bstract Glucagon-like peptide-1 receptor agonists (GLP-1RAs), initially developed for type 2 diabetes and obesity, have evolved into multi-organ potential therapeutics due to their pleiotropic effects beyond glycemic control. Mechanistically, GLP-1 signaling modulates immune and inflammatory pathways, regulates autophagy and pyroptosis, alleviates endoplasmic reticulum stress, and interacts ...
Long-acting glucagon-like peptide (GLP)-1 analogs are currently available in treating diabetes with widely established safety and extensively evaluated efficacy. In recent years, autophagy, as a critical lysosome-dependent self-degradative process to maintain homeostasis, has been shown to be involved in the vascular endothelium damage in diabetes. This level of plasma GLP-1 does not stimulate receptors on target organs due to its low concentration and short half-life. Conversely, a large meal, or post-bariatric surgery, will result in a higher level of endogenous GLP-1 that acts on both the vagal system and receptors on target organs. Whether postprandial endogenous intestinal GLP-1 can reach the brain to modulate food intake requires ... To overcome this limitation, various modifications and delivery strategies to enhance the pharmacokinetic properties and therapeutic efficacy of GLP-1 analogs have been studied. In our study, we hypothesized that liraglutide (LRG, a GLP-1RA representative drug) might regulate lipid metabolism and enhance autophagy to reduce hepatic steatosis. Here we provide a targeted synthesis of recent developments in the field of GLP-1 neurobiology, highlighting studies which have advanced our understanding of how GLP-1 signaling modulates eating, and identify open questions and future challenges we believe still need to be addressed to aid the prevention and/or treatment of obesity.
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