Trindade, SandraRijo-Ferreira, FilipaCarvalho, TâniaNeves, DanielGuegan, Fabien MarcAresta-Branco, FranciscoBento, FabioYoung, Simon A.Pinto, AndreiaVan Den Abbeele, JanRibeiro, Ruy M.Dias, SérgioSmith, Terry K.Figueiredo, Luisa M.2020-12-032020-12-032016Cell Host Microbe. 2016 Jun 8; 19 (6): 837-481931-3128http://hdl.handle.net/10451/45123© 2016 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/)Trypanosoma brucei is an extracellular parasite that causes sleeping sickness. In mammalian hosts, trypanosomes are thought to exist in two major niches: early in infection, they populate the blood; later, they breach the blood-brain barrier. Working with a well-established mouse model, we discovered that adipose tissue constitutes a third major reservoir for T. brucei. Parasites from adipose tissue, here termed adipose tissue forms (ATFs), can replicate and were capable of infecting a naive animal. ATFs were transcriptionally distinct from bloodstream forms, and the genes upregulated included putative fatty acid β-oxidation enzymes. Consistent with this, ATFs were able to utilize exogenous myristate and form β-oxidation intermediates, suggesting that ATF parasites can use fatty acids as an external carbon source. These findings identify the adipose tissue as a niche for T. brucei during its mammalian life cycle and could potentially explain the weight loss associated with sleeping sickness.engAfrican trypanosomesFatFatty acid β-oxidationMetabolismMouse infectionTranscriptomejournal article10.1016/j.chom.2016.05.0021934-6069