Role of Serum Dipeptidyle Peptidase IV (DDP IV) Activity in Development of Non – Alcoholic Steatohepatitis in Patients with Non-Alcoholic Fatty Liver Disease
Journal Title: International Journal of Medical Research Professionals - Year 2018, Vol 4, Issue 5
Abstract
Background: Nonalcoholic fatty liver disease (NAFLD) is defined as the abnormal accumulation of lipids, primarily in the form of triglycerides in individuals who do not consume significant amounts of alcohol (≤ 20 g ethanol/d). It is characterized by a spectrum of disease varying from simple steatosis through to steatohepatitis with fibrosis and scarring, which can lead to cirrhosis. Dipeptidyl peptidase-4 (DPP4), also known as adenosine deaminase complexing protein 2 or CD26 (cluster of differentiation 26) is a protein that, in humans, is encoded by the DPP4 gene. Aim of the work: To study the role of serum dipeptidyle peptidase IV activity in development and progression of simple steatosis to non-alcoholic steatohepatitis in patients with non-alcoholic fatty liver disease and its role in follow up the progression to chronic liver disease. Methods: This study was conducted as a case-control study in Internal Medicine Department of Ain Shams University Hospital and included 30 patients with non-alcoholic fatty liver (group I) and 30 patients with non-alcoholic steatohepatitis (group II) , 30 healthy individuals were taken as a control group (III). All cases are subjected to full history clinical examination full Lab., abdominal sonar and assessment of (DDP IV, CD26). Results: It is suggested that circulating DDP4 may play a role in the progression of non – alcoholic fatty liver disease (NAFLD) to non – alcoholic steatohepatitis because of its ability to differentiate simple steatosis from steatohepatitis. Conclusion: When NAFLD is induced by nutritional overload, hepatic inflammation enhances hepatic DPP4 expression. Accelerated degradation of GLP-1 by DPP4 inhibits insulin secretion and causes hyperglycemia. Hyperglycemia further enhances DPP4 expression, with further worsening in glucose metabolism. The increased hepatic expression of DPP4 in NAFLD patients suggests that DPP4 may be involved in the onset and/or progression of NAFLD. Hepatic inflammation may induce this phenomenon, although DPP4 causes deteriorations in systemic glucose metabolism.
Authors and Affiliations
Khaled Abd Elhamed Mohammed, Inas El Khedr Mohammed, Hany Haroun Kaiser, Khaled Rafik Elbaz, Hesham Drwesh
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