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

Iturriaga, H; Kelly, Melani R.; Bunout, Daniel; Pino, María Eugenia; Pereda, T; Barrera, R.; Petermann, Marcus; Ugarte, G

doi:10.1016/0026-0495(86)90207-6

Cited by 15 publications

(5 citation statements)

References 25 publications

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“…In rodents, it has been proposed that changes in the fat/carbohydrate ratio of ingested food regulate microsomal activity. The deprivation of glucose versus fat, concurrent with low insulin levels, or increased ketone levels, often observed in conditions such as diabetes, fasting, high-fat diets, and alcohol ingestion (Iturriaga et al, 1986;Hirsch et al, 1998), enhances the expression of CYP2E1, mainly through protein stabilization (Song, 1996). Because most obese subjects are insulin resistant, it could be speculated that the lack of insulin action is associated with microsomal induction (Woodcroft and Novak, 1997).…”

Section: Discussionmentioning

confidence: 99%

Changes in Microsomal Activity in Alcoholism and Obesity

Maza

Hirsch

Petermann

et al. 2000

Alcoholism Clin & Exp Res

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Background: Liver damage is more prevalent among obese alcoholics, and cytochrome P-450 -2E1(CYP2E1) induction is involved in its pathogenesis.Objectives: The study was undertaken to assess microsomal function, in alcoholic and nonalcoholic male subjects with different body compositions, through pharmacokinetics of chlorzoxazone (CLZ). We also intended to study the relationship between CLZ hydroxylation and urinary levels of 8-hydroxydiguanosine, and between CLZ levels and liver histology.Methods: Serial measurements of CLZ serum concentration, after a 750 mg dose, were performed in 17 alcoholics (9 normal weight and 8 obese) and 21 nonalcoholic subjects (10 normal weight and 11 obese). Concentration of 6-hydroxy-chlorzoxazone (6-OH-CLZ) was determined at the second hour. Anthropometry, clinical laboratory tests, and urinary 8-hydroxydiguanosine concentrations were measured. Liver biopsies were performed in alcoholics.Results: Five biopsies revealed severe lesions, one in normal-weight and four in obese patients (p ϭ NS). Area under the curve (AUC) of CLZ was higher in normal-weight controls compared with the rest of the groups (ANOVA p ϭ 0.001). This parameter correlated negatively with adiposity in nonalcoholic subjects and did not correlate with liver histology. 6-OH-CLZ/CLZ ratio was lower in normal-weight controls, compared with obese subjects and normal-weight alcoholics (p ϭ 0.02). Both alcoholism and obesity were included as predictors of CLZ AUC in a multiple regression analysis. The two-factor ANOVA showed an additive effect of centripetal body fat distribution and alcoholism. Urinary 8-hydroxydiguanosine levels were extremely variable.Conclusions: Centripetal adiposity and alcoholism are associated with induction of CYP2E1. This may explain the higher prevalence of liver damage among obese alcoholics and also nonalcoholic steatohepatitis.

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Section: Discussionmentioning

confidence: 99%

Changes in Microsomal Activity in Alcoholism and Obesity

Maza

Hirsch

Petermann

et al. 2000

Alcoholism Clin & Exp Res

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“…The relationship has already been noted in other different populations (7,(18)(19). Recent studies appear to indicate, however, that this p h e n o m e n o n is observable only in cases of drinkers without hepatic lesion~s (8). In this case, however, the strenght of the relationsh4p is limited since the partial correlation coefficient between alcohol consumption and glycemia, adjusted for age, sex, and body mass index, is 0.08.…”

Section: (18)mentioning

confidence: 55%

Alcohol consumption and impaired glycoregulation results in a population of 6665 salaried employees

et al. 1988

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Alcohol consumption and glycosuria were found to be associated (p less than 0.001) in a population of 6571 salaried employees who underwent a systematic examination. The prevalence of glycosuria was found to range from 1.3% among 2609 non-drinkers to 5% among 816 heavy drinkers (six glasses or more of alcoholic beverage daily). This association was still significant after adjustment for age, sex and body mass index. Similarly, a positive association was observed between fasting glycemia and alcoholic intake in a subgroup of 998 subjects when such a result was available (p less than 0.05).

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“…This fact could be due to a lower insulin secretion or to a lack of hepatic response to the hormone. In alcoholics, previous reports have shown that they fail to increase ade quately the insulin levels in response to a glucose load, despite having normal basal levels [4], A lack of hepatic response to insu lin is also possible since in other studies a dissociation between peripheral and hepatic responses to the hormone has been found [19], Chronic alcohol consumption leads to an increased rate of ethanol oxidation and hepatic oxygen consumption [22]. An in creased gluconeogenesis could be one of the pathways responsible for this higher oxygen consumption.…”

Section: Discussionmentioning

confidence: 99%

“…These abnormalities in glucose homeostasis in chronic alcoholics are proba bly effected by several opposing factors. In a previous study we found that alcoholic sub jects without liver damage and in early absti nence failed to handle normally a glucose load, showing also a low peripheral insulin response; both abnormalities were corrected after an ethanol infusion [4].…”

Section: Introductionmentioning

confidence: 99%

Glucose Turnover Rate and Peripheral Insulin Sensitivity in Alcoholic Patients without Liver Damage

Bunout¹,

Petermann²,

Bravo³

et al. 1989

Ann Nutr Metab

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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.

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

Cited by 15 publications

References 25 publications

Changes in Microsomal Activity in Alcoholism and Obesity

Changes in Microsomal Activity in Alcoholism and Obesity

Alcohol consumption and impaired glycoregulation results in a population of 6665 salaried employees

Glucose Turnover Rate and Peripheral Insulin Sensitivity in Alcoholic Patients without Liver Damage

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