Serum leptin and ghrelin in chronic hepatitis C patients with steatosis

Abstract

Increased serum leptin before treatment may predict non-SVR, especially in HCV genotype-1 infected patients, whereas increased ghrelin may predict SVR in genotype-1.

Serum leptin and plasma ghrelin concentrations in patients with chronic hepatitis C virus with steatosis: Their effect on the response to antiviral therapy

“…Also we found negative correlations between ghrelin with HOMA-IR and leptin. These results are in agreement with the results of previous studies [20,33] that demonstrated low plasma ghrelin concentrations that tend to decrease more as the grade of steatosis increase in patients with HCV, indicating that ghrelin may prevent or reduce steatosis by negatively regulating leptin [20]. In addition Moreno et al [33] found that, in patients with chronic liver diseases and chronic HCV, plasma ghrelin levels decreased in those with advanced fibrosis, and ghrelin gene hepatic expression correlated with expression of fibrogenic genes, and polymorphisms of the ghrelin gene (-994CT and -604GA) influenced the progression of liver fibrosis, thus Ghrelin exerts antifibrotic effects in the liver and may represent a novel antifibrotic therapy.…”

“…We also evaluated the correlations between pretreatment serum leptin and ghrelin concentrations and liver histology and metabolic factors. Our results are similar to observations made by other investigators [18], suggesting a possible involvement of adipocytokines like leptin and ghrelin in disease progression among the patients with chronic HCV [19,20] .…”

“…In addition, Pavlidis et al [20] found that responders had lower serum leptin and higher plasma ghrelin concentrations at baseline than non-responders, and that ghrelin concentration increased to reach significant levels at the end of treatment, indicating that ghrelin may prevent or reduce steatosis by negatively regulating leptin. This may enhance the likelihood of SVR, since responders also have lower baseline leptin concentrations.…”

“…Leptin may increase insulin resistance and fatty acid concentrations in the liver, leading to enhanced lipid peroxidation and promoting steatosis. Leptin may also induce the release of cytokines, such as TNF-α, INF-γ, IL-18, and TGF-β1, which are involved in the pathogenesis of both liver steatosis and fibrosis [20]. In steatosis, activated hepatic stellate cells, but not quiescent cells, can express leptin [23] .…”

The endocrine effects of acylated and des-acylated ghrelin

“…108 However, in patients with NAFLD and hepatitis C, DAG and AG plasma levels are shown to be higher than in normal individuals. 109,110 In addition, in humans, it was suggested that ghrelin levels should be reduced in response to the development of insulin resistance rather than being influenced by liver damage per se. 111,112 In vivo, peripheral infusion of AG inhibits insulin-induced suppression of hepatic glucose production while stimulating overall glucose uptake in mice.…”