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Energy Metabolism Couples Hepatocyte Integrin-linked Kinase to Liver
Glucoregulation and the Postabsorptive Response of Mice in an Age-dependent
Trefts E, Hughey CC, Lantier L, Lark DS, Boyd KL, Pozzi A, Zent R, Wasserman DH
Submitted Externally on 5/13/2019
American journal of physiology. Endocrinology and metabolism
Volume : Pages
Integrin-linked kinase (ILK) is a critical intracellular signaling node for
integrin receptors. Its role in liver development is complex as ILK deletion at
E10.5 (prior to hepatocyte differentiation) results in biochemical and
morphological differences that resolve as mice age. Nevertheless, mice with ILK
depleted specifically in hepatocytes are protected from hepatic insulin
resistance during obesity. Despite the potential importance of hepatocyte ILK to
metabolic health, it is unknown how ILK controls hepatic metabolism or
glucoregulation. The present study tested the role of ILK in hepatic metabolism
and glucoregulation by deleting it specifically in hepatocytes using a cre-lox
system that begins expression at E15.5 (after initiation of hepatocyte
differentiation). These mice develop the most severe morphological and
glucoregulatory abnormalities at 6 weeks, but these gradually resolve with age.
After identifying when the deletion of ILK caused a severe metabolic phenotype,
in depth studies were performed at this time point to define the metabolic
programs that coordinate control of glucoregulation that are regulated by ILK.
We show 6 week old ILK deficient mice have higher glucose tolerance and
decreased net glycogen synthesis. Additionally, ILK was shown to be necessary
for transcription of mitochondrial-related genes, oxidative metabolism, and
maintenance of cellular energy status. Thus, ILK is required for maintaining
hepatic transcriptional and metabolic programs that sustain oxidative
metabolism, which are required for hepatic maintenance of glucose homeostasis.
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Financial support for this work was provided by the NIDDK Mouse Metabolic Phenotyping Centers (National MMPC, RRID:SCR_008997,
) under the MICROMouse Program, grants DK076169.
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