Katlyn R. Gabriel

TL;DR: Analysis of the transcriptome, lipidome, and genetic interactions of human leukemia cells exposed to palmitate revealed that changes in di-saturated glycerolipids, but not other lipid classes, are central to lipotoxicity in this model.

TL;DR: In this paper, the authors utilized genome-wide screening to identify genes that modulate lipid storage in macrophages, a cell type involved in metabolic diseases, and uncovered a paradigm for a lipid storage response in which binding of MLX transcription factors to LD surfaces adjusts the expression of metabolic genes to lipid storage levels.

TL;DR: It is suggested that hepatic DGat2 deficiency successfully reduces diet‐induced HS and supports development of DGAT2 inhibitors as a therapeutic strategy for treating NAFLD and preventing downstream consequences.

TL;DR: The LD-Portal as discussed by the authors allows users to query multiple datasets describing LD biology, including transcriptional profiles of induced lipid storage, organellar proteomics, genome-wide screen phenotypes, and ties to human genetics.

TL;DR: Dgat1 as well as lysosomal lipid metabolism contribute in vivo to homeostatic 1-OAC levels in an organ-specific manner, indicating tissue-specific mechanisms of regulation.