.22 mg/kg/min); an intravenous ethanol load significantly increased this rate. The euglycemic glucose clamp did not show peripheral insulin resistance in alcoholics, compared with controls.

Among 80 alcoholics in Chile, 43% had normal ADH, 43% atypical ADH and 14% evidently both enzyme types. The pattern of alcoholismic drinking was not related to enzyme type, but the atypical ADH was...

Hepatic alcohol dehydrogenase was measured in liver homogenates from normal, moderate drinkers, and from alcoholics with normal livers, steatosis, and liver cirrhosis.