Regenerative Potential Is a Trait of Mature Tissues, Not an Innate Feature of Newly Born Cells
By LabMedica International staff writers Posted on 25 Mar 2015 |
Image: The photo shows a mouse pancreatic islet as seen by light microscopy. Beta cells can be recognized by the green insulin staining. Glucagon is labeled in red and the nuclei in blue (Photo courtesy of Wikimedia Commons).
Diabetes researchers have found that the ability of insulin-producing beta cells to replicate and respond to elevated glucose concentrations is absent in very young animals and does not appear until after weaning.
Since the ability to regenerate tissue deteriorates with age, it was generally assumed that the younger the animal, the better it could compensate for damage tissues or organs.
Investigators at the Hebrew University of Jerusalem (Israel) examined the effect of young age on compensatory proliferation of pancreatic beta cells in vivo. Much to their surprise, they found that beta cells in suckling mice failed to enter the cell division cycle in response to a diabetes induced injury or increased glycolysis. However, when the mice were weaned to a high carbohydrate diet of pet chow—but not to a high fat diet that mimicked their mothers' milk—they developed the capacity for compensatory proliferation.
Weaning coincided with enhanced glucose-stimulated oxidative phosphorylation and insulin secretion from islets. Transcriptome analysis revealed that weaning increased the expression of genes involved in replication licensing, suggesting a mechanism for increased responsiveness to the mitogenic activity of high glucose. The investigators proposed in a paper published in the March 9, 2015, issue of the journal Developmental Cell that weaning triggered a discrete maturation step of beta cells that elevated both their mitogenic and secretory response to glucose. In light of these findings, the investigators will be searching for the exact molecular signal or pathway that triggered these events.
Senior author Dr. Yuval Dor, professor of developmental biology and cancer research at the Hebrew University of Jerusalem, said, “The data suggest that regenerative potential is a trait of mature tissues, which has to develop actively, similar to functional maturation, rather than an innate feature of newly born cells.”
Related Links:
Hebrew University of Jerusalem
Since the ability to regenerate tissue deteriorates with age, it was generally assumed that the younger the animal, the better it could compensate for damage tissues or organs.
Investigators at the Hebrew University of Jerusalem (Israel) examined the effect of young age on compensatory proliferation of pancreatic beta cells in vivo. Much to their surprise, they found that beta cells in suckling mice failed to enter the cell division cycle in response to a diabetes induced injury or increased glycolysis. However, when the mice were weaned to a high carbohydrate diet of pet chow—but not to a high fat diet that mimicked their mothers' milk—they developed the capacity for compensatory proliferation.
Weaning coincided with enhanced glucose-stimulated oxidative phosphorylation and insulin secretion from islets. Transcriptome analysis revealed that weaning increased the expression of genes involved in replication licensing, suggesting a mechanism for increased responsiveness to the mitogenic activity of high glucose. The investigators proposed in a paper published in the March 9, 2015, issue of the journal Developmental Cell that weaning triggered a discrete maturation step of beta cells that elevated both their mitogenic and secretory response to glucose. In light of these findings, the investigators will be searching for the exact molecular signal or pathway that triggered these events.
Senior author Dr. Yuval Dor, professor of developmental biology and cancer research at the Hebrew University of Jerusalem, said, “The data suggest that regenerative potential is a trait of mature tissues, which has to develop actively, similar to functional maturation, rather than an innate feature of newly born cells.”
Related Links:
Hebrew University of Jerusalem
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