Metabolic and nutritional considerations in nonalcoholic fatty liver

Fong, Derek G.; Nehra, Vandana; Lindor, Keith D.; Buchman, Alan L.

doi:10.1053/jhep.2000.8978

Cited by 155 publications

(121 citation statements)

References 128 publications

(173 reference statements)

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“…[8][9][10][11] Several clinical factors (e.g., the presence of insulin-resistance syndrome) may promote these events, but other potentially important factors (e.g., predisposing genes and environmental factors) remain undefined. 4,13,14,16,[35][36][37][38][39] This study examined differential gene and protein expression profiles of patients within the NAFLD spectrum for whom extensive clinical and histological data were available. This approach has led to the development of a database integrating gene expression, protein expression, and clinical and biochemical data for a large cohort of patients with biopsy-proven NAFLD.…”

Section: Discussionmentioning

confidence: 99%

“…2,4,5 Both endogenous and exogenous factors may influence differential progression of these liver diseases. [11][12][13][14][15][16] For example, environmental factors contributing to oxidative stress may compound hepatic injury in some patients, whereas genetic factors may be more important in others. [17][18][19][20][21] Furthermore, an interaction among these factors may influence the disease course and tip the balance in favor of progression.…”

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confidence: 99%

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A genomic and proteomic study of the spectrum of nonalcoholic fatty liver disease

et al. 2005

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Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, and some of its forms are progressive. This study describes the profiling of hepatic gene expression and serum protein content in patients with different subtypes of NAFLD. Liver biopsy specimens from 98 bariatric surgery patients were classified as normal, steatosis alone, steatosis with nonspecific inflammation, and nonalcoholic steatohepatitis (NASH). Microarray hybridizations were performed in triplicate and the microarray expression levels of a selected group of genes were confirmed using real-time quantitative reverse-transcriptase polymerase chain reaction. Serum protein profiles of the same patients were determined by SELDI-TOF mass spectrometry. Of 98 obese patients, 91 were diagnosed with NAFLD (12 steatosis alone, 52 steatosis with nonspecific inflammation, and 27 NASH), and 7 patients without NAFLD served as obese controls. Each group of NAFLD patients was compared with the obese controls, and 22 genes with more than twofold differences in expression levels were revealed. Proteomics analyses were performed for the same group comparisons and revealed twelve significantly different protein peaks. In conclusion, this genomic/proteomic analysis suggests differential expression of several genes and protein peaks in patients within and across the forms of NAFLD. These findings may help clarify the pathogenesis of NAFLD and identify potential targets for therapeutic intervention. (HEPATOLOGY 2005;42:665-674.)

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

A genomic and proteomic study of the spectrum of nonalcoholic fatty liver disease

et al. 2005

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“…30,31 The increased amount of mesenteric adipose tissue is expected to result in increased free fatty acid flux from portal veins to liver. 32,33 The increased free fatty acid production may lead to reduced fat oxidation and ectopic fat deposition in liver. 30,31 Besides, visceral adipocytes are known to produce a large number of cytokines and vasoactive peptides such as interleukin-6, angiotensin II, plasminogen activator inhibitor-I, which can also be related to the fatty liver and increase of cardiovascular risk.…”

Section: Discussionmentioning

confidence: 99%

Mesenteric fat thickness as an independent determinant of fatty liver

Liu

Chan

et al. 2006

Int J Obes

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Objective: Mesenteric fat is drained by the portal circulation and has been suggested to be a key component in obesity-related health risk, notably the metabolic syndrome. There are increasing epidemiological and experimental data showing that fatty liver is another component of this multifaceted syndrome. Given their intimate anatomical and physiological relationships, we hypothesized that mesenteric fat thickness may be independently associated with the risk of fatty liver. To test this hypothesis, we examined the predictive role of various fat deposits including mesenteric fat thickness, and various metabolic variables on the risk of fatty liver. Subjects and methods: A total of 291 Chinese subjects (134 men and 157 women with a mean BMI of 23.7 kg/m 2 , range: 16.5-33.4 kg/m 2 ) underwent ultrasound examination for measurement of mesenteric, subcutaneous and preperitoneal fat thickness, and for diagnosis of fatty liver. Body mass index, waist circumference, and waist-hip ratio were recorded. Blood pressure was measured. Fasting plasma glucose, insulin resistance, high-density lipoprotein cholesterol (HDL-C), triglycerides, low-density lipoprotein cholesterol (LDL-C), liver enzymes were determined by common methods. Results: The subjects with fatty liver had greater abdominal fat thickness and higher anthropometric indexes than those without fatty liver. The subjects with fatty liver also showed higher blood pressure, worse lipid and glycaemic profile compared with those without fatty liver. Using multiple logistic regression analysis, mesenteric fat thickness was a risk factor of fatty liver, independent of body mass index, age, sex, insulin resistance, fasting plasma glucose, lipid and blood pressure. The odds ratio was 1.5 (95% confidence interval: 1.27-1.77) for every 1 mm increase in the mesenteric fat thickness. Measurement of preperitoneal and subcutaneous fat deposits did not show significant associations with fatty liver. Conclusion: Mesenteric fat thickness measured on ultrasound is an independent determinant of fatty liver.

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“…Effectively, the phenomenon of insulin resistance has been well described in obese individuals and it appears that a loss of insulin sensitivity at the level of the adipocyte or the increase in adipocyte mass may account for the impaired antilipolytic action of insulin in the face of hyperinsulinemia. 14 In this situation, massive lipolysis results in marked mobilization of free fatty acids, which are taken up by the liver. Free fatty acids per se are potentially cytotoxic, causing mitochondrial swelling, increased liposomal fragility, depression of enzyme activity, and impairment of membrane integrity.…”

Section: Discussionmentioning

confidence: 99%

Risk factors of fibrosis in alcohol-induced liver disease

et al. 2002

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In patients with nonalcoholic steatohepatitis (NASH), age, obesity, and diabetes mellitus are independent predictors of the degree of fibrosis. The relative risk for fibrosis adjusted for sex was also associated with increasing grade of Perls stain. The aim of this study was to determine whether the risk factors for fibrosis described in NASH are also risk factors in alcohol-induced liver disease. A total of 268 alcoholic patients with negative hepatitis B virus and hepatitis C virus serology underwent liver biopsy. Fibrosis was assessed semiquantitatively by a score fluctuating between 0 to 8. Liver iron overload was assessed by Perls staining and graded in 4 classes. We have used multivariate regression with partial correlation analysis to assess the variability of fibrosis score according to the value of 7 variables: sex, age, body mass index (BMI) in the past year before the hospitalization when the patient was asymptomatic, daily alcohol intake over the past 5 years, total duration of alcohol abuse, Perls grade, and blood glucose level. In the multivariate regression, fibrosis score was positively correlated with age (P ‫؍‬ .001), BMI (P ‫؍‬ .002), female sex (P < .05), Perls grade (P < .05), and blood glucose level (P < .05). Twenty percent of the variability of fibrosis score was explained by the 7 variables. In conclusion, after adjustment for daily alcohol intake and total duration of alcohol abuse, BMI, Perls grade, and blood glucose are also independent risk factors for fibrosis in alcohol-induced liver disease, raising therapeutic implications for the management of these patients. (HEPATOLOGY 2002;35:635-638.)

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Metabolic and nutritional considerations in nonalcoholic fatty liver

Cited by 155 publications

References 128 publications

A genomic and proteomic study of the spectrum of nonalcoholic fatty liver disease

A genomic and proteomic study of the spectrum of nonalcoholic fatty liver disease

Mesenteric fat thickness as an independent determinant of fatty liver

Risk factors of fibrosis in alcohol-induced liver disease

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