Metformin Ameliorates Hepatic Steatosis and Inflammation without Altering Adipose Phenotype in Diet-Induced Obesity

Non-alcoholic fatty liver disease (NAFLD) is closely associated with obesity and insulin resistance. To better understand the pathophysiology of obesity-associated NAFLD, the present study examined the involvement of liver and adipose tissues in metformin actions on reducing hepatic steatosis and inflammation during obesity. C57BL/6J mice were fed a high-fat diet (HFD) for 12 weeks to induce obesity-associated NAFLD and treated with metformin (150 mg/kg/d) orally for the last four weeks of HFD feeding. Compared with HFD-fed control mice, metformin-treated mice showed improvement in both glucose tolerance and insulin sensitivity. Also, metformin treatment caused a significant decrease in liver weight, but not adiposity. As indicated by histological changes, metformin treatment decreased hepatic steatosis, but not the size of adipocytes. In addition, metformin treatment caused an increase in the phosphorylation of liver AMP-activated protein kinase (AMPK), which was accompanied by an increase in the phosphorylation of liver acetyl-CoA carboxylase and decreases in the phosphorylation of liver c-Jun N-terminal kinase 1 (JNK1) and in the mRNA levels of lipogenic enzymes and proinflammatory cytokines. However, metformin treatment did not significantly alter adipose tissue AMPK phosphorylation and inflammatory responses. In cultured hepatocytes, metformin treatment increased AMPK phosphorylation and decreased fat deposition and inflammatory responses. Additionally, in bone marrow-derived macrophages, metformin treatment partially blunted the effects of lipopolysaccharide on inducing the phosphorylation of JNK1 and nuclear factor kappa B (NF-κB) p65 and on increasing the mRNA levels of proinflammatory cytokines. Taken together, these results suggest that metformin protects against obesity-associated NAFLD largely through direct effects on decreasing hepatocyte fat deposition and on inhibiting inflammatory responses in both hepatocytes and macrophages.

• Publication year

  2014

• Venue

  PLoS ONE

• Publication date

  2014-03-17

• Fields of study

  Biology, Medicine, Chemistry, Environmental Science

• Identifiers
  DOI 10.1371/journal.pone.0091111PMID 24638078PMCID 3956460
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• Metformin directly increased AMPK phosphorylation and reduced fat deposition and inflammatory responses in cultured hepatocytes, and it partially blunted LPS-induced JNK1 and NF-kB p65 phosphorylation and proinflammatory cytokine expression in bone marrow-derived macrophages.

  Confidence 0.94

  박진우 (dztg5apj7m) extractionAnonymous (12632b8b5f) review
• Metformin increased liver AMPK phosphorylation and was accompanied by higher ACC phosphorylation and lower JNK1 phosphorylation together with reduced lipogenic and proinflammatory mRNA levels.

  Confidence 0.96

  박진우 (dztg5apj7m) extractionAnonymous (12632b8b5f) review
• Metformin reduced liver weight and hepatic steatosis without changing adipose tissue phenotype or adipocyte size.

  Confidence 0.95

  박진우 (dztg5apj7m) extractionAnonymous (12632b8b5f) review
• Metformin improved glucose tolerance and insulin sensitivity in the HFD-induced obesity-associated NAFLD mouse model.

  Confidence 0.97

  박진우 (dztg5apj7m) extractionAnonymous (12632b8b5f) review

• adipose tissue phenotype

  phenotype, tissue state

  The adipose-tissue state examined through adiposity, adipocyte size, and adipose AMPK and inflammatory readouts.

  Aliases: adiposity, adipocyte phenotype

  박진우 (dztg5apj7m) extractionAnonymous (12632b8b5f) review
• bone marrow-derived macrophages

  cell type, in vitro system

  Macrophages differentiated from bone marrow cells and used to examine metformin effects on inflammatory signaling in vitro.

  Aliases: BMDMs

  박진우 (dztg5apj7m) extractionAnonymous (12632b8b5f) review
• cultured hepatocytes

  cell type, in vitro system

  Isolated liver parenchymal cells used to test direct cellular effects of metformin in vitro.

  Aliases: hepatocytes

  박진우 (dztg5apj7m) extractionAnonymous (12632b8b5f) review
• hepatic steatosis

  pathology, phenotype

  Excess lipid accumulation in the liver, assessed here by histological changes and liver lipid deposition.

  Aliases: fatty liver, liver steatosis

  박진우 (dztg5apj7m) extractionAnonymous (12632b8b5f) review
• liver ampk phosphorylation

  molecular event, signaling event

  Phosphorylation of AMP-activated protein kinase measured in liver tissue as a signaling readout.

  Aliases: hepatic AMPK phosphorylation, AMPK phosphorylation in liver

  박진우 (dztg5apj7m) extractionAnonymous (12632b8b5f) review
• metformin

  drug, treatment

  An oral antidiabetic drug used in the experiment at 150 mg/kg/day during the final four weeks of high-fat feeding.

  Aliases: MET

  박진우 (dztg5apj7m) extractionAnonymous (12632b8b5f) review
• obesity-associated nafld

  condition, disease model

  A mouse liver disease state induced by high-fat diet feeding and characterized by obesity-related fatty liver changes.

  Aliases: NAFLD, non-alcoholic fatty liver disease

  박진우 (dztg5apj7m) extractionAnonymous (12632b8b5f) review

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