&lt;a name="home"&gt;&lt;/a&gt;Liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver disease

Oliveira, Cláudia Pinto Marques Souza de; Coelho, Ana Maria M.; Barbeiro, Hermes Vieira; Lima, Verônica Castro; Soriano, Francisco Garcia; Ribeiro, Camila Nunes de Morais; Molan, Nilza A.; Alves, Venâncio Avancini Ferreira; Souza, Heraldo Possolo de; Machado, Marcel Cerqueira César; Carrilho, Flair José

doi:10.1590/s0100-879x2006000200004

Cited by 86 publications

(55 citation statements)

References 17 publications

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“…This fact may have occurred because hepatic fibrogenesis probably was not present, as observed by histological analysis. Oxidative stress occurring within a context of triacyglyceride deposition inside the hepatocytes appears to be important for the progression of steatosis to steatohepatitis and fribrosis (19,20) . Several studies have demonstrated that reactive oxygen species are increase in steatohepatitis, whereas antioxidant (vitamin E and glutathione) levels are decreased (10,11) .…”

Section: -Out/dez 2010mentioning

confidence: 99%

Experimental induction of steatosis in different tissues after the ingestion of a carbohydrate-rich diet: effect on the liver, on the heart and on indicators of oxidation

Haubert

Padovan²,

Zucoloto

et al. 2010

Arq. Gastroenterol.

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-Context -The western dietary pattern is characterized by a high calorie intake with a high proportion of simple sugars.This diet is associated with comorbidities such as hepatic fat deposition and is possibly related to non-alcoholic fatty liver disease.Objective -To evaluate the capacity of a hyperglucidic diet to induce steatosis in adult male Wistar rats. After the administration of a carbohydrate-rich diet, we also evaluated the presence of hepatic and cardiac steatosis and the levels of intrinsic antioxidants in the liver. Methods -Forty-six eutrophic adult male Wistar rats were used and 10 of them were chosen, at random, to serve as controls, while the remaining ones formed the experimental group. Control animals received the standard ration offered by the animal house and the experimental group received the hyperglucidic diet. The diets were offered for 21 days and, at the end of this period, tissue samples were collected for analysis of indicators of oxidative stress (malondialdehyde, and reduced glutathione) and of vitamin E. The animals were then sacrificed by decapitation and their viscera were removed for analysis of liver and heart fat. Results -The hyperglucidic diet used induced hepatic fat deposition, with lipid vacuoles being detected in 83% of the livers analyzed by histology.No lipid vacuoles were observed in the heart. Malondialdehyde and reduced glutathione levels remained unchanged when the animals were submitted to the hyperglucidic diet, probably because there was no liver development of fibrosis or inflammation. In contrast, the levels of vitamin E (antioxidant) were reduced, as confirmed in the literature for steatotic animals. Conclusion -The hyperglucidic diet induced hepatic steatosis. In the heart there was an increase in fat content, although no histological changes were observed. These alterations cannot be explained by the presence of malondialdehyde or reduced glutathione (indicators of oxidation), since the values were similar in the groups studied. However, a significant reduction of vitamin E was observed in the experimental group.

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Section: -Out/dez 2010mentioning

confidence: 99%

Experimental induction of steatosis in different tissues after the ingestion of a carbohydrate-rich diet: effect on the liver, on the heart and on indicators of oxidation

Haubert

Padovan²,

Zucoloto

et al. 2010

Arq. Gastroenterol.

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“…It was reported that oxidative stress might contribute to some periparturient infectious, metabolic diseases (1), or abomasal tissue damage because of displacement (obstruction and increased luminal pressure) in DA cases (18). Recently, Oliveira et al (20,21) reported that oxidative stress increased liver steatosis, and could be an important step in the pathogenesis of non-alcoholic fatty liver. Although it is not clear, low cholesterol and lipoprotein concentrations have been associated with sub clinical metabolic disorders (16) or hepatic lipidosis, which might contribute to right-sided abomasal displacement.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of oxidative stress, antioxidant status and lipid profile in cattle with displacement of the abomasum

Durgut¹,

Öztürk²,

Öztürk³

et al. 2016

Ankara Üniversitesi Veteriner Fakültesi Dergisi

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Summary:The aims of the present study were to evaluate serum oxidative and antioxidant status and oxidative stress index, and lipid metabolism profile in cattle with abomasal displacement. A total of thirty-two dairy cows with right-and left-sided abomasal displacement (LDA (n=11) and RDA without volvulus (n=11)) and 10 healthy controls were used in this study. Serum total oxidative status (TOS) and total antioxidant capacity (TAC) were measured by a colorimetric method. The TOS-to-TAC ratio was also calculated as oxidative stress index (OSI) value. Serum lipid profiles were determined by conventional measurement methods as well. Mean TOS and OSI values were significantly (p<0.001) higher in cows with RDA compared to LDA and healthy controls; however, there was no significant differences in serum TAC values among groups. Serum total cholesterol (TC), high density lipoproteins (HDL) and low density lipoproteins (LDL) levels were significantly (p=0.001) decreased, while serum triglyceride (TG) levels were significantly increased in dairy cows with right-and left-sided abomasal displacement compared to healthy controls. The results of current study showed that dairy cows with RDA forming free radicals than LDA and controls due to abomasal tension and increased intraluminal pressure.Key words: Dairy cow, displacement abomasum, oxidative stress. Abomazum deplasmanlı sığırlarda oxidatif stres, antioksidatif seviye ve lipit profilinin değerlendirilmesiÖzet: Bu çalışmanın amacı abomazum deplasmanlı sığırlarda serum oksidan ve antioksidant seviyeleri ve okidatif stres indeksini (OSI) değerlendirmektir. Bu çalışmada toplam sağa ve sola abomasum deplasmanı olan 32 (11 sola deplasman, 11 volvulus olmayan sağa deplasman) ve 10 sağlıklı Holstein sığır kullanıldı. Serum toplam oksidan seviye (TOS) ve toplam antioksidan kapasite (TAC) kolarimetrik bir yöntemle belirlendi. OSI değeri, TAC-TOS oranı hesaplanarak belirlendi. Serum lipid profili ise geleneksel yöntemlerle belirlendi. TOS ve OSI değerleri, sola deplasmanlı sığırlar ve kontrol grubuyla karşılaştırıldığında sağa deplasmanlı sığırlarda önemli oranda (P<0.001) yüksek bulundu. Fakat serum TAC değerlerinde gruplar arasında önemli bir fark yoktu. Sağa ve sola deplasmanı olan sütçü sığırlar kontrolle karşılaştırıldığında serum trigliserit (TG) sevisinde önemli bir artış belirlenirken, serum total kolestrol (TC), yüksek dansiteli lipoproteinler (HDL) ve düşük dansiteli lipoprotein (LDL) seviyelerinde önemli bir azalma belirlendi. Bu çalışmanın sonuçlarında, RDA'lı sütçü sığırlar da intraluminal basınç artışı ve abomazumdaki gerginlikten dolayı LDA ve kontrollerden daha fazla serbest radikaller oluştuğu gösterildi. Anahtar sözcükler: Abomasum deplasmanı, oksidatif stress, sütçü sığır.

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“…The progression of NAFLD to NASH occurs on account of damage caused by lipid peroxidation and free-radical production 5 . Lipid peroxidation is accompanied by an inflammatory response and stellate cell activation, inducing fibrogenesis 6 . Day and James 7 proposed the "two hits" hypothesis to explain the progression of steatosis to inflammation, fibrosis and cirrhosis.…”

Section: Introductionmentioning

confidence: 99%

“…These changes are also present in patients with liver fat accumulation resulting from diseases such as obesity, malnutrition, intestinal malabsorption, endocrine metabolic diseases and thyroid disorders, but only in NASH there are mitochondrial defects in the structure 13 . Mitochondria are responsible for oxidative phosphorylation and ß-oxidation of fatty acids, processes that are the main sources of free radicals and, together with mitochondrial disorders, play a central role in the development of NASH 6 . The mitochondrial abnormalities associated with NAFLD include structural damage, depletion of mitochondrial DNA, decreased activity of respiratory chain complexes and reduced mitochondrial ß-oxidation.…”

Section: Introductionmentioning

confidence: 99%

Fructose and NAFLD: metabolic implications and models of induction in rats

Castro¹,

Cardoso²,

Vannucchi³

et al. 2011

Acta Cir. Bras.

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PURPOSE:The increase in fructose consumption is paralleled by a higher incidence of obesity worldwide. This monosaccharide is linked to metabolic syndrome, being associated with hypertriglyceridemia, hypertension, insulin resistance and diabetes mellitus. It is metabolized principally in the liver, where it can be converted into fatty acids, which are stored in the form of triglycerides leading to NAFLD. Several models of NAFLD use diets high in simple carbohydrates. Thus, this study aimed to describe the major metabolic changes caused by excessive consumption of fructose in humans and animals and to present liver abnormalities resulting from high intakes of fructose in different periods of consumption and experimental designs in Wistar rats. METHODS: Two groups of rats were fasted for 48 hours and reefed for 24 or 48 hours with a diet containing 63% fructose. Another group of rats was fed an diet with 63% fructose for 90 days. RESULTS: Refeeding for 24 hours caused accumulation of large amounts of fat, compromising 100% of the hepatocytes. The amount of liver fat in animals refed for 48 hours decreased, remaining mostly in zone 2 (medium-zonal). In liver plates of Wistar rats fed 63% fructose for 45, 60 and 90 days it's possible to see that there is an increase in hepatocytes with fat accumulation according to the increased time; hepatic steatosis, however, is mild, compromising about 20% of the hepatocytes. CONCLUSIONS: Fructose is highly lipogenic, however the induction of chronic models in NAFLD requires long periods of treatment. The acute supply for 24 or 48 hours, fasted rats can cause big changes, liver steatosis with macrovesicular in all lobular zones. Key words: Fructose. Fatty Liver. Diet. Rats. RESUMO OBJETIVO:O aumento do consumo de frutose é concomitante a maior incidência mundial de obesidade. Este monossacarídeo está relacionado à Síndrome Metabólica, sendo vinculado à hipertrigliceridemia, hipertensão arterial, resistência à insulina e diabetes mellitus. É metabolizada principalmente no fígado, onde pode ser convertida em ácidos graxos, os quais serão estocados na forma de trigligérides ocasionando a esteatose hepática não alcoólica (NAFLD). Vários modelos de NAFLD utilizam dietas ricas em carboidratos simples. Desta forma, este trabalho teve como objetivos descrever as principais alterações metabólicas causadas pelo consumo excessivo de frutose em humanos e em animais e apresentar as alterações hepáticas decorrentes da alta ingestão de frutose em diferentes períodos de consumo e desenhos experimentais em ratos Wistar. MÉTODOS: Dois grupos de ratos Wistar foram mantidos em jejum durante 48 horas e realimentados por 24 ou 48 horas com dieta contendo 63% de frutose. Outro grupo de ratos Wistar foi alimentado com 63% de frutose durante 90 dias. RESULTADOS: A realimentação por 24 horas provocou acúmulo de grande quantidade de gordura. A quantidade de gordura hepática nos animais realimentados por 48 horas diminuiu, mantendo-se principalmente nas zona 2 (medio-zonal). Em fígados de ratos Wi...

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<a name="home"></a>Liver mitochondrial dysfunction and oxidative stress in the pathogenesis of experimental nonalcoholic fatty liver disease

Cited by 86 publications

References 17 publications

Experimental induction of steatosis in different tissues after the ingestion of a carbohydrate-rich diet: effect on the liver, on the heart and on indicators of oxidation

Experimental induction of steatosis in different tissues after the ingestion of a carbohydrate-rich diet: effect on the liver, on the heart and on indicators of oxidation

Evaluation of oxidative stress, antioxidant status and lipid profile in cattle with displacement of the abomasum

Fructose and NAFLD: metabolic implications and models of induction in rats

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