So now that we've covered secondary active transport, in this video, we're going to talk about a specific example of secondary active transport, and that is the glucose active symporter model. Now, this is a classic and relevant example of secondary active transport. And more specifically, we're going to be looking at the intestinal epithelial sodium glucose symporters. And so just to get a better idea of exactly what we're talking about when we refer to intestinal epithelial cells, let's take a look at our image down below. And so notice that we've got our anatomical figure over here and we're zooming into this specific region. And, you can see that we have the stomach, the pancreas, and the intestinal lumen right here. And so if we zoom into the intestinal lumen wall right here in this region, what you'll notice is that the wall is made up of these villi structures that you see right here, these curved structures that give more surface area to the intestinal lumen and allow for better absorption of materials that we eat. And so what you'll notice is that these villi are lined with individual intestinal epithelial cells. And also these villi are closely associated with our bloodstreams, which we have right here in the villi. And so if we zoom into this particular region over here on the right-hand side of our villi, notice that, again, zooming in will show a bunch of individual intestinal epithelial cells. And these little structures that you see here would be the microvilli. Again, allowing cells to increase surface area and increase their absorption of materials that get into our intestines. And so notice that now we're zooming into one individual intestinal epithelial cell here, and that is going to be this image that you see down below. And so really, this image down below is the main image for this lesson, and all of the other images are just there to give you guys a little bit of context. 3 important components that you guys should know. And we've labeled each of these three components as a, b, and c, and you'll be able to see each of these 3 components corresponds with the images that we have down below. So you can see component a is right here, component b is over here, and component c is right here. And so, of course, we know from our previous lesson videos that secondary active transport is indirectly driven by primary active transport. And so that's exactly where we start with component a is primary active transport. And more specifically, it's actually the sodium potassium pump that is going to maintain a transmembrane sodium gradient. And this transmembrane sodium gradient, we know is going to be really high on the outside of the cell, and really low on the inside of the cell. And so if we take a look at our image down below at component a over here, notice that it's just the sodium potassium pump that we talked about from our previous lesson videos. And so we know that it hydrolyzes ATP, and in the process, it transports 3 sodium ions to the outside of the cell as it transports 2 potassium ions to the inside of the cell. And so again, this is establishing a concentration gradient for sodium that is really high on the outside of the cell and really low sodium on the inside of the cell. And so that transitions us directly into the secondary active transport part of this lesson, and that is exactly where the sodium glucose symporters come into play. And so the sodium glucose symporters are going to co-transport, as their name implies, sodium and glucose in the same direction across the membrane. And that's what makes them symporters because the 2 molecules are being transported in the same direction. And so really, what powers the transport of this co-transport here is that there are 2 sodium ions that are going to be imported down their concentration gradients or with their concentration gradients from high to low. And, these 2 sodium ions being imported down their concentration gradients is really what powers the movement of 1 glucose molecule being imported into the cell against its concentration gradient from an area of low concentration to an area of higher concentration. And so if we take a look down below at our image, notice that we have component b up here at the top right, and this is our sodium glucose symporter, our secondary active transporter model. And so notice that no ATP hydrolysis is directly involved here with this, sodium glucose importer. So we know it's gotta be a form of secondary active transport, and it's utilizing the gradient that was established by the sodium potassium pump, the sodium gradient that was established. So there's low sodium on the inside and high sodium on the outside. And so as sodium gets imported down its concentration gradient from high to low, it's powering the movement of glucose from the intestinal tract into the intestinal epithelial cell against its concentration gradient. And so now that transitions us to the last part here of our lesson, part c. And that is just to know that as glucose is pumped into the intestinal epithelial cell from the intestinal tract to the inside of the cell, it's also simultaneously being moved into the bloodstream via a GLUT2 uniporter. And of course, we know uniporters will transport 1 molecule in one direction across the membrane, and that is going to be glucose. And so if we take a look at our image down below, notice down below part c here, we have the GLUT2 uniporter, which is going to transport glucose, in one direction across the membrane so that it can diffuse into the blood. And of course, once glucose is in the blood, that glucose can diffuse to pretty much every cell in our bodies. And so one thing to note here is that the sodium glucose symporter that we talked about in part b and this, GLUT2 uniporter that we just talked about in part c are actually operating on opposite sides of the intestinal epithelial cells. And so if we take a look back down below, notice again that the sodium glucose importer is operating on the intestinal tract, side of the cell. And notice that the GLUT2 uniporter is operating on the opposite side of the cell that's closer to the bloodstream. And so all of these systems here are operating together to allow glucose that gets into our digestive system when we eat foods and transport that glucose from our intestinal tract into our intestinal epithelial cells, and then through, the intestinal epithelial cell into the blood where, again, it can be transported to every cell in our bodies. And so really, it's this sodium glucose importer here that is our example of secondary active transport. And really, this is the conclusion of our lesson on glucose active importer model, and we'll be able to get a bunch of practice in our next couple of videos. So I'll see you guys there.
- 1. Introduction to Biochemistry4h 34m
- What is Biochemistry?5m
- Characteristics of Life12m
- Abiogenesis13m
- Nucleic Acids16m
- Proteins12m
- Carbohydrates8m
- Lipids10m
- Taxonomy10m
- Cell Organelles12m
- Endosymbiotic Theory11m
- Central Dogma22m
- Functional Groups15m
- Chemical Bonds13m
- Organic Chemistry31m
- Entropy17m
- Second Law of Thermodynamics11m
- Equilibrium Constant10m
- Gibbs Free Energy37m
- 2. Water3h 23m
- 3. Amino Acids8h 10m
- Amino Acid Groups8m
- Amino Acid Three Letter Code13m
- Amino Acid One Letter Code37m
- Amino Acid Configuration20m
- Essential Amino Acids14m
- Nonpolar Amino Acids21m
- Aromatic Amino Acids14m
- Polar Amino Acids16m
- Charged Amino Acids40m
- How to Memorize Amino Acids1h 7m
- Zwitterion33m
- Non-Ionizable Vs. Ionizable R-Groups11m
- Isoelectric Point10m
- Isoelectric Point of Amino Acids with Ionizable R-Groups51m
- Titrations of Amino Acids with Non-Ionizable R-Groups44m
- Titrations of Amino Acids with Ionizable R-Groups38m
- Amino Acids and Henderson-Hasselbalch44m
- 4. Protein Structure10h 4m
- Peptide Bond18m
- Primary Structure of Protein31m
- Altering Primary Protein Structure15m
- Drawing a Peptide44m
- Determining Net Charge of a Peptide42m
- Isoelectric Point of a Peptide37m
- Approximating Protein Mass7m
- Peptide Group22m
- Ramachandran Plot26m
- Atypical Ramachandran Plots12m
- Alpha Helix15m
- Alpha Helix Pitch and Rise20m
- Alpha Helix Hydrogen Bonding24m
- Alpha Helix Disruption23m
- Beta Strand12m
- Beta Sheet12m
- Antiparallel and Parallel Beta Sheets39m
- Beta Turns26m
- Tertiary Structure of Protein16m
- Protein Motifs and Domains23m
- Denaturation14m
- Anfinsen Experiment20m
- Protein Folding34m
- Chaperone Proteins19m
- Prions4m
- Quaternary Structure15m
- Simple Vs. Conjugated Proteins10m
- Fibrous and Globular Proteins11m
- 5. Protein Techniques14h 5m
- Protein Purification7m
- Protein Extraction5m
- Differential Centrifugation15m
- Salting Out18m
- Dialysis9m
- Column Chromatography11m
- Ion-Exchange Chromatography35m
- Anion-Exchange Chromatography38m
- Size Exclusion Chromatography28m
- Affinity Chromatography16m
- Specific Activity16m
- HPLC29m
- Spectrophotometry51m
- Native Gel Electrophoresis23m
- SDS-PAGE34m
- SDS-PAGE Strategies16m
- Isoelectric Focusing17m
- 2D-Electrophoresis23m
- Diagonal Electrophoresis29m
- Mass Spectrometry12m
- Mass Spectrum47m
- Tandem Mass Spectrometry16m
- Peptide Mass Fingerprinting16m
- Overview of Direct Protein Sequencing30m
- Amino Acid Hydrolysis10m
- FDNB26m
- Chemical Cleavage of Bonds29m
- Peptidases1h 6m
- Edman Degradation30m
- Edman Degradation Sequenator and Sequencing Data Analysis4m
- Edman Degradation Reaction Efficiency20m
- Ordering Cleaved Fragments21m
- Strategy for Ordering Cleaved Fragments58m
- Indirect Protein Sequencing Via Geneomic Analyses24m
- 6. Enzymes and Enzyme Kinetics13h 38m
- Enzymes24m
- Enzyme-Substrate Complex17m
- Lock and Key Vs. Induced Fit Models23m
- Optimal Enzyme Conditions9m
- Activation Energy24m
- Types of Enzymes41m
- Cofactor15m
- Catalysis19m
- Electrostatic and Metal Ion Catalysis11m
- Covalent Catalysis18m
- Reaction Rate10m
- Enzyme Kinetics24m
- Rate Constants and Rate Law35m
- Reaction Orders52m
- Rate Constant Units11m
- Initial Velocity31m
- Vmax Enzyme27m
- Km Enzyme42m
- Steady-State Conditions25m
- Michaelis-Menten Assumptions18m
- Michaelis-Menten Equation52m
- Lineweaver-Burk Plot43m
- Michaelis-Menten vs. Lineweaver-Burk Plots20m
- Shifting Lineweaver-Burk Plots37m
- Calculating Vmax40m
- Calculating Km31m
- Kcat46m
- Specificity Constant1h 1m
- 7. Enzyme Inhibition and Regulation 8h 42m
- Enzyme Inhibition13m
- Irreversible Inhibition12m
- Reversible Inhibition9m
- Inhibition Constant26m
- Degree of Inhibition15m
- Apparent Km and Vmax29m
- Inhibition Effects on Reaction Rate10m
- Competitive Inhibition52m
- Uncompetitive Inhibition33m
- Mixed Inhibition40m
- Noncompetitive Inhibition26m
- Recap of Reversible Inhibition37m
- Allosteric Regulation7m
- Allosteric Kinetics17m
- Allosteric Enzyme Conformations33m
- Allosteric Effectors18m
- Concerted (MWC) Model25m
- Sequential (KNF) Model20m
- Negative Feedback13m
- Positive Feedback15m
- Post Translational Modification14m
- Ubiquitination19m
- Phosphorylation16m
- Zymogens13m
- 8. Protein Function 9h 41m
- Introduction to Protein-Ligand Interactions15m
- Protein-Ligand Equilibrium Constants22m
- Protein-Ligand Fractional Saturation32m
- Myoglobin vs. Hemoglobin27m
- Heme Prosthetic Group31m
- Hemoglobin Cooperativity23m
- Hill Equation21m
- Hill Plot42m
- Hemoglobin Binding in Tissues & Lungs31m
- Hemoglobin Carbonation & Protonation19m
- Bohr Effect23m
- BPG Regulation of Hemoglobin24m
- Fetal Hemoglobin6m
- Sickle Cell Anemia24m
- Chymotrypsin18m
- Chymotrypsin's Catalytic Mechanism38m
- Glycogen Phosphorylase21m
- Liver vs Muscle Glycogen Phosphorylase21m
- Antibody35m
- ELISA15m
- Motor Proteins14m
- Skeletal Muscle Anatomy22m
- Skeletal Muscle Contraction45m
- 9. Carbohydrates7h 49m
- Carbohydrates19m
- Monosaccharides15m
- Stereochemistry of Monosaccharides33m
- Monosaccharide Configurations32m
- Cyclic Monosaccharides20m
- Hemiacetal vs. Hemiketal19m
- Anomer14m
- Mutarotation13m
- Pyranose Conformations23m
- Common Monosaccharides33m
- Derivatives of Monosaccharides21m
- Reducing Sugars21m
- Reducing Sugars Tests19m
- Glycosidic Bond48m
- Disaccharides40m
- Glycoconjugates12m
- Polysaccharide7m
- Cellulose7m
- Chitin8m
- Peptidoglycan12m
- Starch13m
- Glycogen14m
- Lectins16m
- 10. Lipids5h 49m
- Lipids15m
- Fatty Acids30m
- Fatty Acid Nomenclature11m
- Omega-3 Fatty Acids12m
- Triacylglycerols11m
- Glycerophospholipids24m
- Sphingolipids13m
- Sphingophospholipids8m
- Sphingoglycolipids12m
- Sphingolipid Recap22m
- Waxes5m
- Eicosanoids19m
- Isoprenoids9m
- Steroids14m
- Steroid Hormones11m
- Lipid Vitamins19m
- Comprehensive Final Lipid Map13m
- Biological Membranes16m
- Physical Properties of Biological Membranes18m
- Types of Membrane Proteins8m
- Integral Membrane Proteins16m
- Peripheral Membrane Proteins12m
- Lipid-Linked Membrane Proteins21m
- 11. Biological Membranes and Transport 6h 37m
- Biological Membrane Transport21m
- Passive vs. Active Transport18m
- Passive Membrane Transport21m
- Facilitated Diffusion8m
- Erythrocyte Facilitated Transporter Models30m
- Membrane Transport of Ions29m
- Primary Active Membrane Transport15m
- Sodium-Potassium Ion Pump20m
- SERCA: Calcium Ion Pump10m
- ABC Transporters12m
- Secondary Active Membrane Transport12m
- Glucose Active Symporter Model19m
- Endocytosis & Exocytosis18m
- Neurotransmitter Release23m
- Summary of Membrane Transport21m
- Thermodynamics of Membrane Diffusion: Uncharged Molecule51m
- Thermodynamics of Membrane Diffusion: Charged Ion1h 1m
- 12. Biosignaling9h 45m
- Introduction to Biosignaling44m
- G protein-Coupled Receptors32m
- Stimulatory Adenylate Cyclase GPCR Signaling42m
- cAMP & PKA28m
- Inhibitory Adenylate Cyclase GPCR Signaling29m
- Drugs & Toxins Affecting GPCR Signaling20m
- Recap of Adenylate Cyclase GPCR Signaling5m
- Phosphoinositide GPCR Signaling58m
- PSP Secondary Messengers & PKC27m
- Recap of Phosphoinositide Signaling7m
- Receptor Tyrosine Kinases26m
- Insulin28m
- Insulin Receptor23m
- Insulin Signaling on Glucose Metabolism57m
- Recap Of Insulin Signaling in Glucose Metabolism6m
- Insulin Signaling as a Growth Factor1h 1m
- Recap of Insulin Signaling As A Growth Factor9m
- Recap of Insulin Signaling1m
- Jak-Stat Signaling25m
- Lipid Hormone Signaling15m
- Summary of Biosignaling13m
- Signaling Defects & Cancer20m
- Review 1: Nucleic Acids, Lipids, & Membranes2h 47m
- Nucleic Acids 19m
- Nucleic Acids 211m
- Nucleic Acids 34m
- Nucleic Acids 44m
- DNA Sequencing 19m
- DNA Sequencing 211m
- Lipids 111m
- Lipids 24m
- Membrane Structure 110m
- Membrane Structure 29m
- Membrane Transport 18m
- Membrane Transport 24m
- Membrane Transport 36m
- Practice - Nucleic Acids 111m
- Practice - Nucleic Acids 23m
- Practice - Nucleic Acids 39m
- Lipids11m
- Practice - Membrane Structure 17m
- Practice - Membrane Structure 25m
- Practice - Membrane Transport 16m
- Practice - Membrane Transport 26m
- Review 2: Biosignaling, Glycolysis, Gluconeogenesis, & PP-Pathway3h 12m
- Biosignaling 19m
- Biosignaling 219m
- Biosignaling 311m
- Biosignaling 49m
- Glycolysis 17m
- Glycolysis 27m
- Glycolysis 38m
- Glycolysis 410m
- Fermentation6m
- Gluconeogenesis 18m
- Gluconeogenesis 27m
- Pentose Phosphate Pathway15m
- Practice - Biosignaling13m
- Practice - Bioenergetics 110m
- Practice - Bioenergetics 216m
- Practice - Glycolysis 111m
- Practice - Glycolysis 27m
- Practice - Gluconeogenesis5m
- Practice - Pentose Phosphate Path6m
- Review 3: Pyruvate & Fatty Acid Oxidation, Citric Acid Cycle, & Glycogen Metabolism2h 26m
- Pyruvate Oxidation9m
- Citric Acid Cycle 114m
- Citric Acid Cycle 27m
- Citric Acid Cycle 37m
- Citric Acid Cycle 411m
- Metabolic Regulation 18m
- Metabolic Regulation 213m
- Glycogen Metabolism 16m
- Glycogen Metabolism 28m
- Fatty Acid Oxidation 111m
- Fatty Acid Oxidation 28m
- Citric Acid Cycle Practice 17m
- Citric Acid Cycle Practice 26m
- Citric Acid Cycle Practice 32m
- Glucose and Glycogen Regulation Practice 14m
- Glucose and Glycogen Regulation Practice 26m
- Fatty Acid Oxidation Practice 14m
- Fatty Acid Oxidation Practice 27m
- Review 4: Amino Acid Oxidation, Oxidative Phosphorylation, & Photophosphorylation1h 48m
- Amino Acid Oxidation 15m
- Amino Acid Oxidation 211m
- Oxidative Phosphorylation 18m
- Oxidative Phosphorylation 210m
- Oxidative Phosphorylation 310m
- Oxidative Phosphorylation 47m
- Photophosphorylation 15m
- Photophosphorylation 29m
- Photophosphorylation 310m
- Practice: Amino Acid Oxidation 12m
- Practice: Amino Acid Oxidation 22m
- Practice: Oxidative Phosphorylation 15m
- Practice: Oxidative Phosphorylation 24m
- Practice: Oxidative Phosphorylation 35m
- Practice: Photophosphorylation 15m
- Practice: Photophosphorylation 21m
Glucose Active Symporter Model - Online Tutor, Practice Problems & Exam Prep
The sodium-glucose symporter exemplifies secondary active transport in intestinal epithelial cells. It utilizes the sodium gradient established by the sodium-potassium pump, which transports 3 sodium ions out and 2 potassium ions in, creating a high extracellular sodium concentration. This gradient drives the co-transport of sodium and glucose into the cell, allowing glucose to move against its concentration gradient. Subsequently, glucose exits into the bloodstream via the GLUT2 uniporter, facilitating its distribution throughout the body. This process highlights the interplay between active transport mechanisms and nutrient absorption.
Glucose Active Symporter Model
Video transcript
The Na+-Glucose symporter transports the two molecules into the cell, while the Na+-K+ ATPase uses ATP to transport Na+ ions out of the cell. What would be the result of a mutation leading to a nonfunctional Na+-Glucose symporter?
Imagine that you perform a series of experiments to test the rate of glucose transport (V0) into epithelial cells using the Na+-Glucose symporters. These experimental epithelial cells contain no intracellular Na+ but have the same glucose concentration as their surroundings. In experiment #1, you transfer your cells to test tubes that contain different extracellular [Na+] & then measure the rate of glucose transport (V0). In experiment #2, you introduce leakage Na+ channels into the cell membranes & then repeat the same experiment. Label the data on the plot below as showing results to either Experiment #1 or Experiment #2.
Problem Transcript
Here’s what students ask on this topic:
What is the role of the sodium-potassium pump in the glucose active symporter model?
The sodium-potassium pump plays a crucial role in the glucose active symporter model by establishing a sodium gradient across the intestinal epithelial cell membrane. This pump uses ATP to transport 3 sodium ions out of the cell and 2 potassium ions into the cell, creating a high concentration of sodium outside the cell and a low concentration inside. This gradient is essential for the secondary active transport of glucose. The sodium-glucose symporter utilizes the energy from sodium ions moving down their concentration gradient to co-transport glucose into the cell against its concentration gradient. This process is vital for efficient glucose absorption in the intestines.
How does the sodium-glucose symporter facilitate glucose absorption in the intestines?
The sodium-glucose symporter facilitates glucose absorption in the intestines by coupling the transport of glucose with sodium ions. This symporter is located on the apical side of intestinal epithelial cells. It uses the energy from sodium ions moving down their concentration gradient, established by the sodium-potassium pump, to transport glucose into the cell against its concentration gradient. As sodium ions flow into the cell, they drive the uptake of glucose from the intestinal lumen into the epithelial cells. Once inside, glucose is then transported into the bloodstream via the GLUT2 uniporter, ensuring its distribution throughout the body.
What is the difference between primary and secondary active transport in the context of glucose absorption?
Primary active transport directly uses ATP to move ions against their concentration gradients. In the context of glucose absorption, the sodium-potassium pump is an example of primary active transport. It hydrolyzes ATP to transport 3 sodium ions out of the cell and 2 potassium ions into the cell, creating a sodium gradient. Secondary active transport, on the other hand, does not directly use ATP. Instead, it relies on the energy stored in the ion gradients established by primary active transport. The sodium-glucose symporter is an example of secondary active transport, using the sodium gradient to co-transport glucose into the cell against its concentration gradient.
What is the function of the GLUT2 uniporter in glucose transport?
The GLUT2 uniporter plays a critical role in the final step of glucose transport from the intestinal epithelial cells into the bloodstream. After glucose is co-transported into the epithelial cells by the sodium-glucose symporter, the GLUT2 uniporter facilitates the passive transport of glucose across the basolateral membrane of the epithelial cells into the blood. This uniporter operates by allowing glucose to move down its concentration gradient, ensuring that glucose absorbed from the intestines can enter the bloodstream and be distributed to various tissues and organs throughout the body.
How does the sodium-glucose symporter model exemplify secondary active transport?
The sodium-glucose symporter model exemplifies secondary active transport by using the energy stored in the sodium gradient, established by the sodium-potassium pump, to drive the uptake of glucose into the cell. The sodium-potassium pump, a primary active transporter, creates a high concentration of sodium outside the cell. The sodium-glucose symporter then uses this gradient to co-transport sodium and glucose into the cell. Sodium ions move down their concentration gradient, providing the energy needed to transport glucose against its concentration gradient. This indirect use of ATP, via the sodium gradient, is characteristic of secondary active transport.