Body's own hormone may be liver disease's worst foe
Spanish scientists have discovered healing properties inherent in a stomach hormone produced by the human body naturally. Known as ghrelin, the hormone has been shown to reduce liver fibrosis, oxidative stress and inflammation, and prevent acute liver damage. Details of the study are published in Hepatology, a journal of the American Association for the Study of Liver Diseases. The World Health Organization (WHO) estimates that over 2 billion people worldwide suffer from viral hepatitis, a condition of the liver caused by several factors such as alcohol and infection. Liver diseases include hepatitis viruses (commonly, type A, type B and type C), cirrhosis, and hepatocellular carcinoma (liver cancer). Sufferers of chronic liver disease are threatened by damage caused by fibrosis (liver scaring), which may result in liver failure and, eventually, in the need for a liver transplant. The WHO reports that 21,000 liver transplants were performed globally in 2005 - a small proportion of the many people on liver transplant waiting lists worldwide. Dr Ramón Bataller, part of the team involved in the study from Spain's Hospital Clinic of Barcelona, explained that there are currently no antifibrotic therapies on the market for patients with liver disease. 'Our aim was to determine if recombinant ghrelin could regulate the formation of fibrous tissue associated with chronic liver damage,' he said. Ghrelin is produced primarily in the stomach and is a growth hormone that is crucial for regulating appetite. Studies conducted in the past have shown that it also performs a protective role for the pancreas, heart, gastrointestinal tract, and other parts of the body. In the current study, the team conducted tests that showed that the hormone reduced the amount of fibrogenic cells in animal models by 25%. The researchers also analysed ghrelin serum levels in over 100 blood samples taken from patients with chronic hepatitis C, alcoholic hepatitis, and healthy controls, and found that the ghrelin serum levels in the 2 patient groups were significantly lower than the control. According to Dr Bataller, the researchers were able to 'demonstrate that recombinant ghrelin regulates the fibrogenic response of the liver to acute and chronic disease'. Their findings, he added, showed that ghrelin inhibited the development of fibrosis in both animal models and humans. In studies conducted on patients with anorexia, gastroparesis, cachexia, and chronic heart failure, ghrelin was found to cause only a mild decrease in blood pressure, and was overall well tolerated by the patients. The discovery may now lead to novel fibrosis therapy, signalling a significant step forward in the fight against liver disease. In their paper, the authors noted that subsequent studies need to be conducted into the safety and efficacy of ghrelin in patients with chronic liver disease.
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Spain, United States