GLP-1 and Underlying Beneficial Actions in Alzheimer's Disease, Hypertension, and NASH

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). Howe...

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Published in:Frontiers in endocrinology (Lausanne) 2021-09, Vol.12, p.721198-721198
Main Authors: Li, Qiu-Xuan, Gao, Han, Guo, Yue-Xin, Wang, Bo-Ya, Hua, Rong-Xuan, Gao, Lei, Shang, Hong-Wei, Lu, Xin, Xu, Jing-Dong
Format: Article
Language:English
Subjects:
Alzheimer Disease - etiology
Alzheimer Disease - pathology
Alzheimer Disease - therapy
Alzheimer’s disease
Animals
blood pressure
DPP-4
Endocrinology
GLP-1
Glucagon-Like Peptide 1 - analogs & derivatives
Glucagon-Like Peptide 1 - pharmacology
Glucagon-Like Peptide 1 - physiology
Humans
Hypertension - etiology
Hypertension - pathology
Hypertension - therapy
Incretins - metabolism
Metabolic Networks and Pathways - drug effects
Non-alcoholic Fatty Liver Disease - etiology
Non-alcoholic Fatty Liver Disease - pathology
Non-alcoholic Fatty Liver Disease - therapy
non-alcoholic steatohepatitis
signaling pathway
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Summary: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.
ISSN:1664-2392
1664-2392
DOI:10.3389/fendo.2021.721198