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Non-alcoholic fatty liver disease (NAFLD) represents an excessive fat accumulation within the liver, usually associated with excess body weight. A liver biopsy is the gold standard for diagnosis, but it is inapplicable in population-based studies. In large populations, non-invasive methods could be used, which may also serve to identify potential protective factors. We aimed to (a) estimate NAFLD prevalence in the adult population in Chile by using non-invasive methods and (b) determine the association between the presence of NAFLD and lifestyle habits. The National Health Survey of Chile 2016–2017 was analysed. We included individuals aged 21–75 years, without infectious diseases nor risky alcohol consumption. NAFLD was detected by either fatty liver index (FLI; considers circulating TAG, circulating γ-glutamyl-transferase, BMI and waist circumference), lipid accumulation product (LAP; considers sex, circulating TAG and waist circumference) or their combination. Lifestyle habits were determined by questionnaires. We included 2774 participants, representative of 10 599 094 (9 831 644, 11 366 544) adults in Chile. NAFLD prevalence (95 % CI) was 39·4 % (36·2, 42·8) by FLI, 27·2 % (24·2, 30·4) by LAP and 23·5 % (20·7, 26·5) by their combination. The prevalence progressively increased with increasing BMI. Of note, less smoking and more moderate-vigorous physical activity and whole-grain consumption were associated with lower odds of having NAFLD, independently of BMI. At least one out of four adults in Chile is afflicted with NAFLD. Health promotion strategies focused on controlling excess body weight and promoting specific lifestyle habits are urgently required.

Advanced glycation end products (AGEs) may be associated with nonalcoholic fatty liver disease (NAFLD) from stimulation of oxidative stress, inflammation, and fibrosis. We hypothesized that patients with NAFLD would have a lower concentration of soluble AGEs receptor and higher quantity of serum and liver AGEs and an increase in hepatic smooth muscle actin alpha (α-SMA) and transforming growth factor beta 1 (TGF-β1) compared with a control group. We compared the presence of hepatic and serum AGEs, AGE soluble receptor (sRAGE), and markers associated with hepatic damage between NAFLD patients and controls without disease. Histological characteristics, plasma biochemical parameters, serum AGEs, serum receptor sRAGE, and liver proteins (α-SMA, TGF-β1, AGEs, immunohistochemistry) were assessed in participants aged 18 to 65 years, with NAFLD (simple steatosis [SS]: n = 7; steatohepatitis [NASH]: n = 15) and controls (n = 11). NASH patients presented higher glycated hemoglobin levels (%) (5.7; 5.4-6.3) compared with SS (5.4; 5.2-5.7) and controls (5.4; 5.3-5.5). The NAFLD activity score (NAS) for NASH patients was 4.9 ± 1.3; for SS patients, 2.0 ± 1.0. NASH patients showed higher hepatic AGEs, TGF-β1, and α-SMA compared with SS and control groups. The NAS score indicates that patients with 5 to 8 had higher hepatic AGEs, TGF-β1, and α-SMA compared with a NAS of 1 to 4 and 0. For α-SMA, a NAS of 1 to 4 was higher than NAS 0. No difference was found in serum AGEs and sRAGE between groups. Higher hepatic AGEs, TGF-β1, and α-SMA were observed with increasing disease severity (according to NAS); therefore, endogenous liver AGEs may participate in hepatic damage progression.

Non-alcoholic fatty liver disease (NAFLD) encompasses a wide spectrum of hepatic pathologies ranging from simple steatosis (SS) to hepatocellular carcinoma. Intestinal microbiota (IM) is composed of trillions of microorganisms existing in the gut. It has 150 times more genes than the host. Changes in the composition and function of the IM are associated with different diseases, including NAFLD. In this condition, IM could have a pathogenic role through different mechanisms such as energy salvaging from food, an inflammatory stimulus, a modulation of the innate immune system, regulation of bile acid turnover, alteration of choline metabolism and increasing endogenous ethanol levels. This review is an update on the role of the intestinal microbiota in NAFLD and the possible mechanisms involved.

An altered retinol metabolism might play a role in the development of nonalcoholic fatty liver disease (NAFLD). Tocopherols (TF) modulate metabolic pathways and have been proposed as a complementary treatment of obesity-induced metabolic alterations. Moreover, there is evidence suggesting that TF may modulate retinol metabolism. The aim of this study was to evaluate whether the dietary supplementation of α- and γ-TF modulates the expression of hepatic retinaldehyde dehydrogenases, RALDH1, RALDH2, and RALDH3 (involved in retinol metabolism) and, lipogenic factors sterol regulatory element binding protein-1c (SREBP-1c) and cluster differentiation 36 (CD36) in an animal model of diet-induced NAFLD.Male C57BL/6J mice were divided into four groups: a control diet (CD) group (10% fat, 20% protein, 70% carbohydrates); a CD + TF group (α-tocopherol: 0.7 mg·kg·dTF supplementation in HFD-fed mice decreased the presence of lipid vesicles (90%) and total lipid content (75%) and downregulated the expression of RALDH1, RALDH3, SREBP-1c, and CD36.The present study demonstrated that α- and γ-TF (1:5 ratio) might play a role in modulating retinol metabolism in the prevention of NAFLD induced by a HFD.

Objective The aim of this study was to determine whether hepatic gene expression related to hepatocellular carcinoma (HCC) is associated with disease severity and modifiable lifestyle factors in non-alcoholic fatty liver disease (NAFLD). Methods In a cross-sectional study, the associations between hepatic gene expression and liver histology, insulin resistance, anthropometrics, diet, and physical activity were assessed in patients with non-alcoholic steatohepatitis (NASH; n = 19) or simple steatosis (SS; n = 20). In a group of patients with NASH, we then conducted a 1-y, single-arm, pilot study using ω-3 polyunsaturated fatty acid (PUFA) supplementation to determine whether changes in hepatic PUFA content would have a modulating effect on hepatic gene expression and would affect liver histology. Results In the cross-sectional study, histological features of disease severity correlated with AKR1B10, ANXA2, PEG10, SPP1, STMN2, MT1A, and MT1B in NASH and with EEF1A2, PEG10, and SPP1 in SS. In addition, PEG10, SPP1, ANXA2, and STMN2 expression correlated positively with insulin resistance in NASH. SPP1 and UBD correlated strongly with body mass index in SS. Associations between ENPP2, AKR1B10, SPP1, UBD, and waist circumference depended on sex and diagnosis. Several genes correlated with protein, fat, or carbohydrate intake. PEG10 correlated positively with physical activity in NASH and inversely with plasma vitamin C in both groups. Despite increased erythrocyte and hepatic ω-3 PUFA, supplementation did not alter hepatic gene expression and liver histology. Conclusions HCC-related gene expression was associated with liver histology, body mass index, waist circumference, diet, and physical activity but was not affected by ω-3 PUFA supplementation.

The regulation of food intake and body weight involves two interacting systems: (a) The homeostatic system (including biological regulators of hunger and satiety) and (b) the non-homeostatic system, (involving concepts of food reinforcement and food addiction). Studies have established a strong genetic component in eating behavior and obesity. The TaqI A1 polymorphism (rs1800497) has previously been associated with eating behavior, diminished dopamine D2 receptor (DRD2) density, higher body mass, and food reinforcement, but relations to food addiction remain unclear. To evaluate the association between the polymorphism rs1800497 with eating behavior, food reinforcement and food addiction in Chilean adults. This cross-sectional study recruited a convenience sample of 97 obese, 25 overweight and 99 normal-weight adults (18–35 years). Anthropometric measurements were performed by standard procedures. Eating behavior was assessed using the: Yale Food Addiction Scale (YFAS), the Three Factor Eating Behavior Questionnaire and the Food Reinforcement Value Questionnaire (FRVQ). The DRD2 genotype (rs1800497) was determined by taqman assays. Twenty-two percentage of the participants met the criteria for food addiction. Food addiction was higher in women than men (26% vs 10.7%) and in obese compared to non-obese (40% vs 6%). There was no relationship between food addiction and DRD2 genotype. However when stratified by sex and nutritional status, obese female carriers of the A1 allele reported greater scores on emotional eating and snack food reinforcement compared to non-carriers. The DRD2 polymorphism is associated with some hedonic aspects of eating behavior, namely food reinforcement and emotional eating but not food addiction, and this association may be moderated by sex and obesity status, with obese women who are carriers of this genetic variant at higher risk. Level V: evidence obtained from a cross-sectional descriptive study.

Non-alcoholic fatty liver disease (NAFLD) encompasses a wide spectrum of hepatic pathologies ranging from simple steatosis (SS) to hepatocellular carcinoma. Intestinal microbiota (IM) is composed of trillions of microorganisms existing in the gut. It has 150 times more genes than the host. Changes in the composition and function of the IM are associated with different diseases, including NAFLD. In this condition, IM could have a pathogenic role through different mechanisms such as energy salvaging from food, an inflammatory stimulus, a modulation of the innate immune system, regulation of bile acid turnover, alteration of choline metabolism and increasing endogenous ethanol levels. This review is an update on the role of the intestinal microbiota in NAFLD and the possible mechanisms involved.

We previously reported a lower fecal abundance of Ruminococcus spp., Faecalibacterium prausnitzii , and Coprococcus spp. in nonalcoholic fatty liver disease (NAFLD). In this article, we assess the associations between hepatic gene expression, the specific taxa, and bacterial pathways.The relationships between hepatic genes that were differentially expressed in patients with NAFLD vs healthy controls (HC) and the abundance of these specific taxa were studied. Inferred functional metagenomic analysis using Piphillin was also performed to investigate associations with bacterial pathways.Fifteen patients with NAFLD and 6 HC participated. Of 728 hepatic genes examined, 176 correlated with the abundance of Ruminococcus spp., 138 with F. prausnitzii , and 92 with Coprococcus spp. For Ruminococcus spp., genes were enriched in gene ontology (GO) terms related to apoptotic process, response to external and cytokine stimuli, and regulation of signaling. Several genes related to the Kyoto Encyclopedia of Genes and Genomes pathway insulin resistance were correlated with F. prausnitzii . The hepatic genes associated with F. prausnitzii were enriched in GO terms related to cellular response to different stimuli, apoptotic process, and regulation of metabolic pathways. For Coprococcus spp., only the GO term response to external stimulus was enriched. There was a distinct pattern of associations between hepatic genes and bacterial taxa in NAFLD vs HC. For bacterial pathways, 65 and 18 hepatic genes correlated with bacterial metabolic functions in NAFLD and HC, respectively.Hepatic gene expression related to insulin resistance, inflammation, external stimuli, and apoptosis correlated with bacterial taxa. Patients with NAFLD showed a higher presence of bacterial pathways associated with lipid metabolism.

Non-alcoholic fatty liver disease (NAFLD), especially non-alcoholic steatohepatitis (NASH) is a chronic liver disease commonly associated with hepatic fibrosis. NASH patients have an increased risk for hepatocellular carcinoma (HCC). An altered retinol metabolism is one of the pathways involved in the process of hepatic fibrosis, and enzymes involved in retinol metabolism have been associated with HCC. We aimed to determine the association between plasma retinol levels and hepatic expression of genes related to retinol metabolism, as well as to assess the hepatic expression of transcription factors regulated by retinoic acid in patients with NAFLD. Cross-sectional study where hepatic gene expression (Illumina microarray) and plasma retinol levels (HPLC) were measured in 17 patients with simple steatosis (SS), 15 with NASH, and 22 living liver donors (LD) as controls. Plasma retinol levels were higher in SS (1.53 ± 0.44 μmol/L) and NASH (1.51 ± 0.56 μmol/L) compared to LD (1.21 ± 0.38 μmol/L; p

Background: High calorie foods, especially high in sugar and sodium may have an addictive potential. Experimental rats are able to develop symptoms and neurochemical changes, comparable to those observed in drug abuse, when they are exposed intermittently to sucrose. Aim: To evaluate the association between nutritional status and the prevalence of food addiction in Chilean college students. Material and Methods: Food addiction was assessed using the Yale Food Addiction Scale in 292 Chilean students aged 18-39 years (35% males). Height and weight were measured and body mass index (weight/height²) was calculated. Results: Eleven percent of participants met the criteria for food addiction. Women had a higher prevalence than men (14.4% and 4.8%, respectively). Thirty percent of individuals with a body mass index over 30 kg/m² met the criteria for food addiction. Conclusions: In these Chilean students, food addiction was more prevalent in women and a higher prevalence was observed in obese individuals.

The aim of this study was to evaluate the contribution of tocopherols present in Rosa mosqueta oil (RM) in the prevention of high-fat diet (HFD)-induced alterations.Male C57 BL/6 J mice (n = 9/group) were fed for 12 wk and divided into four groups: control (CD; 10% kcal fat, 20% kcal protein, 70% kcal carbohydrates); HFD (60% as fat, 20% kcal protein, 20% kcal carbohydrates); HFD + RM (0.01 mL/g body weight/d); and HFD + RMLiver steatosis, inflammatory, and oxidative stress parameters were significantly (P 0.05) increased in the HFD + RMThe present study suggests that α- and γ-tocopherols from RM may have an important role in the prevention of alterations induced by HFD.

Evaluation of a physical activity intervention among children with Down's syndrome Introduction: In Chile there are no studies regarding the effects of physical activity on nutritional status of children with Down Syndrome. Objective: To evaluate the impact of a 12 week physical education program on the nutritional status, aerobic capacity and muscle strength in children with Down Syndrome. Subjects and Methods: Between August and November of 2006, a group of 18 children (10 males and 8 females) with Down Syndrome, aged between 5-9 years, underwent to a physical activity program over a 12 week period. A diagnostic and fi nal evaluation of muscle strength variables (dorsal, abdominal and quadriceps) and aerobic capacity was done. Nutritional status was assessed by P/E and T/E (Fundacion Catalana), IMC, IP/T and per- centage of body fat. Results: Signifi cant differences in muscle strength, aerobic capacity, IP/T and waist cir- cumference were observed between the pre-test and post-test (p < 0.05). At the beginning of the intervention, 53% were overweight according to IMC, 26% to P/E and 68% according to IP/T; with an average percentage of body fat of 22.6%. Conclusion: Although the period of intervention was brief, a signifi cant improvement was noted in muscle strength, aerobic capacity, IP/T and waist circumference. According to our results, there is a high prevalence of overweight status and obesity in this population of children with DS in which intervention with adequate physical activity is vital. (Key words: Down syndrome, physical activity, nutritional assessment). Rev Chil Pediatr 2011; 82 (4): 311-318

Introduction: Triglyceride accumulation in the liver is an early feature in the development of nonalcoholic fatty liver disease (NAFLD) associated with human obesity, which is a multifactorial syndrome and whose underlying mechanisms are beginning to be understood. Objectives: Liver peroxisome proliferator-activated receptor-γ (PPAR-γ) mRNA expression was measured as a signaling mechanism related to steatosis in obese patients with NAFLD. Methods: Liver PPAR-γ and sterol receptor element-binding protein 1c (SREBP-1c) mRNA (real-time RT-PCR), serum total adiponectin (RIA), and high molecular weight (HMW)-adiponectin (ELISA) levels, and insulin resistance (IR) evolution (homeostasis model assessment-IR) were determined in 22 obese NAFLD patients (16 with steatosis and six with steatohepatitis) who underwent subtotal gastrectomy with gastrojejunal anastomosis in Roux-en-Y and 16 nonobese subjects who underwent laparoscopic cholecystectomy (controls). Results: Liver PPAR-γ mRNA levels were 112 and 188% higher (P < 0.05) than control values in obese patients with steatosis and steatohepatitis, respectively, who also exhibited 70 and 62% increases in those of SREBP-1c, concomitantly with IR and lower levels of serum total adiponectin and HMW-adiponectin (P < 0.05). Liver PPAR-γ expression showed positive associations with SREBP-1c mRNA levels (r = 0.86; P < 0.0001), serum insulin levels (r = 0.39; P < 0.01), and homeostasis model assessment-IR (r = 0.60; P < 0.0001), and negative correlations with total adiponectin (r = −0.37; P < 0.01) and HMW-adiponectin (r = −0.51; P < 0.001) levels in serum. Conclusions: PPAR-γ is up-regulated in the liver of obese patients with NAFLD, representing an additional reinforcing lipogenic mechanism to SREBP-1c induction in the development of hepatic steatosis.

Steatosis in obese nonalcoholic fatty liver disease (NAFLD) patients is a clinicopathological condition associated with depletion of n-3 polyunsaturated fatty acids (PUFA), a feature that may be related to PUFA desaturation. Liver Delta-6 and Delta-5 desaturase (Delta-6D and Delta-5D) activities, homeostasis model assessment of insulin resistance (HOMA(IR)), and ferric reducing ability of plasma (FRAP) were evaluated in 13 obese patients who underwent subtotal gastrectomy with gastro-jejunal anastomosis in Roux-en-Y and 15 nonobese patients who underwent laparoscopic cholecystectomy (controls). Liver Delta-6D and Delta-5D activities in obese patients were 87% and 66% lower than controls (P0.001), respectively, with a 62% diminution in the Delta-6D/Delta-5D activity ratio (P0.02). Delta-6D inversely correlated with both HOMA(IR) (r = -0.70, P0.0001) and oxidative stress assessed as the reciprocal value of FRAP (r = -0.40, P0.05). Delta-5D negatively correlated with HOMA(IR) (r = -0.48, P0.01) but not with FRAP(-1) (r = -0.13, not significant). In conclusion, liver PUFA desaturation is diminished in obese NAFLD patients, in association with underlying insulin resistance and oxidative stress, which may play a role in altering lipid metabolism favoring fatty infiltration.

The prevalence of childhood obesity has increased substantially in the recent decade as a result of the reduction in physical activity and the availability of high-fat and high-energy-density foods which the paediatric population faces daily. Although children are highly exposed to these foods, there is a wide variation in body weight, suggesting the presence of different patterns of response to an “obesogenic” environment. This wide variability from the point of view of eating behaviour involves a number of social issues (e.g., food availability, cost) as well as genuine behavioural traits such as the response to satiety, energy compensation, eating rate, responsiveness to food, food reward and dietary preferences. This article reviews the main physiological variables related to energy intake affecting eating behaviour in the paediatric population.

High calorie foods, especially high in sugar and sodium may have an addictive potential. Experimental rats are able to develop symptoms and neurochemical changes, comparable to those observed in drug abuse, when they are exposed intermittently to sucrose.To evaluate the association between nutritional status and the prevalence of food addiction in Chilean college students.Food addiction was assessed using the Yale Food Addiction Scale in 292 Chilean students aged 18-39 years (35% males). Height and weight were measured and body mass index (weight/height²) was calculated.Eleven percent of participants met the criteria for food addiction. Women had a higher prevalence than men (14.4% and 4.8%, respectively). Thirty percent of individuals with a body mass index over 30 kg/m² met the criteria for food addiction.In these Chilean students, food addiction was more prevalent in women and a higher prevalence was observed in obese individuals.

Fructose intake has increased considerably in recent years, especially in the form high fructose corn syrup, due its high sweetening power. Several studies have associated high intake of fructose to metabolic alterations, as nonalcoholic fatty liver disease and fructose malabsorption, among other pathologies. This review aims to update about the effect of high intake of fructose in the liver and intestine, mainly associated with processed foods with added fructose.An updated literature search was conducted using databases (Pubmed, Scopus and SciELO), selecting articles published after the year 2000, resulting from the keywords "fructose intake, fructose intolerance, nonalcoholic fatty liver and fructose, fructose malabsorption"Of 735 articles initially retrieved, 78 met the inclusion criteria.Fructose consumption has increased in recent decades, especially due to increased consumption of sweetened beverages and processed foods with added fructose. High fructose intake has been associated to pathologies as NAFLD and fructose malabsorption.La ingesta de fructosa se ha incrementado considerablemente en los últimos años, especialmente bajo la forma de jarabe de maíz alto en fructosa, debido a su gran poder edulcorante. Diversos estudios, han asociado su elevado consumo con alteraciones metabólicas, hígado graso no alcohólico y malabsorción de fructosa, entre otras patologías. Esta revisión tiene como objetivo actualizar acerca del efecto de la alta ingesta de fructosa en el hígado e intestino, asociada principalmente a alimentos procesados con fructosa agregada. Métodos: Para la búsqueda bibliográfica se utilizaron las bases de datos de Pubmed, Scopus y Scielo, seleccionando aquellos artículos publicados después del año 2000 y resultantes de las palabras claves “fructose intake, high fructose corn syrup, nonalcoholic fatty liver and fructose, fructose malabsorption, fructose intolerance/metabolism”. Resultados: La búsqueda arrojó 735 publicaciones de las cuales 78 cumplieron con los criterios de inclusión. Conclusiones: El consumo de fructosa ha aumentado en las últimas décadas, especialmente a través de bebidas endulzadas y productos alimentarios con fructosa agregada. La alta ingesta de fructosa tiene un impacto a nivel intestinal y hepático, asociándose a patologías como hígado graso no alcohólico y malabsorción de fructosa.

Nonalcoholic fatty liver disease in human obesity is characterized by the multifactorial nature of the underlying pathogenic mechanisms, which include misregulation of PPARs signaling. Liver PPAR-αdownregulation with parallel PPAR-γand SREBP-1c up-regulation may trigger major metabolic disturbances betweende novolipogenesis and fatty acid oxidation favouring the former, in association with the onset of steatosis in obesity-induced oxidative stress and related long-chain polyunsaturated fatty acid n-3 (LCPUFA n-3) depletion, insulin resistance, hypoadiponectinemia, and endoplasmic reticulum stress. Considering that antisteatotic strategies targeting PPAR-αrevealed that fibrates have poor effectiveness, thiazolidinediones have weight gain limitations, and dual PPAR-α/γagonists have safety concerns, supplementation with LCPUFA n-3 appears as a promising alternative, which achieves both significant reduction in liver steatosis scores and a positive anti-inflammatory outcome. This latter aspect is of importance as PPAR-αdownregulation associated with LCPUFA n-3 depletion may play a role in increasing the DNA binding capacity of proinflammatory factors, NF-κB and AP-1, thus constituting one of the major mechanisms for the progression of steatosis to steatohepatitis.

Sterol receptor element-binding protein-1c (SREBP-1c) and peroxisome proliferator-activated receptor-alpha (PPAR-alpha) mRNA expression was assessed in liver as signaling mechanisms associated with steatosis in obese patients. Liver SREBP-1c and PPAR-alpha mRNA (RT-PCR), fatty acid synthase (FAS) and carnitine palmitoyltransferase-1a (CPT-1a) mRNA (real-time RT-PCR), and n-3 long-chain polyunsaturated fatty acid (LCPUFA)(GLC) contents, plasma adiponectin levels (RIA), and insulin resistance (IR) evolution (HOMA) were evaluated in 11 obese patients who underwent subtotal gastrectomy with gastro-jejunal anastomosis in Roux-en-Y and 8 non-obese subjects who underwent laparoscopic cholecystectomy (controls). Liver SREBP-1c and FAS mRNA levels were 33% and 70% higher than control values (P

Oxidative stress and insulin resistance (IR) are major contributors in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and in the progression from steatosis to nonalcoholic steatohepatitis (NASH). Our aim was to assess nuclear factor-kappaB (NF-kappaB) and activating protein-1 (AP-1) activation and Toll-like receptor 4 (TLR4) expression as signaling mechanisms related to liver injury in obese NAFLD patients, and examined potential correlations among them, oxidative stress, and IR. Liver NF-kappaB and AP-1 (electromobility shift assay (EMSA)), TLR4 expression (western blot), ferric reducing ability of plasma (FRAP), and IR evolution (HOMA) were evaluated in 17 obese patients who underwent subtotal gastrectomy with gastro-jejunal anastomosis in Roux-en-Y and 10 nonobese subjects who underwent laparoscopic cholecystectomy (controls). Liver NF-kappaB and AP-1 DNA binding were markedly increased in NASH patients (n = 9; P0.05) compared to controls, without significant changes in NAFLD patients with steatosis (n = 8), whereas TLR4 expression was comparable between groups. Hepatic NF-kappaB activation was positively correlated with that of AP-1 (r = 0.79; P0.0001); both liver NF-kappaB and AP-1 DNA binding were inversely associated with FRAP (r = -0.43 and r = -0.40, respectively; P0.05) and directly correlated with HOMA (r = 0.66 and r = 0.62, respectively, P0.001). Data presented show enhanced liver activation of the proinflammatory transcription factors NF-kappaB and AP-1 in obese patients with NASH, parameters that are significantly associated to oxidative stress and IR.

Hepatic steatosis is a major feature associated with NAFLD (non-alcoholic fatty liver disease). The aims of the present study were to assess the levels of PUFA (polyunsaturated fatty acids) in liver total lipids, triacylglycerols (triglycerides) and phospholipids of NAFLD patients in relation to those in adipose tissue and hepatic indexes related to oxidative stress as factors contributing to hepatic steatosis. Eleven control subjects and 19 patients with NAFLD were studied. Analysis of liver and abdominal adipose tissue fatty acids was carried out by GLC. The liver content of protein carbonyl groups and malondialdehyde were taken as indexes related to oxidative stress. NAFLD patients had a depletion in LCPUFA (long-chain PUFA) of the n -6 and n -3 series in liver triacylglycerols, with decreased 20:4, n -6/18:2, n -6 and (20:5, n -3+22:6, n -3)/18:3, n -3 ratios, whereas liver phospholipids contained higher n -6 and lower n -3 LCPUFA. These findings were accompanied by an enhancement of (i) n -6/ n -3 ratio in liver and adipose tissue, (ii) 18:1, n -9 trans levels in adipose tissue, and (iii) hepatic lipid peroxidation and protein oxidation indexes. It is concluded that a marked enhancement in LCPUFA n -6/ n -3 ratio occurs in the liver of NAFLD patients, a condition that may favour lipid synthesis over oxidation and secretion, thereby leading to steatosis. Depletion of hepatic LCPUFA may result from both defective desaturation of PUFA, due to inadequate intake of precursors, such as 18:3, n -3, and higher intake of the 18:1, n -9 trans isomer leading to desaturase inhibition, and from an increased peroxidation of LCPUFA due to oxidative stress.