Changes in food preferences and ingestive behaviors after glucagon-like peptide-1 analog treatment: techniques and opportunities.

BACKGROUND: Glucagon-like peptide-1 (GLP-1) analogs are approved for the treatment of obesity in adults and adolescents. Reports have emerged that the weight loss effect of these medications may be related to changes in food preferences and ingestive behaviors following the treatment. Understanding the mechanisms which impact ingestive behavior could expand opportunities to develop more refined and personalized treatment options for obesity. METHODS: Recent studies investigating the relationship between GLP-1 analogs and ingestive behaviors were retrieved from PubMed using the search terms: "obesity," "food preference," "taste," "ingestive behavior," "weight loss medication," "anti-obesity medication," "GLP-1 analog," "tirzepatide," "liraglutide," "semaglutide." Measurement tools were studied to compare variables used to assess food intake behavior. The main outcomes from each study were analyzed to evaluate the current standing and future directions of appetitive, ingestive, and consummatory behaviors and their association with GLP-1 analogs. RESULTS: Thus far, studies have primarily explored the weight loss phase and report decreased short-term appetite and food intake upon treatment. However, research during the weight maintenance phase and objective measurements of food intake are notably sparse. Additionally, verbal reports have been primarily used to examine food intake, which can be susceptible to subjectivity. CONCLUSIONS: Elucidating the relationship between GLP-1 analogs and ingestive behavior could reveal additional parameters which contribute to their anti-obesity effects. To better understand these mechanisms, it is imperative to consider objective measurements of food intake in future studies. Several measurement tools have been adapted to measure variables of food behavior in humans, and each must be carefully considered with their strengths and limitations to develop optimal investigations.

Gasdermin D kills bacteria.

The recognition of pathogen- or damage- associated molecular patterns (PAMPs/DAMPs) signals a series of coordinated responses as part of innate immunity or host cell defense during infection. The inflammasome is an assemblage of multiprotein complexes in the cytosol that activate inflammatory caspases and release pro-inflammatory mediators. This review examines the two-edged sword activity of gasdermin D (GSDMD). Since its discovery in 2015, GSDMD has played a crucial role in the programmed necrotic type of cell death called pyroptosis. Pyroptosis is an important response in host self-protection against danger signals and infection. Although excessive pyroptosis has a deleterious effect on the host, it proves to have a game-changing therapeutic application against pathogenic invasion when controlled. Here, we explore the mechanism utilized by GSDMD, the best studied member of the gasdermin protein family, in host immune defense against many bacteria. While the protein contributes to the clearance of some bacteria, we also discussed results from previous studies and research, that its presence might hinder effective immunity against other pathogens, thus aiding pathogenic invasion and spread.

Pyroptosis and pyroptosis-inducing cancer drugs.

Pyroptosis, an inflammatory form of lytic cell death, is a type of cell death mediated by the gasdermin (GSDM) protein family. Upon recognizing exogenous or endogenous signals, cells undergo inflammasome assembly, GSDM cleavage, the release of proinflammatory cytokines and other cellular contents, eventually leading to inflammatory cell death. In this review, we discuss the roles of the GSDM family for anti-cancer functions and various antitumor drugs that could activate the pyroptosis pathways.