TY - JOUR
T1 - Heparan sulfate in pancreatic β-cells contributes to normal glucose homeostasis by regulating insulin secretion
AU - Matsuzawa, Takuro
AU - Yoshikawa, Takeo
AU - Iida, Tomomitsu
AU - Kárpáti, Anikó
AU - Kitano, Haruna
AU - Harada, Ryuichi
AU - Nakamura, Tadaho
AU - Sugawara, Akira
AU - Yamaguchi, Yu
AU - Yanai, Kazuhiko
N1 - Funding Information:
This study was supported by Anzai Diabetes Memorial Research Fund , Japan and by the Tohoku University Division For Interdisciplinary Advanced Research . Ins1 - Cre mouse strain (RBRC03934) was provided by Dr. Ken-ichi Yagami at Tsukuba University through the National Bio-Resource Project of the MEXT, Japan. We also acknowledge the support of the Biomedical Research Core of Tohoku University Graduate School of Medicine and the Biomedical Research unit of Tohoku University Hospital .
PY - 2018/5/15
Y1 - 2018/5/15
N2 - Heparan sulfate (HS), a linear polysaccharide, is involved in diverse biological functions of various tissues. HS is expressed in pancreatic β-cells and may be involved in β-cell functions. However, the importance of HS for β-cell function remains unknown. Here, we generated mice with β-cell-specific deletion of Ext1 (βExt1CKO), which encodes an enzyme essential for HS synthesis, to investigate the detailed roles of HS in β-cell function. βExt1CKO mice decreased body weights compared with control mice, despite increased food intake. Additionally, βExt1CKO mice showed impaired glucose tolerance associated with decreased insulin secretion upon glucose challenge. Glucose-induced insulin secretion (GIIS) from isolated βExt1CKO islets was also significantly reduced, highlighting the contribution of HS to insulin secretion and glucose homeostasis. The gene expression essential for GIIS was decreased in βExt1CKO islets. Pdx1 and MafA were downregulated in βExt1CKO islets, indicating that HS promoted β-cell development and maturation. BrdU- or Ki67-positive β-cells were reduced in βExt1CKO pancreatic sections, suggesting the involvement of HS in the proliferation of β-cells. Moreover, insufficient vascularization in βExt1CKO islets may contribute to central distribution of α-cells. These data demonstrate HS plays diverse roles in β-cells, and that loss of HS leads to insufficient insulin secretion and dysregulation of glucose homeostasis.
AB - Heparan sulfate (HS), a linear polysaccharide, is involved in diverse biological functions of various tissues. HS is expressed in pancreatic β-cells and may be involved in β-cell functions. However, the importance of HS for β-cell function remains unknown. Here, we generated mice with β-cell-specific deletion of Ext1 (βExt1CKO), which encodes an enzyme essential for HS synthesis, to investigate the detailed roles of HS in β-cell function. βExt1CKO mice decreased body weights compared with control mice, despite increased food intake. Additionally, βExt1CKO mice showed impaired glucose tolerance associated with decreased insulin secretion upon glucose challenge. Glucose-induced insulin secretion (GIIS) from isolated βExt1CKO islets was also significantly reduced, highlighting the contribution of HS to insulin secretion and glucose homeostasis. The gene expression essential for GIIS was decreased in βExt1CKO islets. Pdx1 and MafA were downregulated in βExt1CKO islets, indicating that HS promoted β-cell development and maturation. BrdU- or Ki67-positive β-cells were reduced in βExt1CKO pancreatic sections, suggesting the involvement of HS in the proliferation of β-cells. Moreover, insufficient vascularization in βExt1CKO islets may contribute to central distribution of α-cells. These data demonstrate HS plays diverse roles in β-cells, and that loss of HS leads to insufficient insulin secretion and dysregulation of glucose homeostasis.
KW - Exostosin1
KW - Heparan sulfate
KW - Insulin secretion
KW - Pancreatic β-cell
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U2 - 10.1016/j.bbrc.2018.03.213
DO - 10.1016/j.bbrc.2018.03.213
M3 - Article
C2 - 29605295
AN - SCOPUS:85044789513
VL - 499
SP - 688
EP - 695
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 3
ER -