Time and metabolic state-dependent effects of GLP-1R agonists on NPY/AgRP and POMC neuronal activity in vivo.

Objective: Long-acting glucagon-like peptide-1 receptor agonists (GLP-1RAs), like liraglutide and semaglutide, are viable treatments for diabetes and obesity. Liraglutide directly activates hypothalamic proopiomelanocortin (POMC) neurons while indirectly inhibiting Neuropeptide Y/Agouti-related peptide (NPY/AgRP) neurons ex vivo. While temporal control of GLP-1R agonist concentration as well as accessibility to tissues/cells can be achieved with relative ease ex vivo, in vivo this is dependent upon the pharmacokinetics of these agonists and relative penetration into structures of interest.

Generation of sRAGE transgenic mice to study inflammaging.

The receptor for advanced glycation end products (RAGE) interacts with multiple ligands and transmits inflammatory signals from damage- and pathogen-associated molecular patterns (DAMPs and PAMPs) to cellular programs. RAGE shares ligands with another group of PRRs, Toll-like receptors. Such ligand-receptor promiscuity generates coordinated and complex signaling patterns that provide a basis for the development of multiple inflammaging diseases.

Mouse RAGE Variant 4 Is a Dominant Membrane Receptor that Does Not Shed to Generate Soluble RAGE.

The receptor for advanced glycation end products (RAGE) is a multi-ligand, immunoglobulin-like receptor that has been implicated in aging-associated diseases. Recent studies have demonstrated that both human and murine Ager genes undergo extensive alternative splicing that generates multiple putative transcripts encoding different receptor isoforms. Except for the soluble isoform (esRAGE), the majority of putative RAGE isoforms remain unstudied.

AGE-RAGE signal generates a specific NF-κB RelA "barcode" that directs collagen I expression.

Advanced glycation end products (AGEs) are sugar-modified biomolecules that accumulate in the body with advancing age, and are implicated in the development of multiple age-associated structural and functional abnormities and diseases. It has been well documented that AGEs signal via their receptor RAGE to activate several cellular programs including NF-κB, leading to inflammation. A large number of stimuli can activate NF-κB; yet different stimuli, or the same stimulus for NF-κB in different cellular settings, produce a very different transcriptional landscape and physiological outcome.

Different effects of omega-3 fatty acids on the cell cycle in C2C12 myoblast proliferation.

Polyunsaturated fatty acids (PUFAs) are important molecules for human health. We investigated the effects of three major omega-3 PUFAs on C2C12 myoblast proliferation. Both docosahexaenoic (DHA) and eicosapentaenoic (EPA) acids decreased cell growth, whereas linolenic (ALA) acid did not, compared with the control.