The Relationship of Resistin with Disease Severity, Inflammation and Insulin Resistance in Cirrhosis Patients

Abstract

Introduction: Glucose intolerance has been shown to play an important role in the progression of early liver disease to cirrhosis. It has been suggested that insulin resistance is responsible for glucose intolerance in patients with chronic liver disease. It is thought that increased resistin through chronic inflammation in chronic liver disease may be responsible for insulin resistance. In our study, we aimed to evaluate the relationship of resistin which is released from adipose tissue with insulin resistance, inflammation markers and disease stage in patients with cirrhosis. Methods: Forty-six patients diagnosed with cirrhosis in Eskişehir Osmangazi University Faculty of Medicine, Department of Gastroenterology between March 2008 and July 2009, and 19 healthy individuals as a control group were included in the study. Patients with a diagnosis of Diabetes Mellitus, other endocrine disease or Hepatocellular Carcinoma, with fasting blood glucose above 126 mg/dl and using drugs that may affect glucose metabolism were excluded from the study. Participants with obesity were determined by skinfold thickness (biceps, triceps, suprailiac and subscapular) measurement. Statistical analyzes were performed by excluding obese patients from the study and control groups. AssayMax Human Resistin ELISA Kit was used to determine serum resistin level. The "Homaostatic Model for Insulin Resistance" (HOMA-IR) formula was used to detect insulin resistance. The studied parameters were statistically compared between the study and control groups and also between the three groups (Child Pugh stage A, B and C) formed according to the disease stage in the study group. Results: All laboratory parameters reflecting insulin resistance, inflammation markers and resistin levels were found to be significantly higher in the study group. As the Child Pugh stage advances, which is used to determine the severity and prognosis of the disease, resistin levels found higher, but it was observed that the rate of patients with decreased insulin resistance had lower levels in total fat ratio. No significant correlation was found between resistin and other markers of insulin resistance except fasting insulin level. Conclusion: In the future metabolism studies which to be performed in patients with cirrhosis detection of skinfold thickness may be useful in determining body fat ratio. Insulin resistance markers are significantly higher in patients with cirrhosis, as disease severity advances resistin levels increases. We are in the opinion that resistin does not contribute to the development of insulin resistance, which occurs with different mechanisms in patients with cirrhosis.