Glucagon like Peptide-1(GLP-1) a Novel Therapeutic Strategy in Non-Alcoholic Fatty Liver Disease (NAFLD)

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a main cause of liver disease and its global prevalence is estimated to be 24%. At present no approved medicines are available for NAFLD treatment. Glucagon-like peptide-1 (GLP-1) is a significant regulator of energy balance, show potential efficacy in the management of NAFLD. GLP-1 and GLP-1 receptor agonist (GLP-1RAs) are attractive options for the treatment of type 2 diabetes (T2D) since they efficiently reduce weight, HbA1C and blood glucose without having a risk of hypoglycaemia. This incretin hormone by normalizing of insulin resistance (IR), oxidative stress, lipid accumulation, lipotoxicity, and liver cell apoptosis is proposed for the management of NAFLD and nonalcoholic steatohepatitis (NASH) patient. Hence, the aim of this review was to discuss the useful effects of GLP-1, GLP-1 receptor agonist (GLP-1RAs) and dipeptidyl peptidase-4 (DPP-4) on NAFLD. In this paper we provided a new finding which highlighted the role of GLP-1 and GLP-1RAs in the treatment of NAFLD.

Probiotic and resveratrol normalize GLP-1 levels and oxidative stress in the intestine of diabetic rats

“…Our study also had some limitations. Firstly, due to rapid degradation of GLP-1 by DPP-4 in the blood circulation, this incretin has a very short half-life (less than 2 min) [ 10 ]. Hence, it was very low and non-significant among various groups in our measurements.…”

“…The clinical worth of GLP-1 is limited by its short half-life and its harmful effects on the gastrointestinal tract at a specific dose. Therefore, an effective approach to increase the therapeutic benefits of GLP-1-based therapy is pharmacological improvement [ 10 , 11 ]. Biochemical modification of these optimized molecules allows for less administration, which places a lower drug burden on the patient [ 12 ].…”

Antioxidative Potentials of Incretin‐Based Medications: A Review of Molecular Mechanisms

“…Lipotoxicity occurs in patients with diabetes, mainly referring to altered lipid metabolism leading to a higher production of toxic byproducts such as MDA, which is the primary marker of oxidative damage [ 105 ]. GLP-1 receptor activation can improve lipid metabolism and reduction of toxic metabolites [ 106 – 108 ]. They can exert these metabolic effects in several ways, such as peroxisome proliferator-activated receptor alpha (PPAR- α ) [ 109 ].…”