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Hepatic protein-tyrosine phosphatase 1B disruption and pharmacological
inhibition attenuate ethanol-induced oxidative stress and ameliorate alcoholic
liver disease in mice.
Authors Hsu MF, Koike S, Mello A, Nagy LE, Haj FG
Submitted By Submitted Externally on 9/28/2020
Status Published
Journal Redox biology
Year 2020
Date Published 9/1/2020
Volume : Pages 36 : 101658
PubMed Reference 32769011
Abstract Alcoholic liver disease (ALD) is a major health problem and a significant cause
of liver-related death. Currently, the mainstay for ALD therapy is alcohol
abstinence highlighting the need to develop pharmacotherapeutic approaches.
Protein-tyrosine phosphatase 1B (PTP1B) is an established regulator of hepatic
functions, but its role in ALD is mostly unexplored. In this study, we used mice
with liver-specific PTP1B disruption as well as pharmacological inhibition to
investigate the in vivo function of this phosphatase in ALD. We report
upregulation of hepatic PTP1B in the chronic plus binge mouse model and,
importantly, in liver biopsies of alcoholic hepatitis patients. Also, mice with
hepatic PTP1B disruption attenuated ethanol-induced injury, inflammation, and
steatosis compared with ethanol-fed control animals. Moreover, PTP1B deficiency
was associated with decreased ethanol-induced oxidative stress in vivo and ex
vivo. Further, pharmacological modulation of oxidative balance in hepatocytes
identified diminished oxidative stress as a contributor to the salutary effects
of PTP1B deficiency. Notably, PTP1B pharmacological inhibition elicited
beneficial effects and mitigated hepatic injury, inflammation, and steatosis
caused by ethanol feeding. In summary, these findings causally link hepatic
PTP1B and ALD and define a potential therapeutic target for the management of
this disease.


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