Niklas Mejhert

TL;DR: This work shows that FA re-esterification during adipocyte lipolysis is mediated by DGAT1, an ER-localized DGAT enzyme that functions to protect the ER from lipotoxic stress and related consequences, such as adipose tissue inflammation.

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: It is shown here that the p.L105P DGAT1 enzyme produced from the mutant allele is less abundant, resulting in partial loss of TG synthesis activity and decreased formation of lipid droplets in patient-derived primary dermal fibroblasts, in contrast with complete loss-of-function alleles of DGat1.

TL;DR: Becuwe et al. show that FIT2 is an acyl coenzyme A diphosphatase, and this activity is crucial for ER homeostasis and cellular lipid storage.