Weaning triggers a maturation step of pancreatic β cells
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Weaning triggers a maturation step of pancreatic β cells. / Stolovich-Rain, Miri; Enk, Jonatan; Vikesa, Jonas; Nielsen, Finn Cilius; Saada, Ann; Glaser, Benjamin; Dor, Yuval.
In: Developmental Cell, Vol. 32, No. 5, 09.03.2015, p. 535-45.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Weaning triggers a maturation step of pancreatic β cells
AU - Stolovich-Rain, Miri
AU - Enk, Jonatan
AU - Vikesa, Jonas
AU - Nielsen, Finn Cilius
AU - Saada, Ann
AU - Glaser, Benjamin
AU - Dor, Yuval
N1 - Copyright © 2015 Elsevier Inc. All rights reserved.
PY - 2015/3/9
Y1 - 2015/3/9
N2 - Because tissue regeneration deteriorates with age, it is generally assumed that the younger the animal, the better it compensates for tissue damage. We have examined the effect of young age on compensatory proliferation of pancreatic β cells in vivo. Surprisingly, β cells in suckling mice fail to enter the cell division cycle in response to a diabetogenic injury or increased glycolysis. The potential of β cells for compensatory proliferation is acquired following premature weaning to normal chow, but not to a diet mimicking maternal milk. In addition, weaning coincides with enhanced glucose-stimulated oxidative phosphorylation and insulin secretion from islets. Transcriptome analysis reveals that weaning increases the expression of genes involved in replication licensing, suggesting a mechanism for increased responsiveness to the mitogenic activity of high glucose. We propose that weaning triggers a discrete maturation step of β cells, elevating both the mitogenic and secretory response to glucose.
AB - Because tissue regeneration deteriorates with age, it is generally assumed that the younger the animal, the better it compensates for tissue damage. We have examined the effect of young age on compensatory proliferation of pancreatic β cells in vivo. Surprisingly, β cells in suckling mice fail to enter the cell division cycle in response to a diabetogenic injury or increased glycolysis. The potential of β cells for compensatory proliferation is acquired following premature weaning to normal chow, but not to a diet mimicking maternal milk. In addition, weaning coincides with enhanced glucose-stimulated oxidative phosphorylation and insulin secretion from islets. Transcriptome analysis reveals that weaning increases the expression of genes involved in replication licensing, suggesting a mechanism for increased responsiveness to the mitogenic activity of high glucose. We propose that weaning triggers a discrete maturation step of β cells, elevating both the mitogenic and secretory response to glucose.
KW - Animals
KW - Apoptosis
KW - Biomarkers
KW - Blotting, Western
KW - Cell Proliferation
KW - Cells, Cultured
KW - Female
KW - Gene Expression Profiling
KW - Glucose
KW - Hypoglycemic Agents
KW - Immunoenzyme Techniques
KW - Insulin
KW - Insulin-Secreting Cells
KW - Islets of Langerhans
KW - Male
KW - Mice
KW - Mice, Inbred ICR
KW - Mice, Transgenic
KW - Oligonucleotide Array Sequence Analysis
KW - RNA, Messenger
KW - Real-Time Polymerase Chain Reaction
KW - Reverse Transcriptase Polymerase Chain Reaction
KW - Weaning
U2 - 10.1016/j.devcel.2015.01.002
DO - 10.1016/j.devcel.2015.01.002
M3 - Journal article
C2 - 25662175
VL - 32
SP - 535
EP - 545
JO - Developmental Cell
JF - Developmental Cell
SN - 1534-5807
IS - 5
ER -
ID: 162858727