Insulin signaling requires glucose to promote lipid anabolism in adipocytes
James R Krycer, Lake-Ee Quek, Deanne Francis, Armella Zadoorian, Fiona C Weiss, Kristen C Cooke, Marin E Nelson, Alexis Diaz-Vegas, Sean J Humphrey, Richard Scalzo, Akiyoshi Hirayama, Satsuki Ikeda, Futaba Shoji, Kumi Suzuki, Kevin Huynh, Corey Giles, Bianca Varney, Shilpa R Nagarajan, Andrew J Hoy, Tomoyoshi Soga Show all
Journal of Biological Chemistry | AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC | Published : 2020
Adipose tissue is essential for metabolic homeostasis, balancing lipid storage and mobilization based on nutritional status. This is coordinated by insulin, which triggers kinase signaling cascades to modulate numerous metabolic proteins, leading to increased glucose uptake and anabolic processes like lipogenesis. Given recent evidence that glucose is dispensable for adipocyte respiration, we sought to test whether glucose is necessary for insulin-stimulated anabolism. Examining lipogenesis in cultured adipocytes, glucose was essential for insulin to stimulate the synthesis of fatty acids and glyceride-glycerol. Importantly, glucose was dispensable for lipogenesis in the absence of insulin, ..View full abstract
Awarded by National Health and Medical Research Council
Awarded by National Health and Medical Research Council Early Career Fellowship
D. E. J. was supported by Senior Principal Research Fellowship APP1019680 and Project Grants GNT1061122 and GNT1086851 from the National Health and Medical Research Council. G. J. C. was supported by a Professorial Research Fellowship from the University of Sydney Medical School. D. E. J. and G. J. C. were also supported by National Health and Medical Research Council Project Grant GNT1086850. J. R. K. was supported by National Health and Medical Research Council Early Career Fellowship APP1072440, an Australian Diabetes Society Skip Martin Early-Career Fellowship, a Diabetes Australia Research Program grant, and a Charles Perkins Centre EarlyCareer Seed Funding Grant. D. F. was funded by a Diabetes Australia Research Program Grant and Charles Perkins Centre EarlyCareer Seed Funding Grant. A. H. was funded by the Research on Development of New Drugs (GAPFREE) from the Japan Agency for Medical Research and Development (AMED). T. S. was funded by the AMED-CREST from AMED. A. H. and T. S. were supported by funds from the Yamagata prefectural government and the City of Tsuruoka.