Leptin has no role in determining severity of steatosis and fibrosis in patients with chronic hepatitis C

Abstract

These findings suggest that the degree of steatosis in patients with CHC does not seem to depend on serum leptin levels or on viral factors, at least as far as HCV viremia and genotype and HGV infection are concerned. The severity of fibrosis does not seem to be influenced by leptin levels, whereas HCV viral load does seem to play some role.

Insulin resistance and liver injury in hepatitis C is not associated with virus-specific changes in adipocytokines

“…33,34 In earlier studies, leptin levels in HCV-infected subjects were similar to those in healthy volunteers matched for age, BMI and gender. 28,35 Serum leptin was found to be associated with IR, 15,37 steatosis 36 and fibrosis 29,30 in some but not all reports. 13,28,30,35,38 With regard to adiponectin, a recent report suggested that adiponectin levels do not differ significantly between healthy subjects and patients with HCV infection after adjusting for age, BMI and gender.…”

“…28,35 Serum leptin was found to be associated with IR, 15,37 steatosis 36 and fibrosis 29,30 in some but not all reports. 13,28,30,35,38 With regard to adiponectin, a recent report suggested that adiponectin levels do not differ significantly between healthy subjects and patients with HCV infection after adjusting for age, BMI and gender. 39 Furthermore, adiponectin levels were not associated with steatosis, portal/periportal inflammation grade, or fibrosis stage.…”

“…41 Other studies have shown that low adiponectin levels are significantly associated with HOMA-IR in HCV. [39][40][41] A major impediment to interpreting these data include small sample size (n Յ 100), 27,29,31-35,37-40 heterogeneous 27 failure to study the effects on IR, 13,[27][28][29][30][32][33][34][35]38 lack of histological correlation, 15,27,37 and failure to examine all cytokines in the same cohort in order to determine independent effects. 13,15,[27][28][29][30][31][32][33][34][35][36][37][38][39][40][41] In contrast, the present study used a large cohort of well-characterized subjects closely matched with controls in the characteristics which modulate IR, with the principal aim of characterizing the independent effects of the four adipocytokines as well as other host and viral factors in relation to IR and hepatic pathology in chronic HCV infection.…”

“…Further, there is no consensus in the literature on whether alterations in these adipocytokines contribute to liver cell injury and inflammation in chronic HCV infection. 13,[27][28][29][30][31][32][33][34][35][36][37][38][39][40][41] In the present study, we tested the hypothesis that TNF␣, IL6, leptin, and adiponectin contribute to the development of HCV-induced IR and liver injury in a prospectively enrolled, well-characterized cohort of untreated non-diabetic, male subjects with chronic HCV infection. We did not assess the serum levels of resistin as its association with obesity, IR, and T2DM in humans is unclear.…”

Insulin resistance, adipocytokines, and hepatitis C virus infection: A missing link?

“…Considering a close link between adipocytokines and IR, 8 it is thus reasonable to speculate that adipocytokines could also contribute, at least in part, to fibrosis progression. Although the association between leptin and steatosis in CHC remains controversial, 3,9 prior studies showed that hypoadiponectinemia was associated with steatosis in CHC. 2 Because the progression from steatosis to fibrosis may take time, 10 the negative association between adipocytokines and the extent of histological injury observed in the present study may be attributed to the time effect.…”