© 2002 by the American Diabetes Association, Inc.
Response to ÖncülInsulin sensitivity in patients with chronic hepatitis C virus infection1 From the First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan We read with great interest the recent letter from Öncül et al. (1) reporting the correlation of serum leptin levels with insulin sensitivity in patients with chronic hepatitis C virus (HCV) infection. Their findings showed that fasting serum insulin levels and serum leptin levels were significantly elevated in patients with chronic HCV infection compared with control subjects and that fasting serum leptin and insulin levels and homeostasis model assessmentestimated insulin sensitivity were correlated in the whole group. Öncül et al. concluded that HCV infection may serve as an additional risk factor for the development of type 2 diabetes due to insulin resistance and hyperleptinemia. Certainly, insulin resistance plays an important role for the development of type 2 diabetes in patients with chronic HCV infection because levels of fasting serum C-peptide were significantly more elevated in noninsulin-treated diabetic patients with (n = 18) than in those without (n = 72) HCV infection (0.73 ± 0.27 vs. 0.57 ± 0.27 nmol/l; P = 0.0321) who were matched by BMI. The authors should show the correlation of serum leptin levels with insulin sensitivity not in the whole group but only in patients with chronic HCV infection, and should exclude the effect of BMI to demonstrate the correlation of serum leptin levels with insulin sensitivity in patients with chronic HCV infection. Conversely, elevated levels of serum leptin and insulin resistance might be correlated regardless of HCV infection (2). Contrary to the conclusion by Öncül et al., that HCV infection may serve as an additional risk factor for the development of type 2 diabetes due to insulin resistance and hyperleptinemia, there are some reports that leptin reverses insulin resistance (3,4). Elevated levels of serum leptin in patients with chronic HCV infection were compatible with previous data (5), although the reason was not fully determined. The mechanism of insulin resistance in patients with chronic HCV infection may be due to decreased liver carbohydrate metabolism and hypersecretion of insulin-resistant cytokines, such as interleukin-6 (6) and tumor necrosis factor (7), which have been shown to be elevated in patients with chronic HCV infection, most likely as a result of HCV-induced inflammation (8,9). Footnotes Address correspondence to Michiaki Fukui, First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto 602-8566, Japan. E-mail: sayarinapm{at}hotmail.com. References
This article has been cited by other articles:
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||