Abstract
GLP-1 is derived from intestinal L cells, which takes effect through binding to GLP-1R and is inactivated by the enzyme dipeptidyl peptidase-4 (DPP-4). Since its discovery, GLP-1 has emerged as an incretin hormone for its facilitation in insulin release and reduction of insulin resistance (IR). However, GLP-1 possesses broader pharmacological effects including anti-inflammation, neuro-protection, regulating blood pressure (BP), and reducing lipotoxicity. These effects are interconnected to the physiological and pathological processes of Alzheimer’s disease (AD), hypertension, and non-alcoholic steatohepatitis (NASH). Currently, the underlying mechanism of these effects is still not fully illustrated and a better understanding of them may help identify promising therapeutic targets of AD, hypertension, and NASH. Therefore, we focus on the biological characteristics of GLP-1, render an overview of the mechanism of GLP-1 effects in diseases, and investigate the potential of GLP-1 analogues for the treatment of related diseases in this review.
Highlights
With the assistance of prediction and decipherment of recombinant cDNA clones, it has been claimed that the anglerfish preproglucagon cDNA encodes a different glucagonrelated peptide [1,2,3]
It is possible that the difference in injection speed and physiological status could account for these opposite blood pressure (BP) alterations which were induced by GLP-1 and GLP-1R agonists
Based on the findings above, this review focuses on the biological characteristics and the underlying mechanistic effects of GLP-1 in AD, BP, and non-alcoholic steatohepatitis (NASH)
Summary
With the assistance of prediction and decipherment of recombinant cDNA clones, it has been claimed that the anglerfish preproglucagon cDNA encodes a different glucagonrelated peptide [1,2,3]. The use of GLP-1 analogues LG and Exendin-4 effectively reduced both their weight and liver fat in NASH patients [19]. The anorectic effects of IP injection of LG and exendin-4 were attenuated by subdiaphragmatic vagal deafferentation in rats, indicating that peripheral GLP-1 could inhibit food intake.
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