AP Biology: Unit 4, Feedback Mechanisms (Drill 16)

Question 1. Based on the table, at which time point does blood glucose reach its peak, and what is the corresponding insulin level?

• A) 30 minutes; 52 uU/mL ✓
• B) 60 minutes; 61 uU/mL
• C) 30 minutes; 61 uU/mL
• D) 60 minutes; 52 uU/mL

Explanation: The table shows blood glucose peaks at 142 mg/dL at 30 minutes, with a corresponding insulin level of 52 uU/mL. B is incorrect because at 60 minutes blood glucose is 128 mg/dL -- declining from its peak, not at maximum. C and D both mix time points -- pairing the 30-minute glucose peak with the 60-minute insulin value or vice versa, reflecting a table-reading error.

Question 2. A student observes that insulin peaks at 60 minutes while blood glucose peaks at 30 minutes. The student claims this delay demonstrates that insulin secretion is triggered by rising glucose levels, not peak glucose levels. Which reasoning best evaluates this claim?

• A) The claim is well-supported because the data show insulin continuing to rise after glucose begins to fall, which is consistent with a delayed secretory response to the rate of glucose increase rather than its absolute level within the described scenario.
• B) The claim is flawed because insulin and blood glucose actually peak at exactly the same time point in the data table, eliminating any delay to interpret.
• C) The claim is partially supported -- the delay is consistent with a lag between glucose stimulus and peak insulin secretion, but the data alone cannot distinguish whether secretion is triggered by rising levels, absolute levels, or both. ✓
• D) The claim is well-supported because glucagon levels are lowest at 60 minutes, confirming that insulin and glucagon are always inversely regulated.

Explanation: The 30-minute lag between glucose peak and insulin peak is consistent with a delayed secretory response, which could reflect the time required for beta cells to detect rising glucose and release insulin. However, the table shows correlation between glucose rise and insulin rise -- it does not isolate whether the trigger is the rate of increase, the absolute level, or a combination. C correctly identifies what the data support and what they cannot distinguish. A overclaims by asserting a specific mechanism not demonstrated by the data. B is factually incorrect -- glucose peaks at 30 minutes and insulin at 60 minutes. D introduces glucagon as supporting evidence but the inverse relationship does not address what specifically triggers insulin secretion.

Question 3. Between 90 and 150 minutes, glucagon levels rise from 72 to 118 pg/mL as blood glucose returns toward baseline. Which cellular mechanism best explains the role of rising glucagon during this period?

• A) Glucagon binds receptors on adipose tissue, stimulating uptake and storage of glucose as glycogen.
• B) Glucagon binds receptors on liver cells, activating glycogen phosphorylase to release glucose from glycogen stores into the blood. ✓
• C) Glucagon stimulates glucose uptake by muscle cells, restoring blood glucose by clearing excess glucose from circulation within this line of reasoning.
• D) Glucagon stimulates intestinal absorption of dietary glucose to restore blood glucose to baseline.

Explanation: Glucagon's primary target is the liver. It binds glucagon receptors on hepatocytes, triggering a cAMP-mediated signaling cascade that activates glycogen phosphorylase, releasing glucose from glycogen stores (glycogenolysis) into the bloodstream to restore blood glucose toward normal. A is incorrect because glucagon does not stimulate glucose uptake or glycogen storage -- those are insulin-mediated effects. C is incorrect because glucagon does not stimulate muscle glucose uptake -- insulin drives glucose entry into muscle cells via GLUT4 transporter recruitment. D is incorrect because glucagon does not act on intestinal absorption.

Question 4. A researcher proposes that the glucose-insulin-glucagon system shown in the table represents a classic negative feedback loop. Which feature of the data is most consistent with this characterization?

• A) Insulin and glucagon levels change in exactly opposite directions throughout the entire observation period, which is the defining feature of negative feedback under the conditions described.
• B) Glucagon levels at 150 minutes are slightly lower than at time 0, suggesting the system overshoots its set point.
• C) Insulin peaks after glucose peaks, confirming that the response always lags behind the stimulus in negative feedback systems.
• D) Blood glucose rises after the meal and is restored toward the pre-meal baseline by 150 minutes, driven by hormonal responses that counteract the initial deviation. ✓

Explanation: The defining feature of negative feedback is that a deviation from a set point triggers a response that counteracts that deviation and restores the system toward baseline. The table shows blood glucose rises after the meal (deviation), insulin rises in response (counteracting signal), and glucose returns to approximately 84-88 mg/dL by 120-150 minutes (restoration toward baseline). D captures this full loop directly. A describes reciprocal hormone changes -- a feature of the mechanism, not the defining characteristic of the loop itself. B misreads the data -- glucagon at 150 minutes (118 pg/mL) is close to but not lower than time 0 (120 pg/mL). C overgeneralizes -- a response lag is not a defining or universal feature of negative feedback systems.

Question 5. A patient with Type 2 diabetes produces insulin normally but has reduced insulin receptor sensitivity in muscle and liver cells. Based on the feedback mechanism shown in the table, which pattern would most likely be observed in this patient following the same standardized meal?

• A) Blood glucose would peak higher and remain elevated longer than in the healthy individual, because target cells do not respond normally to insulin signaling. ✓
• B) Blood glucose would follow the same pattern as the healthy individual because insulin is still being produced at completely normal levels in this patient within this experimental setup.
• C) Glucagon secretion would be permanently suppressed because rising insulin levels would inhibit alpha cells regardless of receptor sensitivity.
• D) Insulin levels would be lower than in the healthy individual because reduced glucose uptake would signal the pancreas to reduce secretion.

Explanation: In Type 2 diabetes, insulin is produced but target cells (muscle, liver) are less responsive to its signal. Glucose uptake and glycogen synthesis in these tissues are therefore reduced, so blood glucose rises higher after the meal and remains elevated longer -- the negative feedback loop is impaired at the effector level. B is incorrect because normal insulin production does not guarantee normal glucose regulation if target cells are unresponsive. C is incorrect because glucagon suppression depends on blood glucose levels and paracrine signaling within the islets -- reduced target cell sensitivity does not mean glucagon is permanently suppressed. D is incorrect because in Type 2 diabetes, chronically elevated blood glucose typically drives increased, not decreased, insulin secretion as the pancreas attempts to compensate.