A link between protein translation and body weight.
Nutrient overload induces obesity, a primary risk factor for type 2 diabetes. Ribosomal biogenesis and protein synthesis, which are controlled by the mammalian target of rapamycin (mTOR), are primary energy-consuming processes in cells. mTOR phosphorylates and inactivates members of the eukaryotic translation initiation factor 4E-binding (eIF4E-binding) protein (4E-BP) family, which are translational repressors of 5' cap-dependent protein synthesis. In this issue of the JCI, Le Bacquer et al. report that simultaneous deletion of both 4E-BP1 and 4E-BP2 in mice results in insulin resistance, decreased energy expenditure, and increased adipogenesis (see the related article beginning on page 387). These findings link protein synthesis, insulin sensitivity, and body weight.
Rui
Liangyou
L
Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA. ruily@umich.edu
D000818:Animals; D001835:Body Weight / Q000502:physiology*; D002352:Carrier Proteins / Q000378:metabolism; D004734:Energy Metabolism; D039561:Eukaryotic Initiation Factor-4E / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D051379:Mice; D008954:Models, Biological; D014176:Protein Biosynthesis; D011494:Protein Kinases / Q000378:metabolism; D019893:Ribosomal Protein S6 Kinases / Q000378:metabolism; D058570:TOR Serine-Threonine Kinases
D002352:Carrier Proteins; D039561:Eukaryotic Initiation Factor-4E; D011494:Protein Kinases; C546842:MTOR protein, human; C546843:mTOR protein, mouse; D019893:Ribosomal Protein S6 Kinases; D058570:TOR Serine-Threonine Kinases; D005947:Glucose