Asset Details
Do you wish to reserve the book?
GLUT1 overexpression enhances glucose metabolism and promotes neonatal heart regeneration
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
GLUT1 overexpression enhances glucose metabolism and promotes neonatal heart regeneration
Do you wish to request the book?
GLUT1 overexpression enhances glucose metabolism and promotes neonatal heart regeneration
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
GLUT1 overexpression enhances glucose metabolism and promotes neonatal heart regeneration
2021
Overview
The mammalian heart switches its main metabolic substrate from glucose to fatty acids shortly after birth. This metabolic switch coincides with the loss of regenerative capacity in the heart. However, it is unknown whether glucose metabolism regulates heart regeneration. Here, we report that glucose metabolism is a determinant of regenerative capacity in the neonatal mammalian heart. Cardiac-specific overexpression of Glut1, the embryonic form of constitutively active glucose transporter, resulted in an increase in glucose uptake and concomitant accumulation of glycogen storage in postnatal heart. Upon cryoinjury, Glut1 transgenic hearts showed higher regenerative capacity with less fibrosis than non-transgenic control hearts. Interestingly, flow cytometry analysis revealed two distinct populations of ventricular cardiomyocytes: Tnnt2-high and Tnnt2-low cardiomyocytes, the latter of which showed significantly higher mitotic activity in response to high intracellular glucose in Glut1 transgenic hearts. Metabolic profiling shows that Glut1-transgenic hearts have a significant increase in the glucose metabolites including nucleotides upon injury. Inhibition of the nucleotide biosynthesis abrogated the regenerative advantage of high intra-cardiomyocyte glucose level, suggesting that the glucose enhances the cardiomyocyte regeneration through the supply of nucleotides. Our data suggest that the increase in glucose metabolism promotes cardiac regeneration in neonatal mouse heart.
Publisher
Springer Science and Business Media LLC,Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 631/80
/ Animals
/ Animals, Newborn - physiology
/ Biomedical and Clinical Sciences
/ Cardiac
/ Embryos
/ Female
/ Fibrosis
/ Glucose
/ Glucose Transporter Type 1 - metabolism
/ Glucose Transporter Type 1 - physiology
/ Glycogen
/ Heart
/ Humanities and Social Sciences
/ Male
/ Mammals
/ Medicine
/ Mice
/ Myocytes
/ Myocytes, Cardiac - metabolism
/ Neonates
/ Newborn
/ Q
/ R
/ Science
