Nonalcoholic fatty liver disease

Younossi, Zobair M.

doi:10.1007/s11894-999-0088-1

Cited by 30 publications

(28 citation statements)

References 33 publications

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“…30, No. 4,1999 HIC than that observed. The maximum HII in our patient population was only 1.36 µmol/g/yr.…”

Section: Discussioncontrasting

confidence: 47%

“…Unlike the patients reported in previous studies, 6,[15][16] our patients were seen at a referral center without a special interest in disorders of iron storage. Given the relatively high prevalence of NAFL (3% and 20% in lean and obese individuals, respectively) 4,8 and C282Y mutation (6.7%) in the general population, 16,19 the co-occurrence of these 2 conditions is possible. However, the 3-to 5-fold higher prevalence of the HFE mutation seen in these previous studies in NAFL patients (21%-31%) 15,16 is most likely the reflection of this referral or ascertainment bias.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4][5][6][7] Risk factors associated with NASH include obesity, type II diabetes, and hyperlipidemia. [8][9] In a more recent study, NASH was described in patients who lacked these risk factors.…”

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confidence: 99%

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Hepatic iron and nonalcoholic fatty liver disease

et al. 1999

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Increased iron is suspected to enhance hepatic injury associated with nonalcoholic fatty liver disease (NAFL).Nonalcoholic steatohepatitis (NASH) is a form of nonalcoholic fatty liver (NAFL) with the potential for progression into cirrhosis. 1-7 Risk factors associated with NASH include obesity, type II diabetes, and hyperlipidemia. [8][9] In a more recent study, NASH was described in patients who lacked these risk factors. 6 Although fatty liver alone seems to be benign, NASH can have a progressive course.

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“…30, No. 4,1999 HIC than that observed. The maximum HII in our patient population was only 1.36 µmol/g/yr.…”

Section: Discussioncontrasting

confidence: 47%

Section: Discussionmentioning

confidence: 99%

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Hepatic iron and nonalcoholic fatty liver disease

et al. 1999

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“…These entities are similar to alcoholic liver diseases in the absence of significant alcohol abuse (40). Simple hepatic steatosis and hepatic steatosis with nonspecific inflammation are believed to be generally benign conditions, whereas NASH can progress to cirrhosis, leading to liver failure as well as to hepatocellular carcinoma (41,42).…”

Section: Discussionmentioning

confidence: 99%

Fatty liver index in polycystic ovary syndrome

Lerchbaum¹,

Gruber²,

Schwetz³

et al. 2011

European Journal of Endocrinology

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Introduction: Women with polycystic ovary syndrome (PCOS) frequently suffer from metabolic disturbances and might be affected by hepatic steatosis. The fatty liver index (FLI) was developed as a simple and accurate predictor of hepatic steatosis. We aimed to analyze the association of FLI with endocrine and metabolic parameters in a cohort of PCOS and control women. Methods: FLI was calculated using body mass index (BMI), waist circumference, triglycerides, and gamma-glutamyl transferase in 611 PCOS and 139 BMI-matched control women within the same age range. Elevated FLI was defined as O60. Metabolic, endocrine, and anthropometric measurements and oral glucose tolerance tests were performed. Results: PCOS women had significantly higher FLI levels than control women in age-adjusted analyses (11.4 (4.3-48.8) and 8.8 (3.9-35.0), respectively, PZ0.001), whereas fibrosis indices were similar (aspartate amino transferase-to-platelet ratio index) or lower (FIB-4) respectively. In binary logistic regression analysis adjusted for age, odds ratio (OR) for elevated FLI was 2.52 (1.31-4.85), PZ0.006, for PCOS women when compared with controls. PCOS women with high FLI levels had an adverse anthropometric, metabolic, and endocrine risk profile. The prevalence of elevated FLI was 88.7% in PCOS women with metabolic syndrome (MS) and 11.3% in PCOS women without MS (P!0.001). In control women, elevated FLI was present in 66.7% of women with MS and 30.8% of women without MS. Conclusion: High FLI levels are a common finding in obese PCOS women and are closely linked to MS. FLI calculation might be a useful tool for identifying PCOS patients at high risk for metabolic and hepatic disturbances.

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“…In general, an intake of <140 g ethanol per week or 20 g ethanol/day is acceptable for the diagnosis as NAFLD (3,4).…”

Section: Introductionmentioning

confidence: 99%

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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Nonalcoholic fatty liver disease

Cited by 30 publications

References 33 publications

Hepatic iron and nonalcoholic fatty liver disease

Hepatic iron and nonalcoholic fatty liver disease

Fatty liver index in polycystic ovary syndrome

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

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