How different is the dietary pattern in non-alcoholic steatohepatitis patients?

Cortez‐Pinto, Helena; Jesus, L.; Barros, Henrique; Lopes, Carla; Moura, Miguel Carneiro de; Camilo, M.

doi:10.1016/j.clnu.2006.01.027

Cited by 228 publications

(202 citation statements)

References 33 publications

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“…This is consistent with the ability of polyunsaturated fatty acids to suppress expression of both sterol regulatory element-binding protein 1c (51,52) and SCD1 (53) and activate genes involved in hepatic fatty acid oxidation (31). Subjects with NAFLD have been shown to consume less polyunsaturated fat than normal control subjects in some (54,55) but not all (56) cross-sectional studies.…”

Section: Discussionsupporting

confidence: 67%

Hepatic Stearoyl-CoA Desaturase (SCD)-1 Activity and Diacylglycerol but Not Ceramide Concentrations Are Increased in the Nonalcoholic Human Fatty Liver

et al. 2009

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OBJECTIVE-To determine whether 1) hepatic ceramide and diacylglycerol concentrations, 2) SCD1 activity, and 3) hepatic lipogenic index are increased in the human nonalcoholic fatty liver.RESEARCH DESIGN AND METHODS-We studied 16 subjects with (n ϭ 8) and without (n ϭ 8) histologically determined nonalcoholic fatty liver (NAFL ϩ and NAFL Ϫ ) matched for age, sex, and BMI. Hepatic concentrations of lipids and fatty acids were quantitated using ultra-performance liquid chromatography coupled to mass spectrometry and gas chromatography. RESULTS-The absolute (nmol/mg) hepatic concentrations of diacylglycerols but not ceramides were increased in the NAFL ϩ group compared with the NAFL Ϫ group. The livers of the NAFL ϩ group contained proportionally less long-chain polyunsaturated fatty acids as compared with the NAFL Ϫ group. Liver fat percent was positively related to hepatic stearoyl-CoA desaturase 1 (SCD1) activity index (r ϭ 0.70, P ϭ 0.003) and the hepatic lipogenic index (r ϭ 0.54, P ϭ 0.030). Hepatic SCD1 activity index was positively related to the concentrations of diacylglycerols (r ϭ 0.71, P ϭ 0.002) but not ceramides (r ϭ 0.07, NS).CONCLUSIONS-We conclude that diacylglycerols but not ceramides are increased in NAFL. The human fatty liver is also characterized by depletion of long polyunsaturated fatty acids in the liver and increases in hepatic SCD1 and lipogenic activities. Diabetes 58: [203][204][205][206][207][208] 2009 N onalcoholic fatty liver disease (NAFLD) is characterized by lipid accumulation in the liver (Ն10% of liver weight), which cannot be attributed to alcohol consumption or any other liver disease (1). NAFLD covers a range from simple nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH) and fibrosis (1). The fatty liver is resistant to the action of insulin to inhibit hepatic glucose (2,3) and VLDL (4) production, resulting in hyperglycemia and hypertriglyceridemia. The mechanisms underlying insulin resistance in human NAFLD are unclear. While triacylglycerols themselves are inert, lipid intermediates may act as important regulators of both oxidative stress (5) and insulin signaling (6). In vitro studies as well as studies in animals suggest that diacylglycerols, which are immediate precursors of triacylglycerols (7), can induce insulin resistance by activating specific isoforms of protein kinase C (PKC) (8,9). The concentrations of diacylglycerols have recently been shown to be increased in human NAFLD compared with subjects with normal liver histology (10). Ceramides are another class of reactive lipids that mediate saturated fat-induced insulin resistance (6). There are no data comparing ceramide and diacylglycerol concentrations in the human liver or relating them to hepatic fat content.Sources of hepatic lipids include dietary chylomicron remnants, free fatty acids released from either adipose tissue triacylglycerols or chylomicrons hydrolyzed at a rate in excess of what can be taken up by tissues (spillover), and de novo lipogenesis (11). Increased lipolysis is a...

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Section: Discussionsupporting

confidence: 67%

Hepatic Stearoyl-CoA Desaturase (SCD)-1 Activity and Diacylglycerol but Not Ceramide Concentrations Are Increased in the Nonalcoholic Human Fatty Liver

et al. 2009

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“…In contrast to these results, previous studies have reported various patterns showing excessive consumption of either mainly carbohydrates or rather mainly fat as being associated with the development of NAFLD and to its severity. [8,9] Dietary patterns of the NAFLD patients in our study varied to a great degree, consistent with the variation of published NAFLD-related diets. We found an energy-dense diet with relatively high amounts of protein and glucose, but poor in fiber and minerals to be associated with NAFLD.…”

Section: Discussionsupporting

confidence: 86%

“…For example, NAFLD patients have been described to consume a fat-rich diet with low amounts of carbohydrates or an energy-dense protein-and carbohydrate-rich diet with high amounts of glucose, fructose, and sucrose. [8,9] Furthermore, high fructose consumption was identified as a major risk factor for the development and severity of NAFLD. [10,11] There is, however, consensus that a weight reduction of at least 7% achieved through calorie restriction through low fat diet [12,13] or Mediterranean diet [14] and increased physical activity is effective in the treatment of overweight NASH patients.…”

Section: Introductionmentioning

confidence: 99%

Non-Alcoholic Fatty Liver Disease is Associated with an Excessive Calorie intake Rather than a Distinctive Dietary Pattern

Wehmeyer¹,

Jagemann²,

Zyriax³

et al. 2016

Journal of Hepatology

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“…In cross-sectional studies, subjects with NAFLD have been shown to consume more fat, especially saturated fat [53] and [54] than subjects without NAFLD. Also, the intake of polyunsaturated fat has been shown to be lower in subjects with NAFLD than in those without in some [54] and [55] but not all [56] studies. Subjects with NAFLD tend to consume products with high glycemic index [57] and more soft drinks [56] as compared to subjects with a normal liver fat content.…”

Section: Causes Of Hepatic Fat Accumulation 251 Acquired Factorsmentioning

confidence: 99%

From the metabolic syndrome to NAFLD or vice versa?

Vanni

Bugianesi

Kotronen

et al. 2010

Digestive and Liver Disease

437

351

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The metabolic syndrome encompasses metabolic and cardiovascular risk factors which predict diabetes and cardiovascular disease (CVD) better than any of its individual components. Nonalcoholic fatty liver disease (NAFLD) comprises a disease spectrum which includes variable degrees of simple steatosis (nonalcoholic fatty liver, NAFL), nonalcoholic steatohepatitis (NASH) and cirrhosis. NAFLD is the hepatic manifestation of the metabolic syndrome, with insulin resistance as the main pathogenetic mechanism. Recent data indicate that hyperinsulinemia is probably the consequence rather than cause of NAFLD and NAFLD can be considered an independent predictor of cardiovascular disease. Serum free fatty acids derived from lipolysis of visceral adipose tissue are the main source of hepatic triglycerides in NAFLD, although hepatic de novo lipogenesis and dietary fat supply contribute to the pathogenesis of NAFLD. Approximately 10-25% NAFLD patients develop NASH, the evolutive form of hepatic steatosis. Presumably in a genetically predisposed environment, this increased lipid overload overwhelms the oxidative capacity and reactive oxygen species are generated, leading to lipid peroxidation, cytokine induction, chemoattraction of inflammatory cells, hepatic stellate cell activation and finally fibrogenesis with extracellular matrix deposition. No currently available therapies for NAFLD and NASH exist. Recently nuclear receptors have emerged as key regulators of lipid and carbohydrate metabolism for which specific pharmacological ligands are available, making them attractive therapeutic targets for NAFLD and NASH.Abbreviations ALT, alanine aminotransferase; BMI, body mass index; CVD, cardiovascular disease; FFA, free fatty acids; HDL, high density lipoprotein; 1H-MRS, proton magnetic resonance spectroscopy; IDF, International Diabetes Federation; LDL, low density lipoprotein; NAFLD, nonalcoholic fatty liver disease; SNP, single nucleotide polymorphism; VLDL, very low density lipoprotein IntroductionThe metabolic syndrome is a cluster of metabolic and cardiovascular risk factors which predicts diabetes and cardiovascular disease (CVD) better than any of its individual components [1]. The latest definition of the metabolic syndrome by International Diabetes Federation (IDF) includes abdominal obesity defined by increased waist circumference (≥94 cm in men and ≥80 cm in women) and two or more of the following features: elevated blood pressure, fasting glucose or triglyceride concentrations, or low HDL cholesterol [1]. The term nonalcoholic fatty liver disease (NAFLD) comprises a disease spectrum which includes variable degrees of simple steatosis (nonalcoholic fatty liver, NAFL), nonalcoholic steatohepatitis (NASH) and cirrhosis [2] and [3]. NAFLD can be considered the hepatic manifestation of the metabolic syndrome. Simple steatosis is benign, whereas NASH is defined by the presence of hepatocyte injury, inflammation and/or fibrosis which can lead to cirrhosis, liver failure and hepatocellular carcinoma. In contrast to t...

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How different is the dietary pattern in non-alcoholic steatohepatitis patients?

Cited by 228 publications

References 33 publications

Hepatic Stearoyl-CoA Desaturase (SCD)-1 Activity and Diacylglycerol but Not Ceramide Concentrations Are Increased in the Nonalcoholic Human Fatty Liver

Hepatic Stearoyl-CoA Desaturase (SCD)-1 Activity and Diacylglycerol but Not Ceramide Concentrations Are Increased in the Nonalcoholic Human Fatty Liver

Non-Alcoholic Fatty Liver Disease is Associated with an Excessive Calorie intake Rather than a Distinctive Dietary Pattern

From the metabolic syndrome to NAFLD or vice versa?

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