Glucose increases plasma insulin by a process that involves
**Core Concept**
Glucose-induced insulin secretion is a critical physiological response that regulates blood glucose levels. This process involves the activation of beta cells in the pancreatic islets, leading to the release of insulin into the bloodstream. The mechanism is mediated by the binding of glucose to specific receptors on the surface of beta cells.
**Why the Correct Answer is Right**
When glucose enters the beta cells, it binds to the glucose transporter 2 (GLUT2) on the cell surface. This binding causes an increase in the influx of glucose into the cell, leading to an increase in the concentration of ATP. The high ATP levels activate the ATP-sensitive potassium channels (K ATP channels), causing a depolarization of the beta cell membrane. The depolarization opens the voltage-dependent calcium channels, allowing an influx of calcium ions into the cell. The increase in intracellular calcium triggers the exocytosis of insulin-containing vesicles, releasing insulin into the bloodstream.
**Why Each Wrong Option is Incorrect**
* **Option A:** This option is not relevant to the glucose-induced insulin secretion pathway.
* **Option B:** This option is incorrect because the glucose transporter 1 (GLUT1) is primarily involved in glucose transport across the blood-brain barrier, not in the regulation of insulin secretion.
* **Option D:** This option is incorrect because the insulin receptor does not play a direct role in glucose-induced insulin secretion; rather, it is involved in the regulation of glucose uptake in peripheral tissues.
**Clinical Pearl / High-Yield Fact**
The glucose-induced insulin secretion pathway is sensitive to the concentration of glucose in the blood, with a threshold of approximately 3-5 mmol/L. This is why fasting glucose levels are often used as a diagnostic criterion for diabetes mellitus.
**Correct Answer: C. The increase in intracellular ATP leads to the activation of ATP-sensitive potassium channels, depolarization of the cell membrane, and the exocytosis of insulin-containing vesicles.**