Jacobs Journal of Internal Medicine

The Entero-Insular-Axis is retained in Patients with Alcoholic Liver Disease

*Christoph Elsing
Department Of Gastroenterology, University Clinic Heidelberg, Germany

*Corresponding Author:
Christoph Elsing
Department Of Gastroenterology, University Clinic Heidelberg, Germany
Email:dr.c.elsing@kkrn.de

Published on: 2016-07-05

Abstract

The incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are secreted after meals and are involved in the pathogenesis of different metabolic diseases, such as non alcoholic liver disease (NALD). GLP-1 agonists are in addition evaluated for the treatment of NALD. The role of incretins is the pathogenesis of alcoholic liver disease (ALD) is however unclear. We determined the secretion of incretins in patients with alcoholic liver disease after oral glucose administration. In 23 patients with alcoholic liver disease in the early withdrawn state and 19 control patients serum levels of total GIP, intact GLP-1, insulin and C-peptide were determined after an oral glucose load (75g glucose after an overnight fasting). In this function test, none of the investigated subjects showed a disturbance of glucose metabolism as indicated by the kinetic of serum glucose. There was a slight tendency for higher insulin resistance and lower insulin sensitivity in alcoholic patients (p = 0.0064). GLP-1 and GIP secretion after the oral stimulation was not different between the two groups, despite marked differences in liver function tests. We conclude that chronic alcohol abuse and alcoholic liver disease is not associated with a disturbed entero-insular axis, which might have influence on treatment options.

Keywords

Alcohol Dependence; Glp-1; Gip; Insulin Secretion; Oral Glucose Tolerance Test

Introduction

Alcohol consumption and abuse is common and in Germany it is estimated that approximately two million people are alcohol dependent. Alcoholic liver disease (ALD) is a major cause of morbidity and mortality in these patients. Approximately 40%-90% of patients with cirrhosis have a history of alcohol abuse and about one third of patients with hepatocellular carcinoma are attributable to alcoholic liver disease. The mechanisms for the development of ALD are multiple. Alcohol itself acts as a potential hepatotoxin with the development of liver disease depending on host factors, such as gender, polymorphism of alcohol-metabolizing enzymes, immunological factors and concomitant diseases like chronic hepatic viral infections, obesity, diabetes and nutritional deficiencies.