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 23 February 2018

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News

Serum leptin in NASH correlates with hepatic steatosis but not fibrosis

A team writing in the journal Hepatology has examined the role of serum leptin in non-alcoholic steatohepatitis and find it correlates with hepatic steatosis, but not fibrosis or inflammation.

News image

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Non-alcoholic steatohepatitis (NASH) is a disorder characterized by hepatic steatosis, inflammation and fibrosis.

Researchers from Australia have determined serum leptin levels in patients with NASH to determine whether relationships exist between leptin levels and severity of hepatic steatosis or fibrosis.

Leptin is an adipocyte-derived anti-obesity hormone. In rodents it has been shown to prevent "lipotoxicity" by limiting triglyceride accumulation.

Leptin also regulates matrix deposition (fibrosis) during wound healing.

The researchers used radioimmunoassay techniques to determine serum leptin concentrations in 27 men and 20 women with NASH.

A further 47 controls, matched for gender and body mass index (BMI) also had their serum leptin levels measured.

These levels were then correlated with hepatic steatosis, fibrosis, and inflammation, each categorized semiquantitatively on liver histology.

The serum leptin values were also correlated with anthropometric indices, serum lipids, glucose, insulin, c-peptide, and alanine aminotransferase (ALT) levels.

In comparison with controls, mean serum leptin levels were raised in both men and women with NASH (men 14 ng/ml vs. 7.2 ng/ml; women 35 ng/ml vs. 15 ng/ml).

Leptin values were found to correlate with serum c-peptide levels but not with BMI.

Leptin - correlates with severity of hepatic steatosis.
Hepatology

However, serum leptin was not an independent predictor of hepatic inflammation or fibrotic severity.

The research group write that the study suggests that hyperleptinemia occurs in NASH. They caution however, that this occurrence cannot be simply explained by gender, obesity, or the presence of type 2 diabetes.

Additionally, leptin levels correlate directly with the severity of hepatic steatosis but not with inflammation or fibrosis.

The research team proposes that the relationship between leptin and steatosis reflect a pathogenic role of leptin in hepatic insulin resistance and/or a failure of the antisteatotic actions of leptin ("peripheral leptin resistance").

Hepatology 2002; 36(2): 403-409
31 July 2002

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