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Quizzes > Science > Biology

How Well Do You Know Hormonal Fuel Metabolism?

Test your grasp on lipoprotein lipase and hormone regulation - dive in!

Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
paper art style icons of lipoprotein lipase insulin glucagon on teal background quiz hormonal regulation of fuel metabolism

Ready to challenge your understanding of hormonal control? Our hormonal regulation of fuel metabolism quiz is designed for students, healthcare pros, and curious minds to test how well you know insulin, glucagon, and lipoprotein lipase activity. Learn pathways, boost recall, and master hormone interactions. You'll tackle fuel metabolism hormone questions like "lipoprotein lipase breaks triglycerides into ______." or identify "hormones that help to regulate blood pressure are ______." Plus, sharpen your skills in the insulin and glucagon regulation quiz section. Dive deeper with a quick lipid metabolism quiz or refresh core concepts in our endocrine system quiz . Start now to ace this free metabolism challenge - begin today!

Which hormone decreases blood glucose levels by promoting glucose uptake into muscle and adipose tissue?
Insulin
Glucagon
Epinephrine
Cortisol
Insulin is the primary hormone responsible for lowering blood glucose by stimulating glucose uptake in muscle and adipose tissue via GLUT4 translocation. It also promotes glycogen synthesis and inhibits gluconeogenesis in the liver. Deficiency or resistance to insulin leads to hyperglycemia as seen in diabetes mellitus. Wikipedia: Insulin
Which enzyme is anchored to the capillary endothelium and hydrolyzes triglycerides in circulating chylomicrons and VLDL?
Lipoprotein lipase
Hormone-sensitive lipase
Hepatic lipase
Pancreatic lipase
Lipoprotein lipase (LPL) is bound to the luminal surface of capillary endothelial cells and hydrolyzes triglycerides in chylomicrons and VLDL into free fatty acids and glycerol. It is activated by insulin and available in adipose and muscle tissue. Defects in LPL activity lead to hypertriglyceridemia. Wikipedia: Lipoprotein lipase
Which hormone increases hepatic glucose production by stimulating gluconeogenesis and glycogenolysis?
Glucagon
Insulin
Growth hormone
Thyroxine
Glucagon, secreted by pancreatic alpha cells, raises blood glucose levels primarily by activating hepatic gluconeogenesis and glycogenolysis through a cAMP-mediated pathway. It opposes the action of insulin during fasting. Excess glucagon activity can worsen hyperglycemia in diabetes. Wikipedia: Glucagon
Which pancreatic cell type secretes glucagon?
Alpha cells
Beta cells
Delta cells
PP cells
Pancreatic alpha cells are responsible for synthesizing and secreting glucagon, which raises blood glucose by promoting gluconeogenesis and glycogenolysis. Beta cells secrete insulin, while delta cells secrete somatostatin and PP cells release pancreatic polypeptide. Dysfunction of alpha cells can affect glucose homeostasis. Wikipedia: Pancreatic alpha cell
Which glucose transporter is insulin-responsive and predominates in muscle and adipose tissue?
GLUT4
GLUT2
GLUT1
GLUT3
GLUT4 is the insulin-regulated glucose transporter found primarily in adipose tissue and skeletal muscle. Insulin stimulates GLUT4 translocation to the plasma membrane, increasing glucose uptake. Defects in this system contribute to insulin resistance. Wikipedia: GLUT4
Insulin inhibits which lipolytic enzyme in adipocytes?
Hormone-sensitive lipase
Lipoprotein lipase
Hepatic lipase
Monoacylglycerol lipase
Insulin activates phosphodiesterase, which reduces cAMP levels and thus inactivates protein kinase A, leading to dephosphorylation and inhibition of hormone-sensitive lipase (HSL). HSL normally hydrolyzes stored triacylglycerols in adipocytes. This inhibition reduces free fatty acid release. Wikipedia: Hormone-sensitive lipase
Which hormone is released by the adrenal medulla to acutely stimulate lipolysis during stress?
Epinephrine
Cortisol
Aldosterone
Norepinephrine
Epinephrine, secreted by the adrenal medulla, binds to ?-adrenergic receptors on adipocytes to increase cAMP and activate hormone-sensitive lipase, triggering rapid lipolysis. Norepinephrine also acts similarly but epinephrine predominates in the blood. This response supplies fatty acids as energy during stress. Wikipedia: Epinephrine
Insulin promotes which process in the liver after a meal?
Glycogen synthesis
Glycogenolysis
Gluconeogenesis
Ketogenesis
After a meal, insulin activates protein phosphatases that dephosphorylate and activate glycogen synthase while inactivating glycogen phosphorylase, promoting hepatic glycogen synthesis. It also inhibits gluconeogenesis and ketogenesis. This coordinates postprandial glucose storage. Wikipedia: Glycogen synthesis
Which coenzyme is required by the pyruvate dehydrogenase complex?
Thiamine pyrophosphate
Biotin
Pyridoxal phosphate
Cobalamin
Thiamine pyrophosphate (TPP) is a coenzyme for the E1 subunit of pyruvate dehydrogenase, facilitating decarboxylation of pyruvate to acetyl-CoA. Biotin is used by carboxylases, pyridoxal phosphate by transaminases, and cobalamin in methyl group transfers. Thiamine deficiency impairs aerobic glucose oxidation. Wikipedia: Pyruvate dehydrogenase
What is the primary fuel for the brain under normal fed conditions?
Glucose
Fatty acids
Ketone bodies
Amino acids
Under normal fed conditions, the brain relies almost exclusively on glucose because fatty acids cannot cross the blood-brain barrier efficiently. During prolonged fasting, it can adapt to using ketone bodies. Amino acids are not a major fuel for the brain. Wikipedia: Brain energy metabolism
During an overnight fast, the main source of blood glucose is:
Hepatic glycogenolysis
Muscle glycogenolysis
Dietary glucose
Renal gluconeogenesis
In an overnight fast (10–12 hours), hepatic glycogenolysis is the primary source of blood glucose, as liver glycogen stores are sufficient. Muscle glycogen is not directly released into circulation. Renal gluconeogenesis contributes later in prolonged fasting. Wikipedia: Gluconeogenesis
Which lipoprotein class transports dietary triglycerides from intestine to peripheral tissues?
Chylomicrons
VLDL
LDL
HDL
Chylomicrons are assembled in enterocytes to transport dietary triglycerides and fat-soluble vitamins through lymphatics into the bloodstream. VLDL is secreted by the liver, LDL carries cholesterol to tissues, and HDL mediates reverse cholesterol transport. Wikipedia: Chylomicron
Hormone-sensitive lipase primarily hydrolyzes:
Stored triglycerides in adipocytes
Plasma triglycerides in chylomicrons
Short-chain fatty acids
Phospholipids in membranes
Hormone-sensitive lipase (HSL) in adipocytes cleaves stored triacylglycerols into diacylglycerol and free fatty acids, which are released into circulation during fasting or stress. It is regulated by hormonal signals such as insulin and catecholamines. Wikipedia: Hormone-sensitive lipase
Which organ is the primary site of gluconeogenesis?
Liver
Kidney
Muscle
Adipose tissue
The liver is the main site for gluconeogenesis, converting lactate, glycerol, and amino acids into glucose during fasting. The kidney contributes only modestly under normal conditions but increases in prolonged fasting. Muscle does not export glucose. Wikipedia: Gluconeogenesis
The insulin receptor belongs to which receptor family?
Receptor tyrosine kinase
G protein–coupled receptor
Nuclear receptor
Cytokine receptor
The insulin receptor is a receptor tyrosine kinase that autophosphorylates upon insulin binding, triggering downstream signaling through IRS proteins and PI3K/Akt pathways. GPCRs use G proteins, nuclear receptors are transcription factors, and cytokine receptors associate with JAK/STAT. Wikipedia: Insulin receptor
Which hormone directly stimulates GLUT4 translocation in adipocytes?
Insulin
Glucagon
Epinephrine
Cortisol
Insulin binding to its receptor initiates a signaling cascade involving IRS-1, PI3K, and Akt, leading to GLUT4 vesicle translocation to the plasma membrane in adipocytes and muscle. This increases glucose uptake. Other hormones do not trigger GLUT4 translocation. Wikipedia: GLUT4
Activation of hormone-sensitive lipase in adipocytes requires which second messenger?
cAMP
IP3
cGMP
Calcium
Hormone-sensitive lipase is activated by phosphorylation via protein kinase A, which is activated by cAMP generated after hormone (e.g., epinephrine) stimulation of ?-adrenergic receptors. IP3 and calcium act in different pathways, and cGMP is primarily in nitric oxide signaling. Wikipedia: cAMP
Which enzyme in glycolysis is allosterically activated by fructose-2,6-bisphosphate?
Phosphofructokinase-1
Hexokinase
Pyruvate kinase
Enolase
Fructose-2,6-bisphosphate is a potent allosteric activator of phosphofructokinase-1 (PFK-1), increasing glycolytic flux. It also inhibits fructose-1,6-bisphosphatase in gluconeogenesis. Hexokinase and pyruvate kinase are regulated differently. Wikipedia: PFK-1
Insulin stimulates fatty acid synthesis by activating which enzyme in the cytosol?
Acetyl-CoA carboxylase
Hormone-sensitive lipase
Carnitine acyltransferase I
Fatty acid synthase
Insulin dephosphorylates and activates acetyl-CoA carboxylase (ACC), the rate-limiting enzyme in fatty acid synthesis that converts acetyl-CoA to malonyl-CoA. Fatty acid synthase catalyzes later steps but is regulated at the transcriptional level. HSL and carnitine acyltransferase I are involved in lipolysis and fatty acid oxidation, respectively. Wikipedia: ACC
Glucagon binding to its hepatic receptor leads to increased activity of which enzyme?
Fructose-1,6-bisphosphatase
Phosphofructokinase-1
Pyruvate kinase
Glycogen synthase
Glucagon raises cAMP, activating protein kinase A, which phosphorylates and activates fructose-1,6-bisphosphatase indirectly by inactivating PFK-2/FBPase-2, favoring gluconeogenesis. PFK-1 and pyruvate kinase drive glycolysis, and glycogen synthase is inhibited by glucagon. Wikipedia: Fructose-bisphosphatase
Which of the following enzymes is NOT directly regulated by phosphorylation?
Hexokinase
Glycogen synthase
Pyruvate dehydrogenase
Hormone-sensitive lipase
Hexokinase is regulated by product inhibition (glucose-6-phosphate) rather than phosphorylation. Glycogen synthase, pyruvate dehydrogenase, and hormone-sensitive lipase are all controlled by reversible phosphorylation. Wikipedia: Hexokinase
Epinephrine increases hepatic glucose output predominantly via activation of:
Glycogen phosphorylase
Glucokinase
Hexokinase
Glycogen synthase
Epinephrine activates the ?-adrenergic receptor in hepatocytes, raising cAMP and activating protein kinase A, which phosphorylates and activates glycogen phosphorylase to break down glycogen. Glucokinase and hexokinase trap glucose, and glycogen synthase is inhibited under this signal. Wikipedia: Glycogen phosphorylase
AMP-activated protein kinase (AMPK) activation in muscle leads to:
Increased GLUT4 translocation
Activation of acetyl-CoA carboxylase
Inhibition of glycolysis
Increased fatty acid synthesis
AMPK activation during energy stress increases GLUT4 translocation and fatty acid oxidation by phosphorylating and inhibiting acetyl-CoA carboxylase, reducing malonyl-CoA. It stimulates glycolysis indirectly, not inhibits it. It suppresses fatty acid synthesis. Wikipedia: AMPK
Insulin signaling leads to activation of Akt, which in turn:
Inactivates glycogen synthase kinase-3
Activates fructose-1,6-bisphosphatase
Inhibits phosphodiesterase
Phosphorylates HSL
Akt phosphorylates and inhibits glycogen synthase kinase-3 (GSK-3), leading to activation of glycogen synthase and increased glycogen synthesis. It does not activate fructose-1,6-bisphosphatase, which is stimulated by glucagon, nor inhibit phosphodiesterase. HSL is inactivated by insulin via phosphodiesterase. Wikipedia: Akt
Which enzyme produces diacylglycerol and IP3 upon activation by Gq-coupled receptors?
Phospholipase C
Adenylate cyclase
Phospholipase A2
Protein kinase C
Phospholipase C (PLC) cleaves membrane phosphatidylinositol 4,5-bisphosphate into diacylglycerol (DAG) and inositol trisphosphate (IP3) upon Gq-coupled receptor activation. DAG activates PKC, while IP3 releases calcium from the ER. Adenylate cyclase generates cAMP. Wikipedia: PLC
During insulin resistance, which tissue exhibits decreased insulin-stimulated glucose uptake first?
Skeletal muscle
Brain
Adipose tissue
Liver
Skeletal muscle is the major site of postprandial glucose disposal and is most sensitive to insulin; it shows decreased uptake early in insulin resistance. The brain relies on GLUT1/3 and is insulin-independent. Adipose and liver contribute but later. Wikipedia: Insulin resistance
Which intermediate of the TCA cycle signals high energy status and inhibits PDH kinase, promoting PDH activity?
Pyruvate
ATP
Acetyl-CoA
NADH
Pyruvate inhibits PDH kinase, reducing phosphorylation of pyruvate dehydrogenase (PDH) and promoting its active dephosphorylated form. ATP, acetyl-CoA, and NADH activate PDH kinase, inhibiting PDH when energy is plentiful. Wikipedia: PDH
Insulin’s effect on hepatic glucokinase is to:
Increase its expression
Promote its phosphorylation
Target it for degradation
Inhibit its transcription
Insulin upregulates glucokinase gene expression in the liver, increasing its capacity to phosphorylate glucose after meals. Phosphorylation is not its primary regulation, and insulin does not degrade or inhibit its transcription. Wikipedia: Glucokinase
Which process is suppressed by insulin in the liver?
Ketogenesis
Glycogen synthesis
Fatty acid synthesis
Protein synthesis
Insulin suppresses ketogenesis by inhibiting hormone-sensitive lipase and reducing fatty acid oxidation in the liver. It also stimulates glycogen synthesis, fatty acid synthesis, and protein synthesis. Wikipedia: Ketogenesis
Cortisol increases blood glucose by upregulating which hepatic enzymes?
Phosphoenolpyruvate carboxykinase and glucose-6-phosphatase
Hexokinase and glucokinase
Pyruvate kinase and pyruvate dehydrogenase
Glycogen synthase and hexokinase
Cortisol, by binding to glucocorticoid receptors, induces transcription of PEPCK and glucose-6-phosphatase, key enzymes in gluconeogenesis. This raises hepatic glucose output during stress. It does not upregulate glycolytic enzymes like hexokinase or pyruvate kinase. Wikipedia: Gluconeogenesis
In the fed state, malonyl-CoA levels rise and inhibit:
Carnitine palmitoyltransferase I
Acetyl-CoA carboxylase
Hormone-sensitive lipase
Glucose-6-phosphatase
Malonyl-CoA, produced by acetyl-CoA carboxylase in the fed state, inhibits carnitine palmitoyltransferase I (CPT1) on the mitochondrial membrane, preventing fatty acid entry for ?-oxidation. This ensures fatty acids are used for lipogenesis, not oxidation. Wikipedia: CPT1
Which G protein subunit activates adenylate cyclase in response to glucagon?
Gs alpha
Gi alpha
Gq alpha
G12 alpha
The Gs alpha subunit binds GTP and activates adenylate cyclase when glucagon binds to its GPCR, increasing cAMP. Gi alpha inhibits AC, Gq alpha activates phospholipase C, and G12 regulates cytoskeleton. Wikipedia: G protein
During prolonged fasting, the brain adapts to using:
Ketone bodies
Fatty acids
Amino acids
Lactate
After days of fasting, the liver generates ketone bodies (?-hydroxybutyrate and acetoacetate), which cross the blood-brain barrier and supply up to 70% of the brain's energy. Fatty acids cannot enter the brain efficiently, and amino acids are used sparingly. Wikipedia: Ketone bodies
Which nuclear receptor mediates the genomic effects of thyroid hormones on metabolism?
Thyroid hormone receptor
Peroxisome proliferator-activated receptor alpha
Glucocorticoid receptor
Estrogen receptor
Thyroid hormone receptors (TR? and TR?) are nuclear receptors that bind T3 and regulate transcription of genes involved in basal metabolic rate, lipid, and carbohydrate metabolism. PPAR? regulates fatty acid oxidation genes. Glucocorticoid and estrogen receptors bind different ligands. Wikipedia: Thyroid hormone receptor
mTOR activation in response to insulin promotes:
Protein synthesis
Autophagy
Gluconeogenesis
Lipolysis
mTOR (mechanistic target of rapamycin) is activated downstream of Akt in response to insulin and amino acids, stimulating protein synthesis and cell growth by phosphorylating S6K and 4E-BP1. It inhibits autophagy. It does not promote gluconeogenesis or lipolysis. Wikipedia: mTOR
The Randle cycle describes competition between oxidation of:
Glucose and fatty acids
Ketone bodies and amino acids
Glucose and ketone bodies
Fatty acids and ketone bodies
The Randle cycle (glucose-fatty acid cycle) posits that elevated fatty acid oxidation inhibits glucose oxidation by increasing acetyl-CoA and citrate, which inhibit PDH and PFK-1. This competition helps regulate fuel choice in muscle. Wikipedia: Randle cycle
Which enzyme complex is inhibited by high levels of malonyl-CoA?
Carnitine palmitoyltransferase I
Pyruvate dehydrogenase complex
Acetyl-CoA carboxylase
Fatty acid synthase
Malonyl-CoA is an allosteric inhibitor of carnitine palmitoyltransferase I (CPT1), controlling fatty acid entry into mitochondria for ?-oxidation. It does not affect the pyruvate dehydrogenase complex or lipogenic enzymes directly. Wikipedia: CPT1
What effect does glucocorticoid receptor activation have on insulin sensitivity in peripheral tissues?
Decreases insulin sensitivity
Increases insulin sensitivity
No effect
Only affects hepatic sensitivity
Chronic glucocorticoid exposure induces insulin resistance in peripheral tissues by promoting gluconeogenesis, lipolysis, and proteolysis, elevating circulating substrates that impair insulin signaling. It affects both muscle and adipose tissue. Wikipedia: Glucocorticoid resistance
Which adipokine enhances insulin sensitivity and has anti-inflammatory effects?
Adiponectin
Leptin
Resistin
TNF-?
Adiponectin is secreted by adipocytes and increases insulin sensitivity by activating AMPK and PPAR? pathways, while exerting anti-inflammatory effects. Leptin regulates appetite, resistin promotes insulin resistance, and TNF-? is pro-inflammatory. Wikipedia: Adiponectin
Which enzyme’s activity increases in liver during early phase of high-carbohydrate feeding to divert glucose into fatty acid synthesis?
ATP-citrate lyase
Malate dehydrogenase
Glucose-6-phosphate dehydrogenase
Citrate synthase
ATP-citrate lyase converts citrate exported from mitochondria into acetyl-CoA in the cytosol, providing substrate for fatty acid synthesis during high-carbohydrate feeding. G6PD provides NADPH, but ACL is the direct link between carbohydrate and lipogenesis. Wikipedia: ACL
Which of these conditions would increase hepatic ketogenesis?
Low insulin-to-glucagon ratio
High carbohydrate intake
High insulin-to-glucagon ratio
Increased malonyl-CoA levels
A low insulin-to-glucagon ratio, as seen in fasting or uncontrolled diabetes, enhances fatty acid release and oxidation in the liver, driving ketogenesis. High carbohydrate intake and high insulin inhibit ketone production. Malonyl-CoA blocks fatty acid entry into mitochondria. Wikipedia: Ketogenesis
Which mechanism describes how insulin increases GLUT4 gene transcription?
Akt-mediated activation of SREBP-1c
PKA-mediated CREB phosphorylation
mTOR-mediated STAT3 activation
AMPK-mediated PGC-1? upregulation
Insulin signaling through Akt promotes SREBP-1c activation which indirectly enhances GLUT4 gene transcription. PKA and CREB act in glucagon signaling, mTOR and STAT3 regulate growth responses, and AMPK/PGC-1? relate to energy stress. NCBI: Insulin and SREBP-1c
In adipocytes, which protein complex scaffolds the insulin receptor to facilitate GLUT4 vesicle docking?
SNARE complex
mTORC1
Phosphoinositide 3-kinase
Adaptor protein complex 2
The SNARE complex, consisting of v-SNAREs (e.g., VAMP2) and t-SNAREs (e.g., syntaxin 4), mediates insulin-stimulated GLUT4 vesicle docking and fusion at the plasma membrane. mTORC1 and PI3K are upstream signaling nodes, and AP-2 is involved in endocytosis. Wikipedia: SNARE
Which modification of the insulin receptor substrate-1 (IRS-1) leads to insulin resistance?
Serine phosphorylation
Tyrosine phosphorylation
Ubiquitination
Acetylation
Serine phosphorylation of IRS-1 by kinases such as JNK impairs insulin signaling by preventing its association with the insulin receptor and PI3K, contributing to insulin resistance. Tyrosine phosphorylation is activating. Ubiquitination targets IRS-1 for degradation, and acetylation is less central. NCBI: IRS-1 regulation
Which transcription factor is directly activated by PPAR? agonists to increase fatty acid oxidation genes?
PGC-1?
ChREBP
SREBP-2
NF-?B
PPAR? agonists activate PPAR? which recruits PGC-1? coactivator to upregulate genes of fatty acid transport and ?-oxidation. ChREBP regulates glycolytic and lipogenic genes, SREBP-2 regulates cholesterol metabolism, and NF-?B modulates inflammation. Wikipedia: PPAR?
How does FGF21, secreted by the liver during fasting, affect adipose tissue?
Increases lipolysis and adiponectin secretion
Decreases HSL activity
Inhibits adiponectin production
Stimulates GLUT4 internalization
Fibroblast growth factor 21 (FGF21) is induced by fasting and enhances adipose lipolysis and adiponectin secretion, improving insulin sensitivity. It does not inhibit HSL or adiponectin, nor does it cause GLUT4 internalization. Wikipedia: FGF21
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Study Outcomes

  1. Analyze Lipoprotein Lipase Activity -

    Explain how lipoprotein lipase breaks triglycerides into glycerol and fatty acids and its role in fuel metabolism.

  2. Evaluate Insulin and Glucagon Regulation -

    Compare how insulin and glucagon coordinate to maintain blood glucose levels during fed and fasting states.

  3. Interpret Nutrient Concentration Shifts -

    Describe changes in nutrient levels across tissues and blood in response to hormonal signals.

  4. Identify Blood Pressure Regulating Hormones -

    List key hormones involved in blood pressure control and outline their mechanisms of action.

  5. Apply Hormonal Concepts to Quiz Scenarios -

    Use your understanding of hormonal regulation to answer targeted questions in the quiz with confidence.

  6. Synthesize Fuel Metabolism Principles -

    Integrate knowledge of hormone-driven energy balance to predict metabolic outcomes under various conditions.

Cheat Sheet

  1. Lipoprotein Lipase Function -

    Lipoprotein lipase (LPL) on endothelial cells hydrolyzes circulating triglycerides from chylomicrons and VLDL into free fatty acids and glycerol (TG + 3H2O → glycerol + 3FFA). This process provides fuel to adipose and muscle tissues. Mnemonic: "LPL Loves Processing Lipids" helps recall LPL's role in lipid uptake.

  2. Insulin: Master Anabolic Regulator -

    Secreted by pancreatic β-cells in response to elevated blood glucose, insulin activates the PI3K/AKT pathway to promote GLUT4 translocation, glycogen synthase activity, and acetyl-CoA carboxylase-driven lipogenesis. A handy acronym "GGLA" (GLUT4, Glycogen synthase, Lipogenesis, Amino acid uptake) outlines its major targets. Insulin's push towards energy storage defines the fed state.

  3. Glucagon and Catabolic Signaling -

    During fasting, pancreatic α-cells release glucagon, which binds Gs-coupled receptors to raise cAMP and activate PKA, stimulating hormone-sensitive lipase and glycogen phosphorylase. This cascade enhances lipolysis and gluconeogenesis ("GNG up, Glycogen down"). Remember "cAMP → PKA" to link second messengers to metabolic breakdown.

  4. Hormonal Control of Blood Pressure -

    Key regulators include angiotensin II (vasoconstrictor via the RAAS pathway), vasopressin (water retention), catecholamines (epinephrine/norepinephrine acting on vascular α1 receptors), and atrial natriuretic peptide (ANP, which lowers blood volume). The RAAS mnemonic "Renin → ANG I → ACE → ANG II" helps track enzymatic steps. Balancing these hormones maintains circulatory homeostasis.

  5. Fuel Selection and Respiratory Quotient -

    The respiratory quotient (RQ = CO₂ produced/O₂ consumed) shifts with fuel usage: RQ ≈1.0 for carbohydrates and ≈0.7 for fats. High insulin levels drive RQ upward by favoring carbohydrate oxidation, while fasting lowers RQ toward fat utilization. Monitoring RQ offers a noninvasive window into metabolic state.

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