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

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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.

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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: 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 2: 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 3: 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 4: 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.

Flashcard 5: 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 6: 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 7: 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 8: 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 9: 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 10: 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 11: 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 12: 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 13: 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 14: 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 15: 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 16: 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 17: 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 18: 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 19: 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 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: 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 22: 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 23: 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 24: Which pancreatic islet cell type secretes glucagon?

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