Blood sugar sensor system

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It has long been known that the pancreas ( pancreas ) on blood glucose concentration over the release of peptide hormones insulin and glucagon acts ( homeostasis ). Insulin is a product of the β-cells, glucagon of the α-cells of the pancreas.

More recent is knowledge of the pancreatic blood sugar sensor system, i. H. the basic principles according to which glucose concentrations are registered and then converted into a release of insulin (glucose level> 5 mmol / l or 90 mg / dl) or glucagon (hunger situation: glucose level <4 mmol / l or 70 mg / dl) . The system of β-cells is now widely known, while for that of α-cells only a few components could be determined.

Sensor system of the pancreatic β-cells

Glucose is absorbed by a low-affinity glucose transporter ( GLUT-1 , Km = 40 mM), proportional to the blood glucose concentration, and introduced into the normal glycolysis pathway via glucokinase (GK) . Its end product, pyruvate , is further metabolized in the mitochondria via the citric acid cycle and the respiratory chain , which ultimately leads to the production of ATP . In the following, ATP has the function of a second messenger : it forwards the glucose signal inside the cell;

Blood sugar sensor systems in pancreatic β cells (left half) or α cells (right part)

The links in the chain of effects are as follows:

  • ATP is an inhibitor of the ATP-regulated potassium channels (K + ATP type). These “ potassium seepage channels ” (sulfonylurea receptor ) are one of the components to which the membrane potential is based: the inside of the cell is set to −60 mV more negative than the surroundings
  • Inhibition (closing) of the potassium channels reduces the membrane potential. As soon as a limit value of −40 mV is reached, voltage-controlled Ca ++ channels open
  • Calcium ions flow in from the outside and cause the migration of insulin-containing granules to the cell membrane, then the exocytosis of insulin. The release of insulin occurs in two phases, i.e. i.e., it includes two types of granules:
    • the readily-released pool , which leads to a transient insulin peak
    • the reserve pool that holds 90% of the insulin

In the case of glucose deficiency, the inhibition of the potassium channels in β-cells does not apply; instead, the complementary situation is set in α-cells.

In the case of the β cells, the known components are shown in the figure, in particular the formation and effect of ATP, which here has second messenger functions. For α-cells it is known that ATP-regulated potassium channels do not play a decisive role. Rather, an action potential is triggered via the voltage-dependent sodium channel, as a result of which the hormone glucagon is secreted. In both cases, hormone release from granules is triggered by a Ca 2+ signal.

Sensor system of the pancreatic α-cells

Potassium seepage channels also contribute to the membrane potential of this cell type, but these are channels of the "K A " type. These are not subject to regulation by ATP.

Glucose transport is brought about by a high-affinity transporter, GLUT-1 (Km = 1 mM), which responds to glucose fluctuations in the lower concentration range. It is not known in detail which signal transduction pathways take place in this cell type when there is excess glucose. However, there is also evidence here that glucokinase (GK) plays a key role.

In glucose deficiency situations, an action potential is triggered by the resting potential temporarily increasing (becoming more negative). This signal leads to the opening of the sodium channels and an immediate collapse of the potential to about −40 mV. At this point the situation corresponds to that which leads to the release of hormones in β cells, but here the hormone is the insulin antagonist glucagon.


  • Leszek Szablewski: Glucose Homeostasis. In: Glucose Homeostasis and Insulin Resistance. Bentham Science Publishers, 2011. ISBN 978-1-60805-189-2 . pp. 46-58.

Individual evidence

  1. Löffler, Georg .: Biochemistry and Pathobiochemistry . 8., completely reworked. Springer, Heidelberg 2007, ISBN 978-3-540-32680-9 .