Beiroa Tarrío, DanielRomero Picó, AmparoLanga, CarmenBernabeu, CarmeloLópez Pérez, Miguel A.López Novoa, José M.Nogueiras Pozo, RubénDiéguez González, Carlos2020-05-012020-05-012013Beiroa D, Romero-Picó A, Langa C, Bernabeu C, López M, López-Novoa JM, et al. (2013) Heterozygous Deficiency of Endoglin Decreases Insulin and Hepatic Triglyceride Levels during High Fat Diet. PLoS ONE 8(1): e54591. https://doi.org/10.1371/journal.pone.0054591http://hdl.handle.net/10347/21951Endoglin is a transmembrane auxiliary receptor for transforming growth factor-beta (TGF-beta) that is predominantly expressed on proliferating endothelial cells. It plays a wide range of physiological roles but its importance on energy balance or insulin sensitivity has been unexplored. Endoglin deficient mice die during midgestation due to cardiovascular defects. Here we report for first time that heterozygous endoglin deficiency in mice decreases high fat diet-induced hepatic triglyceride content and insulin levels. Importantly, these effects are independent of changes in body weight or adiposity. At molecular level, we failed to detect relevant changes in the insulin signalling pathway at basal levels in liver, muscle or adipose tissues that could explain the insulin-dependent effect. However, we found decreased triglyceride content in the liver of endoglin heterozygous mice fed a high fat diet in comparison to their wild type littermates. Overall, our findings indicate that endoglin is a potentially important physiological mediator of insulin levels and hepatic lipid metabolism.eng© 2013 Beiroa et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditedhttps://creativecommons.org/licenses/by/3.0/journal article10.1371/journal.pone.00545911932-6203open access