Serum Level of Omentin-1 in Hepatitis C Decompensated Liver Disease with and without Diabetes Mellitus

Abstract

SUMMARY L iver is one of the largest organs of the body. The liver performs many essential functions related to digestion, metabolism, immunity, and the storage of nutrients within the body. These functions make the liver a vital organ without which the tissues of the body would quickly die from lack of energy and nutrients. Viral hepatitis is liver inflammation due to a viral infection. It may present in acute or chronic forms. The most common causes of chronic viral hepatitis are virus B and virus C. Hepatitis C (originally "non-A non-B hepatitis") is caused by hepatitis C virus (HCV), an RNA virus that is a member of the Flaviviridae family. HCV can be transmitted through blood transfusion, sexual contact and can also cross the placenta. Hepatitis C usually leads to chronic hepatitis and cirrhosis in some people. Cirrhosis is a slowly progressing disease in which healthy liver tissue is replaced with a new fibrous tissue, eventually preventing the liver from functioning properly. Decompensated liver disease is a late stage of liver disease in which complications are obvious on the patients. Chronic liver diseases can induce developing of insulin resistance. Chronic hepatitis C have been demonstrated to induce insulin resistance as proved by numerous epidemiological studies. Chronic hepatitis C induced insulin resistance can aggravate advancement of liver fibrosis, resistance to antiviral treatment and hepatocellular carcinoma. Omentin is a recently demonstrated secretory protein that is highly expressed in visceral fatty tissue with respect to subcutaneous fatty tissue. Omentin-1 may act as an endocrine factor affecting muscles, liver and omental adipose tissue. It can enhance insulin sensitivity and glucose metabolism. Circulating omentin-1 level has been found to be negatively correlated with insulin resistance. Recently, serum omentin-1 represents an independent predictor for hepatocyte ballooning. From this point we designed our study to detect the relationship between circulating level of omentin-1 and diabetes mellitus (insulin resistance) in decompensated liver disease patients. All patients underwent history taking and clinical examination. Laboratory investigations were done including AST, ALT, bilirubin(total and direct), PT, albumin, fasting blood sugar,HbA1c,CBC and serum creatinine. Radiological examination included abdominal ultrasound. Serum omentin, body weight and BMI were measured for both patients and controls. Child pugh score was applied on patients with liver disease. Data were collected, tabulated and statistical analysis was done and revealed that, as general: Omentin-1 was inversely correlated with diabetes mellitus even in patients with decompensated liver disease. Omentin-1level was higher in patienrs with liver cirrhosis than controls. We recorded, level of omentin-1 was higher in patients with HCV (60.0–193.0 pg/ml with Mean ± SD c124.9±42.8) than controls (16.0–42.2 pg/ml with Mean ± SD a31.1±7.3). We recorded, level of omentin-1 was lower in patients with HCV+DM (37.0–92.0 pg/ml with Mean ± SD d54.6±14.3) than in patients with HCV without DM, however, it is higher than controls.