Abstract
One significant health issue that plagues contemporary society is that of Type 2 diabetes (T2D). This disease is characterised by higher-than-average blood glucose levels as a result of a combination of insulin resistance and insufficient insulin secretions from the β-cells of pancreatic islets of Langerhans. Previous developmental research into the pancreas has identified how early precursor genes of pancreatic β-cells, such as Cpal, Ngn3, NeuroD, Ptf1a, and cMyc, play an essential role in the differentiation of these cells. Furthermore, β-cell molecular characterization has also revealed the specific role of β-cell-markers, such as Glut2, MafA, Ins1, Ins2, and Pdx1 in insulin expression. The expression of these genes appears to be suppressed in the T2D β-cells, along with the reappearance of the early endocrine marker genes. Glucose transporters transport glucose into β-cells, thereby controlling insulin release during hyperglycaemia. This stimulates glycolysis through rises in intracellular calcium (a process enhanced by vitamin D) (Norman et al., 1980), activating 2 of 4 proteinases. The rise in calcium activates half of pancreatic β-cell proinsulinases, thus releasing free insulin from granules. The synthesis of ATP from glucose by glycolysis, Krebs cycle and oxidative phosphorylation plays a role in insulin release. Some studies have found that the β-cells contain high levels of the vitamin D receptor; however, the role that this plays in maintaining the maturity of the β-cells remains unknown. Further research is required to develop a more in-depth understanding of the role VDR plays in β-cell function and the processes by which the beta cell function is preserved.
| Original language | English |
|---|---|
| Pages (from-to) | 429-443 |
| Number of pages | 15 |
| Journal | Journal of Diabetes and Its Complications |
| Volume | 32 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - 1 Apr 2018 |
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An overview of type 2 diabetes and importance of vitamin D3-vitamin D receptor interaction in pancreatic β-cells. / Neelankal John, Abraham; Jiang, Fang Xu.
In: Journal of Diabetes and Its Complications, Vol. 32, No. 4, 01.04.2018, p. 429-443.Research output: Contribution to journal › Review article
TY - JOUR
T1 - An overview of type 2 diabetes and importance of vitamin D3-vitamin D receptor interaction in pancreatic β-cells
AU - Neelankal John, Abraham
AU - Jiang, Fang Xu
PY - 2018/4/1
Y1 - 2018/4/1
N2 - One significant health issue that plagues contemporary society is that of Type 2 diabetes (T2D). This disease is characterised by higher-than-average blood glucose levels as a result of a combination of insulin resistance and insufficient insulin secretions from the β-cells of pancreatic islets of Langerhans. Previous developmental research into the pancreas has identified how early precursor genes of pancreatic β-cells, such as Cpal, Ngn3, NeuroD, Ptf1a, and cMyc, play an essential role in the differentiation of these cells. Furthermore, β-cell molecular characterization has also revealed the specific role of β-cell-markers, such as Glut2, MafA, Ins1, Ins2, and Pdx1 in insulin expression. The expression of these genes appears to be suppressed in the T2D β-cells, along with the reappearance of the early endocrine marker genes. Glucose transporters transport glucose into β-cells, thereby controlling insulin release during hyperglycaemia. This stimulates glycolysis through rises in intracellular calcium (a process enhanced by vitamin D) (Norman et al., 1980), activating 2 of 4 proteinases. The rise in calcium activates half of pancreatic β-cell proinsulinases, thus releasing free insulin from granules. The synthesis of ATP from glucose by glycolysis, Krebs cycle and oxidative phosphorylation plays a role in insulin release. Some studies have found that the β-cells contain high levels of the vitamin D receptor; however, the role that this plays in maintaining the maturity of the β-cells remains unknown. Further research is required to develop a more in-depth understanding of the role VDR plays in β-cell function and the processes by which the beta cell function is preserved.
AB - One significant health issue that plagues contemporary society is that of Type 2 diabetes (T2D). This disease is characterised by higher-than-average blood glucose levels as a result of a combination of insulin resistance and insufficient insulin secretions from the β-cells of pancreatic islets of Langerhans. Previous developmental research into the pancreas has identified how early precursor genes of pancreatic β-cells, such as Cpal, Ngn3, NeuroD, Ptf1a, and cMyc, play an essential role in the differentiation of these cells. Furthermore, β-cell molecular characterization has also revealed the specific role of β-cell-markers, such as Glut2, MafA, Ins1, Ins2, and Pdx1 in insulin expression. The expression of these genes appears to be suppressed in the T2D β-cells, along with the reappearance of the early endocrine marker genes. Glucose transporters transport glucose into β-cells, thereby controlling insulin release during hyperglycaemia. This stimulates glycolysis through rises in intracellular calcium (a process enhanced by vitamin D) (Norman et al., 1980), activating 2 of 4 proteinases. The rise in calcium activates half of pancreatic β-cell proinsulinases, thus releasing free insulin from granules. The synthesis of ATP from glucose by glycolysis, Krebs cycle and oxidative phosphorylation plays a role in insulin release. Some studies have found that the β-cells contain high levels of the vitamin D receptor; however, the role that this plays in maintaining the maturity of the β-cells remains unknown. Further research is required to develop a more in-depth understanding of the role VDR plays in β-cell function and the processes by which the beta cell function is preserved.
KW - Insulin release
KW - Islets dedifferentiation
KW - Islets differentiation
KW - Type 2 diabetes
KW - Vitamin D receptor
UR - http://www.scopus.com/inward/record.url?scp=85043397115&partnerID=8YFLogxK
U2 - 10.1016/j.jdiacomp.2017.12.002
DO - 10.1016/j.jdiacomp.2017.12.002
M3 - Review article
VL - 32
SP - 429
EP - 443
JO - Journal of Diabetes and Its Complications
JF - Journal of Diabetes and Its Complications
SN - 1056-8727
IS - 4
ER -