Biomedical Engineering Reference
In-Depth Information
Fig. 6.22
Electrical monitoring pancreatic “-cell activity
following the introduction of glucose into the “-cell-based FET. About five “-cells
were cultured on the gate sensing area, of which the gate width was 10mandthe
gate length was 340m.
The surface potential changes were based on the charge density changes of the
glucose response of about five “-cells. The uptake of glucose into “-cells causes
the increase in ATP/ADP concentration, the depolarization of K AT P channel, the
influx of Ca 2 C through ion channel, and the exocytosis of insulin and C-peptide
together with Zn 2 C to form microcrystals within secretory granules [ 56 ]. In this
study, insulin and C-peptide secretion has been detected by use of enzyme-linked
immunosorbent assay (ELISA) method based on the reaction with anti-insulin
monoclonal antibody, of which the concentration was about 32 ng/ml at 2 h after
glucose addition. The resulting molecular and ion charges at the “-cell/gate interface
induced the surface potential changes of the cell-based FET that prove the electrical
activity of pancreatic “-cells. Furthermore, the positive shift of surface potential
can be assumed to indicate the increase in the concentration of hydrogen ions
at the “-cell/gate interface, because the nonmodified FET device with the Ta 2 O 5
gate insulator is basically more sensitive to hydrogen ion concentration than those
of other ions. This is why we assume that the respiration of “-cells would have
been activated during the insulin secretion process following glucose addition.
After the increase of electrical signal, the surface potential of “-cell-based FET
decreased gradually because of diffusion of hydrogen ions from the cell/gate
interface to the bulk solution accompanied by degradation of respiration activity.
The insulin secretion process would include the respiration activity of “-cells so
that the electrical monitoring by use of the “-cell-based FET might demonstrate the
reduction and exhaustion of glucose-induced insulin secretion.
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