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Proinflammatory Cytokines, Insulin Resistance, and Insulin Secretion in Chronic Hepatitis C Patients: A Case-Control Study

Response to Lecube et al.

¹ Services de Diabétologie et Endocrinologie, Centre Hospitalier Universitaire du Bocage, Dijon, France
² Services d’Hépatogastroenterologie, Centre Hospitalier Universitaire du Bocage, Dijon, France

Address correspondence to Jean Michel Petit, Services de Diabétologie et Endocrinologie, Centre Hospitalier Universitaire du Bocage, BP 77908, 21079 Dijon, France. E-mail: jean-michel.petit{at}chu-dijon.fr

We read with interest the article by Lecube et al. (1), which indicated that tumor necrosis factor (TNF)- is a mechanism by which hepatitis C virus (HCV)-infected patients are more prone to develop type 2 diabetes than patients with other chronic liver diseases. The mechanisms of the development of insulin resistance in patients with chronic HCV infection are not well understood. Insulin resistance in HCV-infected patients occurs already at an early stage in the course of HCV infection (2). Furthermore, although steatosis was more severe in patients infected with genotype 3, insulin resistance was associated with steatosis only in patients infected with genotype 1 (3).

Recently, we investigated the role of adipocytokines in HCV-related steatosis (4). Seventy-one chronic HCV patients were studied to assess the effects of adipocytokines on steatosis. We used an enzyme-linked immunosorbent assay to determine serum TNF receptors (TNF-R) I and II concentrations. Based on the findings in the study by Lecube et al. (1), we investigated whether plasma TNF-RI and TNF-RII concentrations were associated with parameters of insulin resistance in the 68 noncirrhotic subjects of this group of patients. Genotype distributions were as follows: genotype non-3, n = 55; genotype 3, n = 13.

TNF-RII and TNF-RI concentrations were correlated with homeostasis model assessment (r = 0.26, P = 0.02 and r = 0.20, P = 0.09, respectively). Homeostasis model assessment was significantly different in patients with genotype 3 than in patients with genotype non-3 (1.13 vs. 2.46; P = 0.01). There were no significant differences between the two groups for age, BMI, TNF-RI, and TNF-RII concentrations (genotype 3 versus non-3: TNF-RI = 1.64 vs 1.48 pg/ml, P = 0.32; TNF-RII = 3.79 vs. 3.41 pg/ml, P = 0.39).

Our results suggest that the HCV genotype must be included in further study evaluating insulin resistance in HCV-infected patients. Moreover, the lack of difference of TNF-R concentrations between subjects with HCV genotype 3 and non-3, despite a significant difference for homeostasis model assessment level, suggests that factors other than TNF- could be implicated in the development of insulin resistance during HCV chronic infection.

References

1. Lecube A, Hernandez C, Genesca J, Simo R: Proinflammatory cytokines, insulin resistance, and insulin secretion in chronic hepatitis C patients: a case-control study. Diabetes Care 29:1096–1101, 2006[Abstract/Free Full Text]
   
2. Petit JM, Bour JB, Galland-Jos C, Minello A, Verges B, Guiguet M, Brun JM, Hillon P: Risk factors for diabetes mellitus and early insulin resistance in chronic hepatitis C. J Hepatol 35:279–283, 2001[Medline]
   
3. Fartoux L, Poujol-Robert A, Guechot J, Wendum D, Poupon R, Serfaty L: Insulin resistance is a cause of steatosis and fibrosis progression in chronic hepatitis C. Gut 54:1003–1008, 2005[Abstract/Free Full Text]
   
4. Petit JM, Minello A, Jooste V, Bour JB, Galland F, Duvillard L, Verges B, Olsson NO, Gambert P, Hillon P: Decreased plasma adiponectin concentrations are closely related to steatosis in hepatitis C virus-infected patients. J Clin Endocrinol Metab 90:2240–2243, 2005[Abstract/Free Full Text]
   

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				R. Simo Proinflammatory Cytokines, Insulin Resistance, and Insulin Secretion in Chronic Hepatitis C Patients: A Case-Control Study: Response to Petit et al. Diabetes Care, September 1, 2006; 29(9): 2180 - 2181. [Full Text] [PDF]

This Article Extract Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Petit, J. M. Articles by Hillon, P. Search for Related Content PubMed PubMed Citation Articles by Petit, J. M. Articles by Hillon, P. Social Bookmarking                What's this?