Two normal, healthy subjects volunteer for a study on insulin secretion. In Patient 1, blood glucose is increased to 150 mg/dL by direct intravenous infusion. In Patient 2, blood glucose is increased to 150 mg/dL by ingestion of oral glucose. The peak plasma insulin concentration produced in Patient 1 is 70 uU/mL while in Patient 2, it is 95 uU/mL. Which of the following best explains the higher insulin concentration in Patient 2?
Ingestion of glucose results in secretion of a "gut factor" into the blood that subsequently increases insulin secretion by b cells. The most likely candidate for this action is the intestinal peptide known as gastric inhibitory peptide (GIP), which obviously was named for its effects on the stomach. GIP secretion is increased during ingestion of glucose and the blood level produced is sufficient to stimulate insulin secretion. Because of this effect on insulin secretion, GIP is sometimes referred to as glucose-dependent insulinotropic peptide. Activation of the sympathetic innervation to the pancreas inhibits insulin secretion an a2-adrenergic mechanism. Hence, any sympathetic reflexes activated during ingestion of glucose would decrease insulin secretion. While paracrine release of somatostatin by D cells in the islets does inhibit insulin secretion by b cells, there is no reason to suspect that intravenous versus ingested glucose would have a differential effect on somatostatin release. The same holds true for glucagon secretion by a cells. Fuhermore, glucagon has a paracrine effect to increase insulin secretion.
Ingested glucose activates a sympathetic reflex that increases b cell release of insulin
Ingested glucose increases duodenal secretion of gastric inhibitory peptide (GIP), increasing b cell release of insulin
Intravenous glucose increases islet cell secretion of somatostatin, inhibiting b cell release of insulin
Intravenous glucose increases islet cell secretion of glucagon, inhibiting b cell release of insulin