Food effect, also known as food-drug interactions, is a common phenomenon associated with orally administered medications and can be defined as changes in absorption rate or absorption extent. The mechanisms of food effect and their consequences can involve multiple factors, including human post-prandial physiology, properties of the drug, and how the drug is administered. Therefore, it is essential to have a thorough understanding of these mechanisms when recommending whether a specific drug should be taken with or without food. Food-drug interactions can be clinically relevant, especially when they must be avoided to prevent undesirable effects or exploited to optimize medication therapy. This review conducts a literature search that examined studies on food effect. We summarized the literature and identified and discussed common food effect mechanisms. Furthermore, we highlighted drugs that have a clinically significant food effect and discussed the corresponding mechanisms. In addition, this review analyzes the effects of high-fat food or standard meals on the oral drug absorption rate and absorption extent for 229 drugs based on the Biopharmaceutics Drug Disposition Classification System and demonstrates an association between Biopharmaceutics Drug Disposition Classification System class and food effect.

Tumorigenesis is commonly known as a complicated process, in which reactive oxygen species (ROS) plays a critical role to involve in signal transduction, metabolism, cell proliferation and differentiation. Previously, ribosomal protein L10 (RPL10) was suggested to possess extra-ribosomal functions in pancreatic cancer cells in addition to being proposed as a tumor suppressor or transcription co-regulator. To better understand the relationship between RPL10 and tumorigenic potential in pancreatic cancer cells, chromatin immunoprecipitation sequencing reveals that RPL10 is unlikely to be a transcription factor without a specific binding motif for gene transcription. Additionally, transcriptome analysis indicates that RPL10 could regulate the expression of proteins related to ROS production. Moreover, RPL10 in mitochondria is closely associated with the regulation of ROS level by affecting Complex I activity and the subsequent events. Together, the present study suggests that the regulation of ROS level by mitochondrial RPL10 is one of the major extra-ribosomal functions in pancreatic cancer cells, which could be used as an indicator for the tumorigenesis of pancreatic cancer.