Glucose metabolism and oscillatory behavior of pancreatic islets.
A variety of oscillations are observed in pancreatic islets. We establish a model incorporating two oscillatory systems of different time scales: One is the well-known bursting model in pancreatic cells and the other is the glucose-insulin feedback model which considers direct and indirect feedback of secreted insulin. These two are coupled to interact with each other in the combined model, and two basic assumptions are made on the basis of biological observations: The conductance gK(ATP) for the ATP-dependent potassium current is a decreasing function of the glucose concentration whereas the insulin secretion rate is given by a function of the intracellular calcium concentration. Obtained via extensive numerical simulations are complex oscillations including clusters of bursts, slow and fast calcium oscillations, and so on. We also consider how the intracellular glucose concentration depends upon the extracellular glucose concentration, and examine the inhibitory effects of insulin.
Kang
H
H
Department of Physics and Center for Theoretical Physics, Seoul National University, Seoul 151-747, Korea.
Jo
J
J
Kim
H J
HJ
Choi
M Y
MY
Rhee
S W
SW
Koh
D S
DS
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001683:Biological Clocks / Q000502:physiology*; D015220:Calcium Channels / Q000502:physiology*; D020013:Calcium Signaling / Q000502:physiology; D003198:Computer Simulation; D005246:Feedback / Q000502:physiology; D005947:Glucose / Q000378:metabolism*; D051246:Glucose Transport Proteins, Facilitative / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007515:Islets of Langerhans / Q000502:physiology*; D008564:Membrane Potentials / Q000502:physiology; D008954:Models, Biological; D015221:Potassium Channels / Q000502:physiology*
D015220:Calcium Channels; D051246:Glucose Transport Proteins, Facilitative; D007328:Insulin; D015221:Potassium Channels; D000255:Adenosine Triphosphate; D005947:Glucose