Effects of light-to-moderate alcohol consumption on steatosis and steatohepatitis in severely obese patients

Cotrim, Helma Pinchemel; Freitas, Luiz Antônio de; Alves, Erivaldo; Almeida, Aglaya Oliveira Lima Cordeiro de; May, D.; Caldwell, Stephen H.

doi:10.1097/meg.0b013e328328f3ec

Cited by 69 publications

(65 citation statements)

References 20 publications

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“…It was observed that in a well-characterized population with biopsy-proven NAFLD, modest alcohol consumption was associated with decreased prevalence of steatohepatitis (48,49). Furthermore, it was reported that light-to-moderate alcohol consumption protects against insulin resistance in severely obese patients with steatosis and steatohepatitis (50). The above studies suggest that moderate alcohol consumption <20 g/d is not harmful and may be beneficial against several complications.…”

Section: Discussionmentioning

confidence: 92%

Binge Alcohol Consumption Aggravates Oxidative Stress and Promotes Pathogenesis of NASH from Obesity-Induced Simple Steatosis

Minato

Tsutsumi

Tsuchishima

et al. 2014

Mol Med

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The pathogenesis of nonalcoholic steatohepatitis (NASH) is a two-stage process in which steatosis is the "first hit" and an unknown "second hit." We hypothesized that "a binge" could be a "second hit" to develop NASH from obesity-induced simple steatosis. Thirty-week-old male Otsuka Long-Evans Tokushima fatty (OLETF) rats were administered 10 mL of 10% ethanol orally for 5, 3, 2, and 1 d/wk for 3 consecutive weeks. As control, male Otsuka Long-Evans Tokushima (OLET) rats were administered the same amount of alcohol. Various biochemical parameters of obesity, steatosis and NASH were monitored in serum and liver specimens in untreated and ethanol-treated rats. The liver sections were evaluated for histopathological alterations of NASH and stained for cytochrome P-4502E1 (CYP2E1) and 4-hydroxy-nonenal (4-HNE). Simple steatosis, hyperinsulinemia, hyperglycemia, insulin resistance, hypertriglycemia and marked increases in hepatic CYP2E1 and 4-HNE were present in 30-wk-old untreated OLETF rats. Massive steatohepatitis with hepatocyte ballooning was observed in the livers of all OLETF rats treated with ethanol. Serum and hepatic triglyceride levels as well as tumor necrosis factor (TNF)-α mRNA were markedly increased in all ethanol-treated OLETF rats. Staining for CYP2E1 and 4-NHE demonstrated marked increases in the hepatic tissue of all the groups of OLETF rats treated with ethanol compared with OLET rats. Our data demonstrated that "a binge" serves as a "second hit" for development of NASH from obesity-induced simple steatosis through aggravation of oxidative stress. The enhanced levels of CYP2E1 and increased oxidative stress in obesity play a significant role in this process.

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Section: Discussionmentioning

confidence: 92%

Binge Alcohol Consumption Aggravates Oxidative Stress and Promotes Pathogenesis of NASH from Obesity-Induced Simple Steatosis

Minato

Tsutsumi

Tsuchishima

et al. 2014

Mol Med

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“…By contrast, modest alcohol intake and obesity seem to have additive effect on liver disease progression, and in a large prospective study any degree of alcohol consumption increased by 3.6-fold the risk of hepatocellular carcinoma in NASH-related cirrhosis [122,123].…”

Section: Implications For Future Researchmentioning

confidence: 94%

Impact of current treatments on liver disease, glucose metabolism and cardiovascular risk in non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of randomised trials

et al. 2012

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Aims/hypothesis Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum ranging from simple steatosis to non-alcoholic steatohepatitis (NASH): NAFLD causes an increased risk of cardiovascular disease, diabetes and liverrelated complications (the latter confined to NASH). The effect of proposed treatments on liver disease, glucose metabolism and cardiovascular risk in NAFLD is unknown. We reviewed the evidence for the management of liver disease and cardiometabolic risk in NAFLD. Methods Publications through November 2011 were systematically reviewed by two authors. Outcomes evaluated though standard methods were: histological/radiological/biochemical features of NAFLD, variables of glucose metabolism and cardiovascular risk factors. Seventy-eight randomised trials were included (38 in NASH, 40 in NAFLD): 41% assessed post-treatment histology, 71% assessed glucose metabolism and 88% assessed cardiovascular risk factors. Lifestyle intervention, thiazolidinediones, metformin and antioxidants were most extensively evaluated. Results Lifestyle-induced weight loss was safe and improved cardio-metabolic risk profile; a weight loss ≥7% improved histological disease activity, but was achieved by <50%

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“…The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines heavy or at-risk drinking as more than 4 drinks on any day or more than 14 drinks per week in men or more than 3 drinks on any day or 7 drinks per week in women. 146 Several recent cross-sectional studies [147][148][149][150][151][152][153] suggest a beneficial effect of light alcohol consumption (on average less than one drink per day) on the presence (defined either biochemically or by imaging) and severity of NAFLD. There are no studies reporting the effect of ongoing alcohol consumption on disease severity or natural history of NAFLD or NASH.…”

Section: Bariatric Surgerymentioning

confidence: 99%

The diagnosis and management of non-alcoholic fatty liver disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association

et al. 2012

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Effects of light-to-moderate alcohol consumption on steatosis and steatohepatitis in severely obese patients

Abstract: The results suggest that LMAC may have a protection effect against IR in severely obese patients. However, it had no impact on the severity of activity and stage of liver disease.

Cited by 69 publications

References 20 publications

Binge Alcohol Consumption Aggravates Oxidative Stress and Promotes Pathogenesis of NASH from Obesity-Induced Simple Steatosis

Binge Alcohol Consumption Aggravates Oxidative Stress and Promotes Pathogenesis of NASH from Obesity-Induced Simple Steatosis

Impact of current treatments on liver disease, glucose metabolism and cardiovascular risk in non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of randomised trials

The diagnosis and management of non-alcoholic fatty liver disease: Practice Guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association

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