MCAT Biological and Biochemical Foundations of Living Systems Flashcards: 1d Metabolic Regulation Hormonal Integration

What this deck covers

This deck focuses on 1d Metabolic Regulation Hormonal Integration, giving you a quick way to review the definitions, rules, and examples that matter most for MCAT Biological and Biochemical Foundations of Living Systems.

How to use these flashcards

Work through these flashcards in short sessions. Try to answer each prompt before flipping the card, then revisit any cards you miss until the explanation feels automatic.

Flashcard 1: What is the primary metabolic effect of glucagon on the liver during fasting?

Answer: Increases glycogenolysis and gluconeogenesis; increases hepatic glucose output. Glucagon counters low blood glucose by stimulating hepatic glucose release through breakdown of glycogen and synthesis from non-carbohydrate precursors.

Flashcard 2: Which pancreatic islet cell type secretes insulin?

Answer: Beta ($\beta$) cells. Pancreatic beta cells respond to elevated blood glucose by releasing insulin to regulate postprandial metabolism.

Flashcard 3: What is the net effect of PKA on glycogen metabolism in the liver during fasting?

Answer: Activates glycogen phosphorylase; inhibits glycogen synthase. PKA phosphorylation shifts glycogen metabolism toward breakdown to release glucose during fasting.

Flashcard 4: Identify the primary fuel used by the brain in early fasting versus prolonged starvation.

Answer: Early: glucose; prolonged: ketone bodies (with reduced glucose requirement). The brain initially depends on glucose but adapts to ketone utilization to spare glucose during extended nutrient deprivation.

Flashcard 5: What is the rate-limiting enzyme of glycolysis, and how does insulin affect it in liver?

Answer: PFK-1; insulin activates it indirectly via $\uparrow$ fructose-$2,6$-bisphosphate. Insulin promotes glycolysis by increasing levels of the allosteric activator fructose-2,6-bisphosphate for PFK-1.

Flashcard 6: Which hormone increases blood glucose by promoting glycogenolysis in liver and muscle?

Answer: Epinephrine (adrenal medulla catecholamine). Epinephrine rapidly mobilizes glucose stores via adrenergic signaling to support fight-or-flight responses.

Flashcard 7: Which metabolic state is characterized by high insulin-to-glucagon ratio?

Answer: Fed (absorptive) state. Elevated insulin relative to glucagon promotes anabolic processes like glycogenesis and lipogenesis after meals.

Flashcard 8: Which enzyme is activated by epinephrine in adipose tissue to mobilize stored fat?

Answer: Hormone-sensitive lipase (HSL) via PKA phosphorylation. Epinephrine activates beta-adrenergic receptors, increasing cAMP and PKA to phosphorylate HSL for triglyceride hydrolysis.

Flashcard 9: What second messenger pathway is used by glucagon receptors on hepatocytes?

Answer: Gs $\rightarrow$ adenylyl cyclase $\rightarrow$ $\uparrow$ cAMP $\rightarrow$ PKA. Glucagon stimulates Gs-protein coupled receptors, elevating cAMP to activate PKA for gluconeogenic and glycogenolytic effects.

Flashcard 10: What is the immediate mechanism by which insulin increases glucose uptake in skeletal muscle?

Answer: Translocation of GLUT4 to the plasma membrane. Insulin signaling via PI3K/Akt promotes GLUT4 vesicle fusion with the cell membrane, facilitating glucose entry.

Flashcard 11: Which pancreatic islet cell type secretes glucagon?

Answer: Alpha ($\alpha$) cells. Alpha cells release glucagon in response to hypoglycemia to maintain blood glucose homeostasis.

Flashcard 12: Which pancreatic islet cell type secretes somatostatin, and what is its net effect?

Answer: Delta ($\delta$) cells; inhibits insulin and glucagon release. Somatostatin from delta cells modulates pancreatic hormone secretion to fine-tune glucose regulation.

Flashcard 13: What second messenger pathway is used by the insulin receptor?

Answer: Receptor tyrosine kinase (RTK) signaling (PI3K/Akt pathway). Insulin binding activates its receptor's tyrosine kinase activity, triggering downstream signaling for metabolic effects.

Flashcard 14: Which tissues have insulin-dependent GLUT4-mediated glucose uptake?

Answer: Skeletal muscle and adipose tissue. These tissues require insulin-stimulated GLUT4 for efficient glucose uptake during fed states to store energy.

Flashcard 15: Which GLUT transporter in liver and pancreatic $\beta$ cells senses blood glucose levels?

Answer: GLUT2. GLUT2's high Km allows it to function as a glucose sensor, modulating insulin secretion and hepatic glucose handling.

Flashcard 16: What is the key regulatory enzyme that makes fructose-$2,6$-bisphosphate in liver?

Answer: PFK-2 (part of the bifunctional PFK-2/FBPase-2 enzyme). PFK-2 generates fructose-2,6-bisphosphate, which activates glycolysis and inhibits gluconeogenesis in the liver.

Flashcard 17: Which hormone state favors hepatic PFK-2 activity over FBPase-2 activity?

Answer: Fed state (high insulin). High insulin dephosphorylates the bifunctional enzyme, favoring PFK-2 to promote glycolysis in nutrient abundance.

Flashcard 18: What is the rate-limiting enzyme of gluconeogenesis, and what is its key activator?

Answer: Fructose-$1,6$-bisphosphatase; activated by low fructose-$2,6$-bisphosphate. Low fructose-2,6-bisphosphate relieves inhibition, allowing gluconeogenesis to proceed during fasting states.

Flashcard 19: What is the net effect of glucagon on hepatic glycolysis versus gluconeogenesis?

Answer: Decreases glycolysis; increases gluconeogenesis. Glucagon signaling lowers fructose-2,6-bisphosphate, inhibiting glycolysis while promoting gluconeogenesis for glucose production.

Flashcard 20: What is the rate-limiting enzyme of fatty acid synthesis, and how does insulin affect it?

Answer: Acetyl-CoA carboxylase; insulin activates it (dephosphorylation). Insulin dephosphorylates ACC to catalyze malonyl-CoA formation, initiating fatty acid synthesis in fed states.

Flashcard 21: What is the effect of malonyl-CoA on fatty acid oxidation?

Answer: Inhibits CPT-I, decreasing mitochondrial $\beta$-oxidation. Malonyl-CoA allosterically inhibits CPT-I, preventing fatty acid entry into mitochondria to favor synthesis over oxidation.

Flashcard 22: Which metabolic state is characterized by low insulin-to-glucagon ratio?

Answer: Fasting (postabsorptive) state. Decreased insulin and increased glucagon drive catabolic processes to maintain blood glucose between meals.

Flashcard 23: Which hormone increases ketone body production during prolonged fasting, and in which organ?

Answer: Glucagon; liver (increases ketogenesis from fatty acids). Low insulin and high glucagon during fasting enhance hepatic fatty acid oxidation and ketone synthesis for alternative fuel.

Flashcard 24: What is the primary metabolic effect of insulin in liver, muscle, and adipose tissue?

Answer: Promotes glucose uptake/storage; increases glycogenesis, lipogenesis, protein synthesis. Insulin acts anabolically to store nutrients post-meal by enhancing glucose transport and metabolic pathways for energy storage in key tissues.