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OBJECTIVES: To prospectively evaluate demographic, anthropometric and health-related quality of life (HRQoL) in pediatric patients with laboratory-confirmed coronavirus disease 2019 (COVID-19) METHODS: This was a longitudinal observational study of surviving pediatric post-COVID-19 patients (n=53) and pediatric subjects without laboratory-confirmed COVID-19 included as controls (n=52) was performed. RESULTS: The median duration between COVID-19 diagnosis (n=53) and follow-up was 4.4 months (0.8-10.7). Twenty-three of 53 (43%) patients reported at least one persistent symptom at the longitudinal follow-up visit and 12/53 (23%) had long COVID-19, with at least one symptom lasting for >12 weeks. The most frequently reported symptoms at the longitudinal follow-up visit were headache (19%), severe recurrent headache (9%), tiredness (9%), dyspnea (8%), and concentration difficulty (4%). At the longitudinal follow-up visit, the frequencies of anemia (11% versus 0%, p=0.030), lymphopenia (42% versus 18%, p=0.020), C-reactive protein level of >30 mg/L (35% versus 0%, p=0.0001), and D-dimer level of >1000 ng/mL (43% versus 6%, p=0.0004) significantly reduced compared with baseline values. Chest X-ray abnormalities (11% versus 2%, p=0.178) and cardiac alterations on echocardiogram (33% versus 22%, p=0.462) were similar at both visits. Comparison of characteristic data between patients with COVID-19 at the longitudinal follow-up visit and controls showed similar age (p=0.962), proportion of male sex (p=0.907), ethnicity (p=0.566), family minimum monthly wage (p=0.664), body mass index (p=0.601), and pediatric pre-existing chronic conditions (p=1.000). The Pediatric Quality of Live Inventory 4.0 scores, median physical score (69 [0-100] versus 81 [34-100], p=0.012), and school score (60 [15-100] versus 70 [15-95], p=0.028) were significantly lower in pediatric patients with COVID-19 at the longitudinal follow-up visit than in controls. CONCLUSIONS: Pediatric patients with COVID-19 showed a longitudinal impact on HRQoL parameters, particularly in physical/school domains, reinforcing the need for a prospective multidisciplinary approach for these patients. These data highlight the importance of closer monitoring of children and adolescents by the clinical team after COVID-19.

Background Cachexia is a paraneoplastic syndrome related with poor prognosis. The tumour micro‐environment contributes to systemic inflammation and increased oxidative stress as well as to fibrosis. The aim of the present study was to characterise the inflammatory circulating factors and tumour micro‐environment profile, as potentially contributing to tumour fibrosis in cachectic cancer patients. Methods 74 patients (weight stable cancer n = 31; cachectic cancer n = 43) diagnosed with colorectal cancer were recruited, and tumour biopsies were collected during surgery. Multiplex assay was performed to study inflammatory cytokines and growth factors. Immunohistochemistry analysis was carried out to study extracellular matrix components. Results Higher protein expression of inflammatory cytokines and growth factors such as epidermal growth factor, granulocyte–macrophage colony‐stimulating factor, interferon‐α, and interleukin (IL)‐8 was observed in the tumour and serum of cachectic cancer patients in comparison with weight‐stable counterparts. Also, IL‐8 was positively correlated with weight loss in cachectic patients (P = 0.04; r = 0.627). Immunohistochemistry staining showed intense collagen deposition (P = 0.0006) and increased presence of α‐smooth muscle actin (P

This study aimed to evaluate the impact of a 12-week calorie-restricted diet and recreational sports training on gene expressions IL-15, ATROGIN-1 and MURF-1 in skeletal muscle of T2D patients.Older adults with T2D (n = 39, 60 ± 6.0 years, BMI 33.5 ± 0.6 kg/mTotal body weight was reduced in ~4 kg representing body fat mass in all groups after 12-weeks (P 0.05). HbA1c values decreased in all groups post-intervention. Lipids profile improved in the training groups (P 0.05) after 12-weeks. ATROGIN-1 and MURF-1 mRNA reduced in the DS (1.084 ± 0.14 vs. 0.754 ± 1.14 and 1.175 ± 0.34 vs. 0.693 ± 0.12, respectively; P 0.05), while IL-15 mRNA increased in the DR (1.056 ± 0.12 vs. 1.308 ± 0.13; P 0.05) after 12-weeks intervention.Recreational training with a moderate calorie-restricted diet can downregulates the expression of atrophy-associated myokines and increases the expression of anti-inflammatory gene IL-15.

Summary Cancer-associated cachexia is a complex metabolic syndrome characterized by weight loss and systemic inflammation. Muscle loss and fatty infiltration into muscle are associated with poor prognosis in cancer patients. Skeletal muscle secretes myokines, factors with autocrine, paracrine and/or endocrine action, which may be modified by or play a role in cachexia. This study examined myokine content in the plasma, skeletal muscle and tumor homogenates from treatment-naive patients with gastric or colorectal stages I-IV cancer with cachexia (CC, N = 62), or not (weight stable cancer, WSC, N = 32). Myostatin, interleukin (IL) 15, follistatin-like protein 1 (FSTL-1), fatty acid binding protein 3 (FABP3), irisin and brain-derived neurotrophic factor (BDNF) protein content in samples was measured with Multiplex technology; body composition and muscle lipid infiltration were evaluated in computed tomography, and quantification of triacylglycerol (TAG) in the skeletal muscle. Cachectic patients presented lower muscle FSTL-1 expression (p = 0.047), higher FABP3 plasma content (p = 0.0301) and higher tumor tissue expression of FABP3 (p = 0.0182), IL-15 (p = 0.007) and irisin (p = 0.0110), compared to WSC. Neither muscle TAG content, nor muscle attenuation were different between weight stable and cachectic patients. Lumbar adipose tissue (AT) index, visceral AT index and subcutaneous AT index were lower in CC (p = 0.0149, p = 0.0455 and p = 0.0087, respectively), who also presented lower muscularity in the cohort (69.2% of patients; p = 0.0301), compared to WSC. The results indicate the myokine profile in skeletal muscle, plasma and tumor is impacted by cachexia. These findings show that myokines eventually affecting muscle wasting may not solely derive from the muscle itself (as the tumor also may contribute to the systemic scenario), and put forward new perspectives on cachexia treatment targeting myokines and associated receptors and pathways.

International audience; An idiopathic myopathy characterized by central nuclei in muscle fibers, a hallmark of muscle regeneration, has been observed in cancer patients. In cancer cachexia skeletal muscle is incapable of regeneration, consequently, this observation remains unaccounted for. In C26-tumor bearing, cachectic mice, we observed muscle fibers with central nuclei in the absence of molecular markers of bona fide regeneration. These clustered, non-peripheral nuclei were present in NCAM-expressing muscle fibers. Since NCAM expression is upregulated in denervated myofibers, we searched for additional makers of denervation, including AchRs, MUSK, and HDAC. This last one being also consistently upregulated in cachectic muscles, correlated with an increase of central myonuclei. This held true in the musculature of patients suffering from gastrointestinal cancer, where a progressive increase in the number of central myonuclei was observed in weight stable and in cachectic patients, compared to healthy subjects. Based on all of the above, the presence of central myonuclei in cancer patients and animal models of cachexia is consistent with motor neuron loss or NMJ perturbation and could underlie a previously neglected phenomenon of denervation, rather than representing myofiber damage and regeneration in cachexia. Similarly to aging, denervation-dependent myofiber atrophy could contribute to muscle wasting in cancer cachexia.

Cachexia is a wasting syndrome characterized by the continuous loss of skeletal muscle mass due to imbalance between protein synthesis and degradation, which is related with poor prognosis and compromised quality of life. Dysfunctional mitochondria are associated with lower muscle strength and muscle atrophy in cancer patients, yet poorly described in human cachexia. We herein investigated mitochondrial morphology, autophagy and apoptosis in the skeletal muscle of patients with gastrointestinal cancer-associated cachexia (CC), as compared with a weight-stable cancer group (WSC). CC showed prominent weight loss and increased circulating levels of serum C-reactive protein, lower body mass index and decreased circulating hemoglobin, when compared to WSC. Electron microscopy analysis revealed an increase in intermyofibrillar mitochondrial area in CC, as compared to WSC. Relative gene expression of Fission 1, a protein related to mitochondrial fission, was increased in CC, as compared to WSC. LC3 II, autophagy-related (ATG) 5 and 7 essential proteins for autophagosome formation, presented higher content in the cachectic group. Protein levels of phosphorylated p53 (Ser46), activated caspase 8 (Asp384) and 9 (Asp315) were also increased in the skeletal muscle of CC. Overall, our results demonstrate that human cancer-associated cachexia leads to exacerbated muscle-stress response that may culminate in muscle loss, which is in part due to disruption of mitochondrial morphology, dysfunctional autophagy and increased apoptosis. To the best of our knowledge, this is the first report showing quantitative morphological alterations in skeletal muscle mitochondria in cachectic patients.

Obesity and related diseases are becoming more prevalent. Conjugated linoleic acid (CLA) might be a useful coadjutant treatment helping to decrease fat mass. However, the precise impact of CLA is unclear because the decreased body fat mass is followed by an increase in insulin resistance. This study aimed to evaluate some of the consequences of a high dose of CLA in rats fed a normal low fat or a high fat diet for 30 days. Male Wistar rats were separated into 4 groups (each n = 10): Control group receiving 7% fat (soybean oil); CLA group receiving 4% soybean oil and 3% CLA mixture; animal fat (AF) group, receiving 45% fat (lard); and animal fat plus CLA (AF+CLA) group, receiving 42% lard and 3% CLA mixture. The CLA mixture contained 39.32 mole% c9,t11-CLA and 40.50 mole% t10,c12-CLA. After 30 days, both CLA groups (CLA and AF+CLA groups) developed insulin resistance, with an increase in glucose in the fasting state and in an insulin tolerance test. The CLA group had increased liver weight and percentage of saturated fatty acids in liver and adipose tissue. Feeding the high fat diet resulted in increased hepatic triacylglycerol accumulation and this was exacerbated by dietary CLA. It is concluded that a high dose of CLA mixture increases insulin resistance and exacerbates hepatic steatosis when combined with a high fat diet.

Aim To examine the effects of creatine (Cr) supplementation on liver fat accumulation in rats fed a choline-deficient diet. Methods Twenty-four rats were divided into 3 groups of 8 based on 4 weeks of feeding an AIN-93 control diet (C), a choline-deficient diet (CDD) or a CDD supplemented with 2% Cr. The CDD diet was AIN-93 without choline. Results The CDD significantly increased plasma homocysteine and TNFα concentration, as well as ALT activity. In liver, the CDD enhanced concentrations of total fat (55%), cholesterol (25%), triglycerides (87%), MDA (30%), TNFα (241%) and decreased SAM concentrations (25%) and the SAM/SAH ratio (33%). Cr supplementation prevented all these metabolic changes, except for hepatic SAM and the SAM/SAH ratio. However, no changes in PEMT gene expression or liver phosphatidylcholine levels were observed among the three experimental groups, and there were no changes in hepatic triglyceride transfer protein (MTP) mRNA level. On the contrary, Cr supplementation normalized expression of the transcription factors PPARα and PPARγ that were altered by the CDD. Further, the downstream targets and fatty acids metabolism genes, UCP2, LCAD and CPT1a, were also normalized in the Cr group as compared to CDD-fed rats. Conclusion Cr supplementation prevented fat liver accumulation and hepatic injures in rats fed with a CDD for 4 weeks. Our results demonstrated that one-carbon metabolism may have a small role in mitigating hepatic fat accumulation by Cr supplementation. The modulation of key genes related to fatty acid oxidation pathway suggests a new mechanism by which Cr prevents liver fat accumulation.

Fasting and then refeeding on a high-carbohydrate diet increases serum and hepatic triacylglycerol (TAG) concentrations compared to standard diets. Fructose is a lipogenic monosaccharide which stimulates de novo fatty acid synthesis. Omega-3 (n-3) fatty acids stimulate hepatic β-oxidation, partitioning fatty acids away from TAG synthesis. This study investigated whether dietary n-3 fatty acids from fish oil (FO) improve the hepatic lipid metabolic response seen in rats fasted and then refed on a high-fructose diet. During the post-prandial (fed) period, rats fed a FO rich diet showed an increase in hepatic peroxisome proliferator-activated receptor α (PPAR-α) gene expression and decreased expression of carbohydrate responsive element binding protein (ChREBP), fatty acid synthase (FAS) and microsomal triglyceride transfer protein (MTTP). Feeding a FO rich diet for 7 days prior to 48 h of fasting resulted in lower hepatic TAG, lower PPAR-α expression and maintenance of hepatic n-3 fatty acid content. Refeeding on a high fructose diet promoted an increase in hepatic and serum TAG and in hepatic PPAR-α, ChREBP and MTTP expression. FO did not prevent the increase in serum and hepatic TAG after fructose refeeding, but did decrease hepatic expression of lipogenic genes and increased the n-3 fatty acid content of the liver. n-3 Fatty acids can modify some components of the hepatic lipid metabolic response to later feeding with a high fructose diet.

Objective The aim of this study was to investigate how maternal polyunsaturated fatty acid intake at different periods during pregnancy affects the composition of polyunsaturated fatty acids in mature human milk. Methods A prospective study was conducted involving 45 pregnant women, aged between 18 and 35 y, who had full-term pregnancies and practiced exclusive or predominant breast-feeding. Mature breast milk samples were collected after the 5th postpartum week by manual expression; fatty acid composition was determined by gas chromatography. Fatty acid intake during pregnancy and puerperium was estimated through multiple 24-h dietary recalls. Linear regression models, adjusted by postpartum body mass index and deattenuated, were used to determine associations between estimated fatty acids in maternal diet during each trimester of pregnancy and fatty acid content in mature human milk. Results A positive association was identified between maternal intake of eicosapentaenoic acid (β, 1.873; 95% confidence interval [CI], 0.545, 3.203) and docosahexaenoic acid (β, 0.464; 95% CI, 0.212–0.714) during the third trimester of pregnancy, as well as the maternal dietary ω-3 to ω-6 ratio (β, 0.093; 95% CI, 0.016–0.170) during the second and third trimesters and postpartum period, with these fatty acids content in mature breast milk. Conclusions The maternal dietary docosahexaenoic acid and eicosapentaenoic acid content during late pregnancy may affect the fatty acid composition of mature breast milk. Additionally, the maternal dietary intake of ω-3 to ω-6 fatty acid ratio, during late pregnancy and the postpartum period, can affect the polyunsaturated fatty acid composition of breast milk.

PURPOSE: To assess oxidative stress and the profile of fatty acids incorporated into the hepatic tissue of animals refed with high-fat (HF) diets after acute food restriction.METHODS: Fifty male Wistar rats were divided into five groups and fasting for 48 hours. One group was sacrificed without refeeding (NR), a control group (C) was refed with the standard AIN-93 diet and the remaining groups with HF diets respectively consisting of hydrogenated vegetable oil (PHVO), trans-free (TF) margarine and trans-free margarine enriched with ω-3 and ω-6 (O). After this period the animals were sacrificed for malondialdehyde (MDA), catalase and hepatic fatty acid determination.RESULTS: The groups refed with HF diets showed elevation of MDA levels compared to the C group (p

Summary Background & aims Non-alcoholic fatty liver disease (NAFLD) is a common liver disease in Western countries. Metabolic disorders which are increasing in prevalence, such as dyslipidaemias, obesity and type 2 diabetes, are closely related to NAFLD. Insulin resistance is a prominent risk factor for NAFLD. Marine omega-3 (n-3) polyunsaturated fatty acids (PUFAs) are able to decrease plasma triacylglycerol and diets rich in marine n-3 PUFAs are associated with a lower cardiovascular risk. Furthermore, marine n-3 PUFAs are precursors of pro-resolving and anti-inflammatory mediators. They can modulate lipid metabolism by enhancing fatty acid β-oxidation and decreasing de novo lipogenesis. Therefore, they may play an important role in prevention and therapy of NAFLD. Methods This review aims to gather the currently information about marine n-3 PUFAs as a therapeutic approach in NAFLD. Actions of marine n-3 PUFAs on hepatic fat metabolism are reported, as well as studies addressing the effects of marine n-3 PUFAs in human subjects with NAFLD. Results A total seventeen published human studies investigating the effects of n-3 PUFAs on markers of NAFLD were found and twelve of these reported a decrease in liver fat and/or other markers of NAFLD after supplementation with n-3 PUFAs. The failure of n-3 PUFAs to decrease markers of NAFLD in five studies may be due to short duration, poor compliance, patient specific factors and the sensitivity of the methods used. Conclusions Marine n-3 PUFAs are likely to be an important tool for NAFLD treatment, although further studies are required to confirm this.

Background The marine n-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) exert numerous beneficial effects on health, but their potency to improve treatment of type 2 diabetic (T2D) patients remains poorly characterized. We aimed to evaluate the effect of a combination intervention using EPA + DHA and the insulin-sensitizing drug pioglitazone in overweight/obese T2D patients already treated with metformin. Methods In a parallel-group, four-arm, randomized trial, 69 patients (66 % men) were assigned to 24-week-intervention using: (i) corn oil (5 g/day; Placebo), (ii) pioglitazone (15 mg/day; Pio), (iii) EPA + DHA concentrate (5 g/day, containing ~2.8 g EPA + DHA; Omega-3), or (iv) pioglitazone and EPA + DHA concentrate (Pio& Omega-3). Data from 60 patients were used for the final evaluation. At baseline and after intervention, various metabolic markers, adiponectin and cytokines were evaluated in serum using standard procedures, EPA + DHA content in serum phospholipids was evaluated using shotgun lipidomics and mass spectrometry, and hyperinsulinemic-euglycemic clamp and meal test were also performed. Indirect calorimetry was conducted after the intervention. Primary endpoints were changes from baseline in insulin sensitivity evaluated using hyperinsulinemic-euglycemic clamp and in serum triacylglycerol concentrations in fasting state. Secondary endpoints included changes in fasting glycemia and glycated hemoglobin (HbA1c), changes in postprandial glucose, free fatty acid and triacylglycerol concentrations, metabolic flexibility assessed by indirect calorimetry, and inflammatory markers. Results Omega-3 and Pio& Omega-3 increased EPA + DHA content in serum phospholipids. Pio and Pio& Omega-3 increased body weight and adiponectin levels. Both fasting glycemia and HbA1c were increased by Omega-3, but were unchanged by Pio& Omega-3. Insulin sensitivity was not affected by Omega-3, while it was improved by Pio& Omega-3. Fasting triacylglycerol concentrations and inflammatory markers were not significantly affected by any of the interventions. Lipid metabolism in the meal test and metabolic flexibility were additively improved by Pio& Omega-3. Conclusion Besides preventing a modest negative effect of n-3 fatty acids on glycemic control, the combination of pioglitazone and EPA + DHA can be used to improve lipid metabolism in T2D patients on stable metformin therapy. Trial registration EudraCT number 2009-011106-42. Electronic supplementary material The online version of this article (doi:10.1186/s12986-015-0047-9) contains supplementary material, which is available to authorized users.

Over the last few years, consistent data have demonstrated that creatine (Cr) supplementation prevents the accumulation of fat in rat liver as well as the progression of fatty liver disease in different situations. Studies have demonstrated that Cr is effective and prevents fatty liver in high-fat and choline-deficient diets and in hepatoma cells in vitro. Because Cr synthesis is responsible for a considerable consumption of hepatic methyl groups, studies have tested the idea that Cr supplementation could modulate phospholipid formation and VLDL secretion. Studies have also demonstrated Cr is able to modulate the expression of key genes related to fatty acid oxidation in hepatocyte cell culture and in rat liver. However, to date, the mechanism by which Cr exerts protective effects against fatty liver is poorly understood. Therefore, the present review aims to summarize the studies involving the therapeutic use of Cr supplementation on fatty liver disease and to explore the mechanisms involved in one-carbon and fatty acid metabolism for the preventive effects of Cr supplementation on fat liver accumulation. Although a small number of studies have been conducted to date, we consider Cr as a new and promising therapeutic strategy to control fat accumulation in the liver as well as the progression of fatty liver disease.

There is no consensus about the effects of conjugated linoleic acid (CLA) on lipid metabolism, especially in animals fed a high-fat diet. Therefore, the objective of the present study was to evaluate the incorporation of CLA isomers into serum, liver and adipose tissue, as well as the oxidative stress generated in rats refed with high-fat diets after a 48 hour fast. Rats were refed with diets containing soybean oil, rich in linoleic acid [7% (Control Group - C) or 20% (LA Group)], CLA [CLA Group - 20% CLA mixture (39.32 mole% c9,t11-CLA and 40.59 mole% t10,c12- CLA)], soybean oil + CLA (LA+CLA Group - 15.4% soybean oil and 4.6% CLA) or animal fat (AF, 20% lard). The CLA group showed lower weight gain and liver weight after refeeding, as well as increased serum cholesterol. The high dietary fat intake induced fat accumulation and an increase in -tocopherol in the liver, which were not observed in the CLA group. Circulating -tocopherol was increased in the CLA and CLA+LA groups. The high- fat diets reduced liver catalase activity. CLA isomers were incorporated into serum and tissues. In this shortterm refeeding experimental model, CLA prevented hepatic fat accumulation, although it produced an increase in serum cholesterol.No hay consenso acerca de los efectos del ácido linoleico conjugado (CLA) sobre el metabolismo lipídico, especialmente en animales alimentados con una dieta alta en grasa. Por lo tanto, el objetivo del presente estudio fue evaluar la incorporación de isómeros de CLA en el suero, hígado y tejido adiposo, así como el estrés oxidativo generado en ratas realimentadas con dietas altas en grasa después de 48 horas de ayuno. Los animales fueron realimentados con dietas que contenían aceite de soja, rico en ácido linoleico [7% (Groupo Control - C)], o 20% (Groupo LA)], CLA [Groupo CLA - 20% de mezcla de CLA (39,32% moles del c9,t11-CLA y 40.59% moles del t10,c12-CLA)], aceite de soja + CLA (Grupo LA+- CLA - 15.4 % de aceite de soja y 4,6% de CLA) o grasa animal (Grupo AF, 20% de manteca de cerdo). El grupo CLA tuvo menor aumento de peso y menor peso hepático después de la realimentación, así como aumento del colesterol total em el suero. La dieta alta en grasa indujo la acumulación de grasa y un aumento de -tocoferol en el hígado, que no se observaron en el grupo CLA. El -tocoferol serico fue mayor en los grupos CLA y LA+CLA. Las dietas altas en grasa redujeron la actividad de la catalasa hepática. Isómeros de CLA fueron incorporados em el suero y tejidos. En este modelo de realimentación de corto prlazo, el CLA ha impedido la acumulación de grasa hepática, aunque genero un aumento del colesterol total sérico.

Objectives: To evaluate the fatty acid composition of mature human milk of women living far from the coastal area of Brazil. Methods: Mature breast milk samples were obtained from 47 lactating women aged between 18 and 35 years, who delivered their babies at term and who exclusively or predominantly breastfed. Milk collection took place after the fifth week postpartum by hand expression. The fatty acid composition of the milk was determined by gas chromatography. Results: It was observed that the concentration of eicosapentaenoic acid (0.08%) was higher than that observed in previous studies in Brazil. However, the content of docosahexaenoic acid (0.09%) found in human milk was one of the lowest verified in the world. The content of trans fatty acids (2.05%) was similar to that reported in national studies previous to the mandatory declaration of this fatty acid content in food labels, suggesting that this measure had no effect on reducing the content of this fatty acid in the usual diet of women. Conclusions: Low levels of docosahexaenoic acid and high concentrations of trans fatty acids were observed in mature breast milk of women living far from the coastal area in Brazil. Resumo: Objetivos: Avaliar a composição de ácidos graxos do leite humano maduro de mulheres residentes em área distante da costa litorânea brasileira. Métodos: Amostras de leite materno maduro foram obtidas de 47 mulheres lactantes com idade entre 18 e 35 anos, que tiveram partos a termo e em aleitamento exclusivo ou predominante. A coleta de leite se deu a partir da 5ª semana pós-parto, por meio de ordenha manual. A composição de ácidos graxos do leite foi determinada por cromatografia gasosa. Resultados: Verificou-se que a concentração de eicosapentaenoico (0,08%) foi superior ao observado em estudos brasileiros prévios. Entretanto, o teor de docosa-hexaenoico (0,09%) encontrado no leite humano foi um dos menores já verificados no mundo. O teor de ácidos graxos trans (2,05%) foi similar ao relatado em estudos nacionais prévios à obrigatoriedade de declaração do teor deste em rótulos de alimentos, sugerindo que esta medida não surtiu efeito na redução de seu teor na dieta habitual das mulheres. Keywords: Fatty acids, Human breast milk, Lactation, Palavras-chave: Ácidos graxos, Leite materno, Lactação

The high consumption of fructose is linked to the increase in various characteristics of the metabolic syndrome. Fish oil is beneficial for the treatment of these comorbidities, such as insulin resistance, dyslipidemia, and hepatic steatosis. The objective of this study was to evaluate the consequences of the administration of fish oil concomitant to fructose ingestion during the experiment (45 days) and during the final 15 days in high-fructose-fed rats. Male Wistar rats were divided into 5 groups: control; those receiving 10% fish oil (FO); those receiving 60% fructose (Fr); those receiving 60% fructose and 10% fish oil for 45 days (FrFO); and those receiving fructose plus soybean oil for 30 days and fish oil for the final 15 days of the study (FrFO15). There was an increase in triacylglycerol, serum total cholesterol, and hepatic volume in the Fr group. The FO and FrFO groups experienced an increase in lipid peroxidation and a decrease in serum reduced glutathione. The FrFO group suffered greater hepatic injury, with increased alanine aminotransferase levels and DNA damage. Marked n-3 incorporation occurred in the groups receiving fish oil, favoring a better response to the oral glucose tolerance test. Fructose induced comorbidities of the metabolic syndrome, and the use of fish oil promoted a better glucose tolerance, although it was accompanied by more hepatocyte damage.

OBJETIVO: Esta pesquisa investigou a composicao lipidica dos tecidos hepatico e adiposo de ratos Wistar tratados durante 21 dias com uma dieta rica em gordura saturada (grupo gordura saturada, n=6) ou rica em gordura hidrogenada, ou seja, 50% da gordura consistindo de gordura vegetal parcialmente hidrogenada (grupo gordura hidrogenada, n=6) e compara-los a um grupo-controle (grupo-controle, n=6). METODOS: As quantidades de tecido adiposo e gordura hepatica total foram maiores no grupo gordura saturada do que no grupo gordura hidrogenada. A peroxidacao lipidica hepatica foi maior no grupo gordura saturada, com consequente diminuicao dos niveis hepaticos de vitaminas E e A. Por outro lado, o nivel serico de vitamina A foi maior no grupo gordura saturada do que nos outros grupos. A analise das fracoes lipidicas hepaticas revelou mais colesterol e menos colesterol da lipoproteina de alta densidade no grupo gordura hidrogenada. O grupo gordura hidrogenada apresentou os maiores niveis de triglicerides, seguido do grupo gordura saturada. Quantidades significativas de acidos graxos trans foram detectados nos tecidos hepatico e adiposo do grupo gordura hidrogenada. RESULTADOS: Dentre os acidos graxos identificados, o 18:1n9 apresentou uma associacao positiva maior com o colesterol hepatico e triglicerides, e uma associacao negativa maior com o colesterol da lipoproteina de alta densidade. A gordura vegetal parcialmente hidrogenada promove um maior acumulo de colesterol e triglicerides no figado do que a gordura saturada. CONCLUSAO: Os acidos graxos trans foram incorporados aos hepatocitos e adipocitos de forma altamente eficiente.