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Adipocyte JAK2 Regulates Hepatic Insulin Sensitivity Independently of Body
Composition, Liver Lipid Content, and Hepatic Insulin Signaling.
Authors Corbit KC, Camporez JPG, Edmunds LR, Tran JL, Vera NB, Erion DM, Deo RC, Perry
RJ, Shulman GI, Jurczak MJ, Weiss EJ
Submitted By Submitted Externally on 2/19/2018
Status Published
Journal Diabetes
Year 2018
Date Published 2/1/2018
Volume : Pages 67 : 208 - 221
PubMed Reference 29203511
Abstract Disruption of hepatocyte growth hormone (GH) signaling through disruption
ofJak2(JAK2L) leads to fatty liver. Previously, we demonstrated that development
of fatty liver depends on adipocyte GH signaling. We sought to determine the
individual roles of hepatocyte and adipocyteJak2on whole-body and tissue insulin
sensitivity and liver metabolism. On chow, JAK2L mice had hepatic steatosis and
severe whole-body and hepatic insulin resistance. However, concomitant deletion
ofJak2in hepatocytes and adipocytes (JAK2LA) completely normalized insulin
sensitivity while reducing liver lipid content. On high-fat diet, JAK2L mice had
hepatic steatosis and insulin resistance despite protection from diet-induced
obesity. JAK2LA mice had higher liver lipid content and no protection from
obesity but retained exquisite hepatic insulin sensitivity. AKT activity was
selectively attenuated in JAK2L adipose tissue, whereas hepatic insulin
signaling remained intact despite profound hepatic insulin resistance.
Therefore, JAK2 in adipose tissue is epistatic to liver with regard to insulin
sensitivity and responsiveness, despite fatty liver and obesity. However,
hepatocyte autonomous JAK2 signaling regulates liver lipid deposition under
conditions of excess dietary fat. This work demonstrates how various tissues
integrate JAK2 signals to regulate insulin/glucose and lipid metabolism.


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