Upregulated hepatokine fetuin B aggravates myocardial ischemia/reperfusion injury through inhibiting insulin signaling in diabetic mice.

Journal of Molecular and Cellular Cardiology
Wenjuan XingHai-Feng Zhang

Abstract

Patients with type 2 diabetes mellitus (T2DM) are more susceptible to acute myocardial ischemia/reperfusion (MI/R) injury. However, the mechanism remains largely elusive. Clinical observation showed that high levels of hepatokine fetuin-B (FetB) in plasma are significantly associated with both diabetes and coronary artery diseases. This study was aimed to determine whether FetB mostly derived from liver exacerbates MI/R-induced injury and the underlying mechanisms in T2DM. Mice were given high-fat diet and streptozotocin to induce T2DM model and subjected to 30 min MI followed by reperfusion. Diabetes caused increased hepatic FetB expression and greater myocardial injury as evidenced by increased apoptosis and myocardial enzymes release following MI/R. In T2DM hearts, insulin-induced phosphorylations of insulin receptor substrate 1 at Tyr608 site and Akt at Ser473 site and glucose transporter 4 membrane translocation were markedly reduced. Interaction between FetB and insulin receptor-β subunit (IRβ) was enhanced assessed by immunoprecipitation analysis. More importantly, FetB knockdown via AAV9 alleviated MI/R injury and improved cardiac insulin-induced signaling in T2DM mice. Conversely, upregulation of FetB in normal mice ca...Continue Reading

References

Nov 1, 1992·BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology·W M BrownK M Dziegielewska
Oct 6, 1997·Lancet·H WangK J Tracey
Mar 29, 2005·American Journal of Physiology. Heart and Circulatory Physiology·Maria A PotenzaMonica Montagnani
Jul 10, 2008·JAMA : the Journal of the American Medical Association·Joachim H IxUNKNOWN Health ABC Study
Jul 18, 2008·Diabetes·Norbert StefanMatthias B Schulze
Nov 26, 2008·Circulation·Cornelia WeikertAndreas Fritsche
Jul 11, 2009·Apoptosis : an International Journal on Programmed Cell Death·Wenjuan XingFeng Gao
Nov 6, 2010·Cardiovascular Research·Qiujun YuXin L Ma
Jul 5, 2011·European Journal of Heart Failure·Antoine H Chaanine, Roger J Hajjar
Dec 25, 2012·Cardiovascular Research·Prasanth PuthanveetilBrian Rodrigues
Nov 20, 2015·Cardiovascular Diabetology·Tamás BaranyaiZoltán Giricz
Apr 2, 2016·Circulation Research·Christian Riehle, E Dale Abel
May 28, 2016·Circulation Research·Samuel T KeatingAssam El-Osta
Aug 4, 2016·Journal of Nuclear Cardiology : Official Publication of the American Society of Nuclear Cardiology·Paola Gargiulo, Pasquale Perrone-Filardi
Feb 12, 2017·Metabolism: Clinical and Experimental·Susan KralischThomas Ebert
Mar 8, 2017·Journal of Diabetes Investigation·Kyoichiro Tsuchiya, Yoshihiro Ogawa
Apr 25, 2017·Diabetes Research and Clinical Practice·K OgurtsovaL E Makaroff
Feb 1, 2019·Circulation·Emelia J BenjaminUNKNOWN American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee
Sep 2, 2019·Phytomedicine : International Journal of Phytotherapy and Phytopharmacology·Penghua FangLe Bu

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Citations

Sep 18, 2021·Frontiers in Physiology·Junfa XueLixin Xie

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