Perspectives on Nonalcoholic Fatty Liver Disease: An Overview of Present and Future Therapies

Vizuete, John; Camero, Alfredo; Malakouti, Mazyar; Garapati, Karthik; Gutiérrez, Julio

doi:10.14218/jcth.2016.00061

Cited by 20 publications

(14 citation statements)

References 89 publications

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“…Collectively, these findings point toward oxidative stress as an important acting factor in the development in HFD‐dependent liver steatosis and establishment of a pro‐inflammatory state, which can further increase in NASH to progress into fibrosis and cirrhosis . Hence, abrogation of hepatic steatosis by combined DHA and HT would represent a crucial therapeutic strategy eluding disease progression into stages lacking efficacious handling at present time …”

Section: Discussionmentioning

confidence: 99%

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Docosahexaenoic acid and hydroxytyrosol co‐administration fully prevents liver steatosis and related parameters in mice subjected to high‐fat diet: A molecular approach

et al. 2019

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Attenuation of high‐fat diet (HFD)‐induced liver steatosis is accomplished by different nutritional interventions. Considering that the n‐3 PUFA docosahexaenoic acid (DHA) modulates lipid metabolism and the antioxidant hydroxytyrosol (HT) diminishes oxidative stress underlying fatty liver, it is hypothesized that HFD‐induced steatosis is suppressed by DHA and HT co‐administration. Male C57BL/6J mice were fed a control diet (CD; 10% fat, 20% protein, 70% carbohydrates) or a HFD (60% fat, 20% protein, 20% carbohydrates) for 12 weeks, without and with supplementation of DHA (50 mg/kg/day), HT (5 mg/kg/day) or both. The combined DHA + HT protocol fully prevented liver steatosis and the concomitant pro‐inflammatory state induced by HFD, with suppression of lipogenic and oxidative stress signaling, recovery of fatty acid oxidation capacity and enhancement in resolvin availability affording higher inflammation resolution capability. Abrogation of HFD‐induced hepatic steatosis by DHA and HT co‐administration represents a crucial therapeutic strategy eluding disease progression into stages lacking efficacious handling at present time.

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Section: Discussionmentioning

confidence: 99%

“…70,71 Hence, abrogation of hepatic steatosis by combined DHA and HT would represent a crucial therapeutic strategy eluding disease progression into stages lacking efficacious handling at present time. [4][5][6]…”

Section: Liver Molecular Changes Associated Withmentioning

confidence: 99%

Docosahexaenoic acid and hydroxytyrosol co‐administration fully prevents liver steatosis and related parameters in mice subjected to high‐fat diet: A molecular approach

et al. 2019

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“…The use of metformin to prevent progressive liver injury in NAFLD/NASH has been heavily debated . Many studies have shown an improvement in liver enzymes while taking metformin, but effects on histological endpoints have been less convincing .…”

Section: Discussionmentioning

confidence: 99%

Hepatic exposure of metformin in patients with non‐alcoholic fatty liver disease

Sundelin

Gormsen

Heebøll

et al. 2019

Brit J Clinical Pharma

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Aims: Metformin is first-line treatment of type 2 diabetes mellitus and reduces cardiovascular events in patients with insulin resistance and type 2 diabetes. Target tissue for metformin action is thought to be the liver, where metformin distribution depends on facilitated transport by polyspecific transmembrane organic cation transporters (OCTs). Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in the western world with strong associations to insulin resistance and the metabolic syndrome, but whether NAFLD affects metformin biodistribution to the liver is not known. In this study, the primary aim was to investigate in vivo hepatic uptake of metformin dynamically in humans with variable degrees of liver affection.As a secondary aim, we wished to correlate hepatic metformin distribution with OCT gene transcription determined in diagnostic liver biopsies.Methods: Eighteen patients with biopsy-proven NAFLD were investigated using 11C-metformin PET/CT technique. Gene transcripts of OCTs were determined by real-time polymerase chain reaction (PCR). Results:We observed similar hepatic volume of distribution of metformin between patients with simple steatosis and non-alcoholic steatohepatitis (NASH) (Vd 2.38 ± 0.56 vs. 2.10 ± 0.39, P = 0.3). There was no association between hepatic exposure to metformin and the degree of inflammation or fibrosis, and no clear correlation between metformin distribution and OCT gene transcription.The authors confirm that the PI for this paper is M.D., Ph. D Elias Sundelin and that he had direct clinical responsibility for patients.

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“…Estresse oxidativo, inflamação hepática, disfunção mitocondrial, citocinas próinflamatórias desequilibradas, fibrose, resistência à insulina, hiperinsulinemia, ácidos graxos livres plasmáticos, fígado gorduroso e lesão de hepatócitos são condições que apoiam o desenvolvimento da esteato-hepatite gordurosa não alcoólica e fibrogênese. [8][9][10][11] A disfunção do tecido adiposo em doença hepática gordurosa não alcoólica tem sido associada a redução do catabolismo de aminoácidos de cadeia ramificada (BCAA) e ácidos graxos. Essa alteração está inversamente relacionada aos teores séricos de BCAA e de conteúdo hepático de gordura.…”

Section: Fisiopatologiaunclassified

Doença Hepática Gordurosa Não Alcoólica: Atualização Sobre A Fisiopalogia

Silva¹,

Brito²,

Rodrigues³

et al. 2015

RBM

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Objetivo. Revisar a fisiopatologia da doença hepática gordurosa não alcoólica com destaque para novos aspectos relacionados a resistência insulínica como ácidos biliares e microbiota intestinal. Método. Revisão de literatura nas bases Pubmed e Lilacs, utilizando-se os termos patogênese e fisiopatologia da doença hepática gordurosa não alcoólica. Palavras-chave. Hepatopatia gordurosa não alcoólica; obesidade; diabetes mellitus tipo 2; síndrome metabólica ABSTRACT Objective. To review the pathophysiology of non-alcoholic fatty liver disease with emphasis on the new aspects related to insulin resistance, such as bile acids and intestinal microbiota. Method. Review of literature on the bases Pubmed and Lilacs using the terms pathogenesis and pathophysiology of non-alcoholic fatty liver disease. Results. Non-alcoholic fatty liver disease will be the major cause of liver morbidity and mortality in the next twenty years. The spectrum of non-alcoholic fatty liver disease involves a continuous and complex process involving simple deposition of fat, with possible evolution to inflammation, called steatohepatitis and risk of progression to fibrosis, Débora Gonçalves da Silva-médica, endocrinologista, coordenadora do

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Perspectives on Nonalcoholic Fatty Liver Disease: An Overview of Present and Future Therapies

Cited by 20 publications

References 89 publications

Docosahexaenoic acid and hydroxytyrosol co‐administration fully prevents liver steatosis and related parameters in mice subjected to high‐fat diet: A molecular approach

Docosahexaenoic acid and hydroxytyrosol co‐administration fully prevents liver steatosis and related parameters in mice subjected to high‐fat diet: A molecular approach

Hepatic exposure of metformin in patients with non‐alcoholic fatty liver disease

Doença Hepática Gordurosa Não Alcoólica: Atualização Sobre A Fisiopalogia

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