Regulation of Secretion of Insulin

  1. Plasma glucose: The primary stimulus of insulin secretion is elevated plasma glucose levels. If the plasma glucose concentrations increase above 100mg/dL glucose uptake through the GLUT2 transporter in the beta cells is increased. Note: GLUT2 transporters are not dependent upon insulin like the GLUT4 transporters. Once in the beta cell the glucose is metabolized resulting in an increase in ATP production. Increased ATP interacts with ATP-sensitive K+ channels which causes them to close, resulting in depolarization of the cell membrane. The depolarization results in the opening of voltage-gated Ca++ channels allowing Ca++ to enter the cell. The increase in intracellular Ca++ stimulates exocytosis of the insulin containing vesicles. When glucose levels drop below 100 mg/dL ATP levels drop, the K+ channels open and insulin secretion stops. This is a classic example of negative feedback control.

  1. Plasma amino acids: amino acids in the blood have a similar, albeit slower effect than glucose on the release of insulin by the beta cells.

  1. Gastrointestinal hormones: Prior to any increase in blood glucose or amino acids, insulin release will be increased 50% because of hormones released from cells in the intestines. The primary hormones involved are glucagon-like peptide-1 and gastric inhibitory peptide (these hormones are known collectively as incretins). Both hormones are released from cells of the small intestines in response to nutrient ingestion. This is a type of feed forward mechanism (Bio 264: module 1) to help prevent a sudden surge in plasma glucose concentrations.

  1. Autonomic nervous system: Parasympathetic activity increases insulin release while sympathetic activity decreases insulin release. It may seem odd that sympathetic activity decreases insulin release since that would limit glucose uptake in the very tissues that need additional energy during physical exertion, namely skeletal muscle. However, as mentioned above, exercise results in incorporation of GLUT4 transporters in the active muscles allowing glucose to enter those muscles.

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