23Insulin and Glucagon Relationship Quiz
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Questions and Answers

Which of the following describes the relationship between insulin and glucagon release?

  • Insulin stimulates glucagon release, and glucagon inhibits insulin release.
  • Insulin inhibits glucagon release, and glucagon stimulates insulin release. (correct)
  • Both insulin and glucagon inhibit their own release.
  • Both insulin and glucagon stimulate each other's release.
  • What is the initial form of insulin synthesized in the cell?

  • Mature insulin
  • Pre-proinsulin (correct)
  • C-peptide
  • Proinsulin
  • What is the role of somatostatin in regulating insulin and glucagon?

  • It stimulates insulin and inhibits glucagon release.
  • It inhibits insulin and stimulates glucagon release.
  • It stimulates both insulin and glucagon release.
  • It inhibits both insulin and glucagon release. (correct)
  • Where does the formation of disulfide bonds between the A and B chains of insulin occur?

    <p>Golgi apparatus (A)</p> Signup and view all the answers

    What is the fate of C-peptide after it's cleaved from proinsulin?

    <p>It is secreted along with insulin. (D)</p> Signup and view all the answers

    What is the enzyme responsible for the degradation of insulin?

    <p>Insulinases (C)</p> Signup and view all the answers

    What is the approximate half-life of mature insulin in the bloodstream?

    <p>3-5 minutes (D)</p> Signup and view all the answers

    In which cellular structure is proinsulin cleaved into mature insulin?

    <p>Secretory granules (B)</p> Signup and view all the answers

    What is the primary effect of insulin on glucose uptake?

    <p>Increases glucose uptake in muscle and adipose tissue, excluding brain neurons. (D)</p> Signup and view all the answers

    Which glucose transporter is directly dependent on insulin?

    <p>GLUT4 (A)</p> Signup and view all the answers

    What is the immediate effect of insulin binding to its receptor on muscle cells?

    <p>Fusion of GLUT4 vesicles with the cell membrane. (D)</p> Signup and view all the answers

    What happens to GLUT4 transporters when insulin levels decrease?

    <p>They are endocytosed and recycled back into intracellular vesicles. (B)</p> Signup and view all the answers

    Which of the following is NOT an effect of insulin on carbohydrate metabolism?

    <p>Increased gluconeogenesis. (B)</p> Signup and view all the answers

    Which tissue utilizes GLUT5 for glucose transport via secondary active transport using a Na+ gradient?

    <p>Jejunum and kidney tubules (A)</p> Signup and view all the answers

    What is the fate of insulin receptors after insulin binds to them on the cell surface?

    <p>They are endocytosed and then recycled back to the membrane. (C)</p> Signup and view all the answers

    Which statement best describes the directionality of glucose transport via GLUT2?

    <p>Bidirectional transport across cell membrane. (A)</p> Signup and view all the answers

    Which of the following directly triggers the initial, immediate phase of insulin release?

    <p>A sharp increase in blood glucose levels (2-3x above normal fasting) (A)</p> Signup and view all the answers

    What is the primary role of glucokinase in the insulin secretion pathway?

    <p>To produce ATP, which influences potassium channel activity (A)</p> Signup and view all the answers

    Which of these gastrointestinal hormones is known to enhance insulin secretion?

    <p>Glucagon-like Peptide-1 (GLP-1) (D)</p> Signup and view all the answers

    Which of the following describes a characteristic of the delayed phase of insulin release?

    <p>Contribution of newly synthesized insulin to the sustained release (A)</p> Signup and view all the answers

    How does insulin binding to its receptor initiate intracellular signaling?

    <p>Via autophosphorylation of the receptor's beta subunits (D)</p> Signup and view all the answers

    What effect does insulin have on liver cells regarding glucose metabolism?

    <p>Promotes glucose uptake and glycogen synthesis (B)</p> Signup and view all the answers

    Apart from glucose uptake, which of the following is directly stimulated by insulin?

    <p>Lipogenesis (B)</p> Signup and view all the answers

    Which of the following is NOT a direct effect of insulin binding to its receptor?

    <p>Downregulation of specific enzymes involved in glucose metabolism (C)</p> Signup and view all the answers

    What is the primary effect of insulin on lipid metabolism in adipose tissue?

    <p>Promoting lipogenesis through FA uptake and triglyceride synthesis. (B)</p> Signup and view all the answers

    Which process is directly inhibited by insulin in adipose tissue, leading to reduced fatty acid release?

    <p>Hormone-sensitive lipase activity. (C)</p> Signup and view all the answers

    How does insulin influence protein metabolism?

    <p>Enhances protein synthesis and reduces protein breakdown. (D)</p> Signup and view all the answers

    What is one of the key ways insulin contributes to increased lipogenesis in adipose tissue?

    <p>Stimulating the breakdown of VLDL and chylomicrons via lipoprotein lipase. (B)</p> Signup and view all the answers

    Which metabolic process is favored by insulin when glycogen stores are full in the liver?

    <p>Fatty acid synthesis and VLDL formation. (B)</p> Signup and view all the answers

    What effect does insulin deficiency have on lipid metabolism?

    <p>Increased use of stored fat for energy and risk of ketosis. (B)</p> Signup and view all the answers

    How does insulin inhibit gluconeogenesis in the liver?

    <p>By inhibiting the enzymes involved in gluconeogenesis. (A)</p> Signup and view all the answers

    When insulin levels are high, what happens to glucose transport into muscle and adipose tissue?

    <p>Glucose transport into these cells increases via GLUT4. (B)</p> Signup and view all the answers

    What is the primary reason C-peptide is a useful marker for assessing endogenous insulin secretion?

    <p>C-peptide is produced in a 1:1 ratio with insulin and is retained during portal circulation. (D)</p> Signup and view all the answers

    Which cellular event directly precedes the release of insulin and C-peptide from the beta cell?

    <p>Membrane depolarization due to the influx of calcium ions, culminating in exocytosis of insulin containing vesicles. (C)</p> Signup and view all the answers

    What is the role of glucokinase in the regulation of insulin secretion?

    <p>It acts as a glucose sensor and is stimulated by insulin and helps to determine the rate of glycolysis. (B)</p> Signup and view all the answers

    How do sulfonylurea drugs enhance insulin release?

    <p>By closing K⁺ channels, mimicking the effects of high ATP levels and inducing membrane depolarization. (D)</p> Signup and view all the answers

    Which of the following correctly describes the role of gut hormones like GLP-1 and GIP on insulin secretion?

    <p>They increase cAMP, which enhances calcium influx into the beta cells, leading to an increase in insulin secretion. (B)</p> Signup and view all the answers

    What is the direct effect of adrenaline and somatostatin on insulin secretion?

    <p>They inhibit adenylate cyclase, reducing cAMP and calcium influx, which suppresses insulin release. (C)</p> Signup and view all the answers

    What initial event leads to an increase in ATP in the beta cells after a meal?

    <p>Increased glucose entering the beta-cells through GLUT2, which promotes glycolysis and respiration. (B)</p> Signup and view all the answers

    What is a direct consequence of mutations in K⁺ channels that can cause neonatal hyperinsulinemia?

    <p>The potassium channels become non-functional, leading to a state of constant depolarization, and therefore constant insulin secretion. (D)</p> Signup and view all the answers

    What is the primary action of insulin on gluconeogenesis?

    <p>It inhibits enzymes involved in gluconeogenesis. (A)</p> Signup and view all the answers

    Which of the following hormones is primarily responsible for breaking down glycogen in the liver?

    <p>Epinephrine (D)</p> Signup and view all the answers

    What effect does glucocorticoids have on protein metabolism?

    <p>It promotes protein breakdown in muscle and liver. (C)</p> Signup and view all the answers

    What is the effect of insulin on lipolysis in adipose tissue?

    <p>It inhibits lipolysis. (D)</p> Signup and view all the answers

    During high glucose levels, where is glucose primarily directed when glycogen stores are full?

    <p>To fatty acid synthesis. (C)</p> Signup and view all the answers

    Which hormone is known to reduce glucose uptake in muscle cells, thus promoting insulin resistance?

    <p>Growth Hormone (C)</p> Signup and view all the answers

    What is the normal fasting blood glucose range?

    <p>3.9–5.6 mmol/L (D)</p> Signup and view all the answers

    Which metabolic process is stimulated by both glucocorticoids and Growth Hormone?

    <p>Gluconeogenesis (A)</p> Signup and view all the answers

    Flashcards

    Insulin

    A hormone produced by beta (β) cells in the pancreas that helps regulate blood sugar levels by promoting glucose uptake by cells.

    Glucagon

    A hormone produced by alpha (α) cells in the pancreas that raises blood sugar levels by stimulating the liver to release glucose.

    Somatostatin

    A hormone produced by delta (δ) cells in the pancreas that inhibits the release of both insulin and glucagon, acting as a local regulator.

    Pre-proinsulin

    A single polypeptide chain synthesized in the rough endoplasmic reticulum (ER) of beta cells, the precursor to insulin.

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    Proinsulin

    A shorter polypeptide chain formed after pre-proinsulin is cleaved in the ER. It's transported to the Golgi apparatus.

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    Insulin Processing

    The process of converting proinsulin to mature insulin. This involves the formation of disulfide bonds, packaging into secretory granules, and cleavage of C-peptide.

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    Insulin Processing Time

    The time it takes for insulin to be processed and released from beta cells, ranging from 30 to 120 minutes.

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    Insulinases

    Enzymes found in the liver and kidneys primarily responsible for breaking down insulin, regulating blood sugar levels.

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    What triggers insulin release?

    Glucose is the main trigger for insulin release. When blood glucose levels rise, it stimulates the beta cells in the pancreas to release insulin.

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    Explain the two phases of insulin release.

    Insulin release occurs in two phases: the immediate phase and the delayed phase. The immediate phase is a rapid spike in insulin release triggered by a sudden rise in blood glucose, while the delayed phase is a gradual increase in insulin release that lasts over an hour, reflecting the release of both preformed insulin and newly synthesized insulin.

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    What is the primary effect of insulin on liver cells?

    Insulin binds to its receptor on liver cells, triggering glucose uptake into the cells, thus lowering blood glucose levels.

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    How does insulin affect glycogen production?

    Insulin promotes the conversion of excess glucose into glycogen for storage in the liver. This process, known as glycogenesis, helps regulate blood sugar levels by storing glucose for later use.

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    How does insulin affect glucose breakdown?

    Insulin stimulates the breakdown of glucose for energy through a process called glycolysis. This process ensures that cells have a constant supply of energy from glucose when needed.

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    What role does insulin play in fat synthesis?

    Insulin promotes the synthesis of fats (lipogenesis) from excess glucose, allowing for energy storage for future use.

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    What is the role of insulin in protein synthesis?

    Insulin promotes protein synthesis, building and repairing tissues, contributing to overall growth and development.

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    List some other factors that stimulate insulin secretion.

    Besides glucose itself, certain gastrointestinal hormones, such as GIP, GLP-1, and CCK, also stimulate insulin release, further enhancing the response to glucose.

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    What is C-peptide?

    C-peptide is a protein produced alongside insulin in a 1:1 ratio. It has a longer half-life than insulin, making it a useful indicator of your body's natural insulin production.

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    Why is C-peptide useful in diabetes?

    C-peptide is valuable in evaluating insulin secretion in diabetes patients because it reflects the body's intrinsic insulin production.

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    What is the initial step in insulin secretion?

    Elevated blood glucose levels trigger the uptake of glucose into beta cells via GLUT2 transporters. This increase in glucose metabolism leads to higher ATP production.

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    What happens after glucose enters the beta cells?

    Increased ATP levels close ATP-sensitive potassium channels, reducing potassium efflux, which causes the cell membrane to depolarize.

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    What happens after the cell depolarizes?

    Depolarization of the beta cell membrane opens voltage-gated calcium channels, allowing calcium ions to flow into the cell.

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    How is insulin released?

    Calcium influx triggers the fusion of insulin-containing vesicles with the cell membrane, leading to exocytosis and the release of insulin and C-peptide into the bloodstream.

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    How do sulfonylureas work?

    Sulfonylureas are drugs that mimic the effect of glucose by closing potassium channels, boosting insulin secretion.

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    How do gut hormones affect insulin secretion?

    Gut hormones like GIP and GLP-1 increase cAMP production, which enhances calcium influx and insulin secretion.

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    Insulin & Fat Storage

    Insulin promotes the conversion of glucose into fat (triglycerides) for storage in adipose tissues.

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    Insulin Deficiency & Fat Breakdown

    In the absence of insulin, the body utilizes stored fat for energy, leading to an increase in plasma free fatty acids.

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    Insulin & Liver: VLDL Production

    Increased insulin levels stimulate the liver to convert excess glucose into fatty acids for later use, ultimately promoting the production of VLDL (very low-density lipoprotein).

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    Insulin & Protein Synthesis

    High insulin levels increase protein synthesis by stimulating amino acid uptake and increasing gene transcription for protein production.

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    Insulin & Protein Breakdown

    Insulin reduces protein breakdown (catabolism) by reducing the release of amino acids from muscle and other tissues, preserving them for protein synthesis.

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    Insulin & Gluconeogenesis

    Insulin reduces the production of glucose (gluconeogenesis) from amino acids in the liver by inhibiting key enzymes, sparing amino acids for protein synthesis.

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    Insulin & Glycogen Synthesis

    When insulin levels are high, the liver activates glycogen synthase and promotes the conversion of glucose into glycogen for storage.

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    Insulin & Glucose Uptake

    Insulin stimulates the uptake of glucose into muscle and adipose tissue by activating the GLUT4 transporter, increasing glucose utilization for energy.

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    Insulin's primary effect on glucose uptake

    Glucose uptake in muscle and adipose tissue is increased by insulin, but brain neurons don't need insulin for glucose uptake.

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    How does GLUT4 help with glucose uptake?

    GLUT4 is a protein transporter that helps move glucose into cells. It's stored in vesicles, and insulin triggers its movement to the cell membrane, allowing glucose to enter.

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    What happens when insulin is removed?

    When insulin is removed, GLUT4 transporters return to their storage vesicles, decreasing glucose uptake. This is like turning off the delivery service.

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    Why is GLUT2 different from GLUT4?

    Liver cells use GLUT2, a different transporter, allowing glucose to enter or leave depending on the body's needs.

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    How does insulin affect glucose uptake via GLUT4?

    Insulin promotes increased glucose uptake into muscle and adipose tissue by activating GLUT4.

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    Insulin's impact on glycogen storage

    Insulin stimulates the enzyme that builds glycogen (glycogen synthase) and inhibits the enzyme that breaks down glycogen (glycogen phosphorylase) leading to glycogen storage.

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    How does insulin affect glucose storage in the liver?

    Insulin increases the activity of glucokinase, an enzyme involved in glucose storage, increasing glucose storage in the liver.

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    Insulin's impact on gluconeogenesis

    Insulin helps to reduce the production of glucose in the liver by decreasing gluconeogenesis. This limits glucose output from the liver.

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    Insulin's role in glucose homeostasis

    Insulin promotes glucose uptake by cells, inhibits glycogen breakdown, fat breakdown, and gluconeogenesis, while stimulating protein synthesis.

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    Catecholamines' impact on glucose metabolism

    Catecholamines (epinephrine and norepinephrine) increase glycogen breakdown, fat breakdown, and plasma lactate levels, preparing the body for fight or flight.

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    Cortisol's role in glucose metabolism

    Cortisol promotes protein breakdown, fat mobilization, and gluconeogenesis, helping the body cope with stress.

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    Growth hormone's effects on glucose metabolism

    Growth hormone promotes lipolysis, gluconeogenesis, and reduces glucose uptake, contributing to glucose homeostasis.

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    Insulin counterregulatory hormones

    Insulin counterregulatory hormones oppose the actions of insulin, raising blood glucose levels when needed.

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    Glycogenolysis

    Glycogenolysis is the breakdown of glycogen, a stored form of glucose, into glucose molecules.

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    Lipolysis

    Lipolysis is the process of breaking down fat (triglycerides) into fatty acids and glycerol.

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    Gluconeogenesis

    Gluconeogenesis is the process of producing glucose from non-carbohydrate sources like amino acids and glycerol.

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    Study Notes

    Insulin Synthesis, Release, and Action

    • Insulin is a peptide hormone produced in the pancreas.
    • Its main function is enabling glucose entry into tissues (muscle and adipose) and efficient glucose utilization, reducing blood glucose levels.
    • Diabetes Mellitus arises from the inability to synthesize insulin (Type 1) or respond to it (Type 2), leading to elevated blood glucose.

    Pancreas

    • The pancreas consists of exocrine and endocrine cells.
    • Exocrine cells (acinus cells) secrete digestive juices into the duodenum.
    • Endocrine cells (Islets of Langerhans) secrete hormones like insulin, glucagon, somatostatin, and pancreatic polypeptide, important for blood glucose control.
    • Islet cells are highly vascularized (10-15% of blood flow) and innervated by the parasympathetic and sympathetic nervous systems.

    Pancreas: Tissues & Cells

    • Five endocrine cell types reside in the islets of Langerhans.
    • Each cell type synthesizes and secretes a specific hormone.
      • Alpha cells: glucagon
      • Beta cells: insulin
      • Delta cells: somatostatin
      • PP cells (F cells): pancreatic polypeptide
      • Epsilon cells: ghrelin

    Paracrine Signals in the Islet

    • Alpha cells produce glucagon.
    • Glucagon can stimulate beta cells to release insulin, but insulin inhibits glucagon release.
    • Beta cells produce insulin.
    • Insulin inhibits glucagon release from alpha cells and modulates somatostatin release from delta cells.
    • Delta cells produce somatostatin, which inhibits both insulin and glucagon release.

    Synthesis of Insulin

    • Insulin, a polypeptide hormone with two chains (A and B), comprises 51 amino acids.
    • Pre-proinsulin is synthesized in rough ER ribosomes as a single polypeptide chain that becomes proinsulin.
    • In the ER, pre-proinsulin is cleaved into proinsulin, which is then transported to the Golgi apparatus.
    • Within the Golgi, disulfide bonds form between A and B chains, and proinsulin is packaged into secretory granules.
    • In secretory granules, proinsulin is cleaved into insulin and C-peptide.
    • Insulin and C-peptide are ready for exocytosis.

    Synthesis of Insulin: Processing

    • Proteases cleave C-peptide from proinsulin, yielding mature insulin.
    • Mature insulin forms crystalline granules with zinc inside vesicles.
    • Vesicles fuse with the plasma membrane via exocytosis to release insulin and C-peptide.
    • Insulin (3-5 minutes) and C-peptide have different half-lives (35 minutes).
    • Insulinases degrade excess insulin.

    C-Peptide (Clinical Relevance)

    • C-peptide reflects insulin secretion in a 1:1 ratio with insulin.
    • C-peptide has a longer half-life (35 minutes) compared to insulin (3-8 minutes).
    • C-peptide is retained during portal circulation, unlike insulin.
    • C-peptide is useful for assessing endogenous insulin secretion in diabetic patients

    Mechanism of Insulin Secretion

    • High blood glucose triggers glucose uptake through GLUT2, increasing glycolysis and respiration, and further increasing ATP.
    • ATP-sensitive K channels close, reducing potassium efflux.
    • Membrane depolarization opens voltage-gated Ca2+ channels, increasing Ca2+ influx.
    • Fusion of vesicles with the membrane releases insulin and C-peptide via exocytosis.

    Modulation of Insulin Secretion - Key Pathways

    • Glucose metabolism is the primary trigger for insulin secretion.
    • Increased ATP resulting from glucose metabolism closes ATP-sensitive K+ channels, thus increasing insulin secretion.
    • Mutations in K+ channels can cause neonatal hyperinsulinemia.
    • Sulfonylurea drugs close K+ channels, enhancing insulin secretion by mimicking glucose action.
    • Voltage-gated calcium channels (VGCC) are activated by gut hormones.
    • Gut hormones increase cAMP and enhance calcium influx, stimulating insulin secretion.
    • Adrenaline and somatostatin inhibit adenylate cyclase, reducing cAMP and calcium influx, suppressing insulin release.

    Regulation of Insulin Secretion - Factors Involved

    • Meal constituents (glucose, amino acids, free fatty acids) directly stimulate insulin secretion.
    • Gastrointestinal hormones like GIP, GLP-1, and CCK enhance insulin secretion.
    • Inhibitors like somatostatin and certain epinephrine receptors can reduce insulin secretion.

    Phases of Insulin Release

    • Insulin release occurs in two phases:
      • Immediate phase (3-5 minutes): triggered by a rise in glucose; a rapid burst of insulin release.
      • Delayed phase (over 1 hour): gradual increase in insulin release following the initial burst; primarily from newly synthesized insulin.
    • Phase 1 insulin is stored in granules near capillaries.
    • Phase 2 insulin is stored in granules further from capillaries and comprises newly synthesized insulin.

    Insulin Receptor Activation and Effects

    • Insulin binding induces autophosphorylation of the receptor's beta subunits, activating tyrosine kinase activity.
    • Phosphorylation of insulin receptor substrate (IRS) proteins initiates downstream signaling cascades.

    Effect of Insulin

    • Insulin facilitates glucose uptake into cells.
    • Insulin stimulates glycogen synthesis and inhibits glycogenolysis, promoting glucose storage.
    • Insulin stimulates glycolysis, breaking down glucose for energy.
    • Insulin stimulates lipogenesis, the synthesis of fats.
    • Insulin promotes protein synthesis.

    Glucose Transport and Insulin Action

    • Insulin's primary effect is increasing glucose uptake into muscle and adipose tissues.
    • Brain neurons do not require insulin for glucose uptake.
    • GLUT4 (insulin-dependent glucose transporter) is stored in intracellular vesicles in muscle and fat cells.
    • Insulin binding triggers vesicle fusion with the cell membrane, inserting GLUT4 transporters into the membrane to enable glucose uptake.
    • When insulin is removed, GLUT4 transporters are recycled back to intracellular vesicles, decreasing glucose uptake.

    Glucose Transporters

    • GLUT1, GLUT2, GLUT3, GLUT4, and GLUT5 are glucose transporters that facilitate glucose uptake into target tissues.
    • GLUT4 is insulin-dependent and located in muscle, fat, and heart tissues (facilitated diffusion).
    • GLUT1, GLUT2, and GLUT3 are not insulin-dependent and are ubiquitous in various cells (facilitated diffusion).
    • GLUT5 is not insulin-dependent and located in the jejunum, intestine, and kidney tubules (secondary active transport).

    Effects of Insulin on Metabolism (Carbohydrates)

    • Insulin increases glucose uptake into muscle and adipose tissue by activating the GLUT4 transporter.
    • Insulin activates glycogen synthase, increasing glycogen synthesis.
    • Insulin inhibits glycogen phosphorylase, which reduces glycogen breakdown.
    • Insulin enhances liver glucokinase activity, promoting glucose storage in the liver.
    • Insulin supports NADPH production in the pentose phosphate pathway, required for biosynthesis.
    • Insulin reduces hepatic glucose production (gluconeogenesis).

    Effects of Insulin on Metabolism (Lipids)

    • Insulin promotes lipogenesis (fat storage) by activating capillary lipoprotein lipase, enabling free fatty acid uptake by adipocytes and stimulating glycerol-3-phosphate and triglyceride synthesis.
    • Insulin inhibits hormone-sensitive lipase in adipose tissue, reducing lipolysis (fat breakdown).
    • In the liver, glucose is directed towards fatty acid synthesis when glycogen stores are full, leading to VLDL formation.

    Effects of Insulin on Metabolism (Proteins)

    • Insulin increases protein synthesis by stimulating gene transcription and amino acid uptake by cells.
    • Insulin reduces protein breakdown and amino acid release from muscle and other tissues, thus promoting protein synthesis.
    • Insulin inhibits enzymes involved in gluconeogenesis, preserving amino acids for protein synthesis.

    Insulin Deficiency & Lipid Metabolism

    • Without insulin, lipolysis increases, releasing free fatty acids from adipose tissue.
    • This rise in free fatty acids leads to increased plasma cholesterol and lipoproteins.
    • Uncontrolled fat breakdown potentially increases the risk of ketoacidosis.

    Insulin Counterregulatory Hormones

    • Catecholamines (epinephrine and norepinephrine) increase glycogenolysis, lipolysis, and plasma lactate levels, thus opposing insulin's effects.
    • Glucocorticoids (cortisol) increase protein breakdown, fatty acid mobilization, and gluconeogenesis.
    • Growth hormone (GH) increases lipolysis, gluconeogenesis, and reduces glucose uptake promoting insulin resistance.

    Glucose Homeostasis - Hyperglycemia & Hypoglycemia

    • Normal fasting blood glucose is 3.9-5.6 mmol/L (70-100 mg/dL).
    • Hypoglycemia (<3.9 mmol/L) can lead to severe neurological complications.
    • Causes of hypoglycemia include acute complications, hyperinsulinism, and insufficient counterregulatory hormones.
    • Chronic hyperglycemia damages tissues, leading to diabetes, nephropathy, and neuropathy.

    Hyperinsulinism and Hypoglycemia

    • Hyperinsulinism, or excessive insulin production or activity, can cause hypoglycemia.
    • Causes of hyperinsulinism include congenital hyperinsulinism, genetic disorders, and tumours (insulinomas).
    • Drug-induced hyperinsulinism (e.g., sulfonylureas) can also lead to elevated insulin levels, which often result in hypoglycemia.
    • Diagnosis often requires differentiating from insulinoma based on differing C-peptide levels.

    Diabetes Mellitus - Classification

    • Type 1 diabetes (T1D) is characterized by autoimmune destruction of beta cells leading to insulin deficiency.
    • Type 2 diabetes (T2D) is characterized by insulin resistance coupled with reduced insulin production.
    • Risk factors for T2D include obesity and older age.
    • Lifestyle modification and/or drugs like Metformin, Thiazolidinediones, Sulfonylureas, and GLP-1 Receptor Agonists can manage T2D.

    Diabetes: Diagnostic Criteria

    • Diagnostic criteria for diabetes include fasting plasma glucose (FPG) ≥ 7.0 mmol/L (126 mg/dL), random plasma glucose ≥ 11.1 mmol/L (200 mg/dL) in the presence of symptoms, HbA1c ≥ 6.5%, and oral glucose tolerance test (OGTT) ≥ 11.1 mmol/L (200 mg/dL) 2 hours post a 75g glucose load.

    Diabetic Ketoacidosis (DKA)

    • Diabetic ketoacidosis (DKA) occurs in uncontrolled diabetes, usually type 1, leading to ketone build-up in the blood.
    • DKA is life-threatening and requires immediate treatment.
    • Symptoms of DKA include shortness of breath (Kussmaul breathing), fruity-smelling breath (acetone), abdominal pain, nausea, and vomiting.

    Other Resources

    • Relevant readings on human endocrinology and essential endocrinology are Gard and Brook & Marshall.
    • Guyton & Hall and other cited publications provide further information on this subject.

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    Description

    Test your knowledge on the interplay between insulin and glucagon with this quiz. Explore key concepts such as the synthesis and role of insulin, the effects on glucose uptake, and the regulation of these hormones in the body. Perfect for students of endocrinology or anyone interested in metabolic processes.

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