Leptin and TNF alpha levels in hepatitis C and its relationship withhepatic fibrosis

Crespo, Javier; Amado, J. A.; García‐Unzueta, María Teresa; Almohalla, C.; García-Pajares, Félix; Castro, Beatriz; Pons‐Romero, F.

doi:10.1016/s0168-8278(00)80581-4

Cited by 42 publications

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“…[29][30][31] However, another study revealed no relationship between TNF␣ levels and the grading of steatosis or portal inflammation. 30 To date, no studies have assessed the relationship of serum IL6 to HCV-associated IR. Serum IL6 levels were not significantly different between HCVinfected subjects and controls.…”

Section: Discussionmentioning

confidence: 99%

“…Several reports have demonstrated that the serum levels of TNF␣ are increased in HCV-infected subjects compared with controls, 27,30,32 and have shown a correlation with IR, 31 and the histological severity of inflammation, 32 and fibrosis. [29][30][31] However, another study revealed no relationship between TNF␣ levels and the grading of steatosis or portal inflammation. 30 To date, no studies have assessed the relationship of serum IL6 to HCV-associated IR.…”

Section: Discussionmentioning

confidence: 99%

“…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.…”

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

et al. 2007

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The role of tumor necrosis factor ␣, interleukin 6, leptin, and adiponectin in the pathogenesis of hepatitis C virus (HCV)-associated insulin resistance (IR) remains controversial. We tested the hypothesis that these adipocytokines contribute to chronic HCV-associated IR and liver injury by first comparing their serum levels and homeostasis model assessment of insulin resistance (HOMA-IR) in 154 untreated, non-diabetic, HCV-infected male subjects with fibrosis stage 0-2, to that in 75 healthy volunteers matched for age, body mass index (BMI), and waist-hip ratio (WHR). We next examined whether the adipocytokine levels were associated with the extent of hepatic steatosis, portal/periportal inflammation and fibrosis in our total cohort of 240 HCVinfected male subjects. Significantly higher levels of HOMA-IR (2.12 versus 1.63, P ‫؍‬ 0.01), TNF␣ (1.28 versus 0.60 pg/ml, P < 0.001) and IL6 (2.42 versus 1.15 pg/ml, P ‫؍‬ 0.001) were noted in the HCV cohort compared with healthy controls respectively, but there were no significant differences in leptin and adiponectin concentrations. C hronic hepatitis C virus (HCV) infection is associated with the development of hepatic steatosis 1-5 and unique, virus-specific alterations in host metabolism leading to the development of insulin resistance (IR) and type 2 diabetes mellitus (T2DM). [6][7][8][9] We and others have shown that chronic HCV infection is associated with the development of IR in the absence of overt T2DM, irrespective of the presence or absence of cirrhosis. 6,10 Further, IR as assessed by the homeostasis model (HOMA-IR) 11 was independently associated with virally-mediated portal inflammation and an increased rate of fibrosis progression, indicating that IR is a cause rather than a consequence of hepatic fibrosis in HCV infection. 6 Despite recent recognition of the important role of IR in the progression of liver injury in HCV infection [12][13][14] and the response to antiviral therapy, 12,14,15 the mechanism of HCV-induced IR is not known. There is an abundance of literature to suggest that adipose tissue-derived cytokines (adipocytokines) may play a key role in the development of obesity-related IR. 16,17 TNF␣, IL6 and leptin are proinflammatory cytokines that can directly alter glucose and lipid metabolism. [16][17][18] In contrast, adiponectin, the most abundant of all the adipocytokines has an opposite effect, increasing insulin sensitivity [16][17][18] and having anti-steatotic, 19 anti-inflammatory 20 and antifibrotic effects. 21 In nonalcoholic fatty liver disease, it has been shown that serum levels of the various adipocyto-

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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

et al. 2007

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“…Rather, IR in CHC seems to be due to direct virus-specific effects on insulin signaling. Thus, initial studies noted increased serum levels of TNF-α in subjects with CHC [66][67][68] or showed a correlation with IR [69] but did not adequately correct for potential confounders. A later well-controlled study compared 154 HCV-infected non-diabetic males with 75 matched uninfected controls [65] .…”

Section: Inflammation and Irmentioning

confidence: 99%

Molecular mechanisms of insulin resistance in chronic hepatitis C

Douglas

George²

2009

WJG

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It is now widely recognized that chronic hepatitis C (CHC) is associated with insulin resistance (IR) and type 2 diabetes, so can be considered a metabolic disease. IR is most strongly associated with hepatitis C virus (HCV) genotype 1, in contrast to hepatic steatosis, which is associated with genotype 3 infection. Apart from the well-described complications of diabetes, IR in CHC predicts faster progression to fibrosis and cirrhosis that may culminate in liver failure and hepatocellular carcinoma. More recently, it has been recognized that IR in CHC predicts a poor response to antiviral therapy. The molecular mechanisms for the association between IR and HCV infection are not well defined. This review will elaborate on the clinical associations between CHC and IR and summarize current knowledge regarding the molecular mechanisms that potentially mediate HCV-associated IR.

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“…In patients with chronic hepatitis C, blood leptin levels correlate with the grade of fibrosis (12).…”

Section: Introductionmentioning

confidence: 99%

Relationship between the frequency of hepatitis B virus infections and levels of serum adipokines in patients with hepatosteatosis and insulin resistance

Balkan¹,

Gülşen²,

Balkan³

et al. 2017

Eur J Ther

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Objective:Although the steatogenic effect of hepatitis B virus (HBV) has been established in several studies, it is not yet known whether it leads to hepatosteatosis in anti-HBc IgG-positive patients. This study aimed to investigate the relationship between the frequency of HBV and levels of serum adipokines in patients with hepatosteatosis and insulin resistance. Methods: Eighty patients diagnosed with hepatosteatosis by ultrasonography, who were admitted to our polyclinic between July 2011 and June 2012 for various reasons, and who had insulin resistance were included. Homeostasis model assessment-insulin resistance of >2.7 was considered as insulin resistance, and these patients was investigated for anti-HBc IgG. The anti-HBc IgG level was analyzed by enzyme-linked immunosorbent assay. Levels of adiponectin, resistin, and leptin in serum samples were analyzed in anti-HBc IgG (+) and anti-HBc IgG (−) groups. Results: Anti-HBc IgG was positive in 29 (36.2%) patients and negative in 51 (63.8%). While the level of leptin in the anti-HBc IgG (+) group was 31569.72±14027.64 ng/mL, it was 25410.73±10978.26 ng/mL in the anti-HBc IgG (−) group. The levels of leptin in the anti-HBc IgG (+) and anti-HBc IgG (−) groups were statistically significant (p=0.047). However, levels of adiponectin and resistin were not different between the groups. Conclusion: These results suggest that anti-HBc IgG positivity is involved in the etiology of hepatosteatosis and insulin resistance as well.

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Leptin and TNF alpha levels in hepatitis C and its relationship withhepatic fibrosis

Cited by 42 publications

References 0 publications

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

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

Molecular mechanisms of insulin resistance in chronic hepatitis C

Relationship between the frequency of hepatitis B virus infections and levels of serum adipokines in patients with hepatosteatosis and insulin resistance

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