Journal article

RABL2 is required for hepatic fatty acid homeostasis and its dysfunction leads to steatosis and a diabetes-like state

JCY Lo, AE O'Connor, ZB Andrews, C Lo, T Tiganis, MJ Watt, MK O'Bryan

Endocrinology | ENDOCRINE SOC | Published : 2016

Abstract

Fatty liver, or hepatic steatosis, is an alarmingly common pathology in western societies, in large part because if left unheeded, it can lead to life-threatening forms of nonalcoholic fatty liver disease, including nonalcoholic steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. As such, it is essential that we attain a greater understanding of the pathways that control energy partitioning in the liver and ultimately how they are impacted by environmental factors. Here, we define the essential requirement for a member of the Ras-related protein in the brain (RAB)-like (RABL) clade of small GTPases, RABL2, in fatty acid metabolism including in microtubule-associated mitochond..

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Grants

Awarded by National Health and Medical Research Council (NHMRC)


Awarded by NHMRC


Funding Acknowledgements

This work was supported by the National Health and Medical Research Council (NHMRC) Grant 606445 (to M.K.O.), a NHMRC PhD scholarship (J.C.Y.L.), the NHMRC Principal Research Fellowship APP1058356 (to M.K.O.), the NHMRC Senior Research Fellowship APP1077703 (to M.J.W.), the NHMRC Career Development Fellowship APP1084344 (to Z.B.A.), and the NHMRC Principal Research Fellowship APP1002693 (to T.T.).