In this video, we're going to introduce yet another way that cells can regulate their biochemical reactions, and that is through negative feedback. And so negative feedback is also sometimes referred to as just feedback inhibition. And so negative feedback or feedback inhibition is an efficient and a very common means for biochemical regulation. And so cells use negative feedback all the time to regulate their reactions. Now really the purpose of negative feedback is to prevent the overproduction as well as the wasteful production of a product. And so as we'll see moving forward, negative feedback is really just a way for molecules such as a product to regulate the production of its own activity. And so negative feedback inhibition is when the final product or just a later product in a metabolic pathway can come back and inhibit an earlier step in the same exact metabolic pathway that led to that product's production. And so ultimately, this is going to slow down the entire metabolic pathway, and that is going to begin to decrease the final concentration of that product that acted to inhibit the reaction. And so, as we'll see down below in our example, negative feedback inhibitors really do, inhibitors, really do act as inhibitors. And recall that inhibitors are commonly represented with a negative symbol. And so these negative feedback inhibitors are going to bind to an allosteric an allosteric site on the allosteric enzyme and of course that means that it's not going to bind to the enzyme's active site. And so down below in our example, notice we're saying that negative feedback inhibition really acts like the red light, to inhibit metabolic pathways. And so over here what we have is a red light to show you that, really negative feedback acts like a red light and slows down these, metabolic pathways. And so over here we're showing you an example of a metabolic pathway. And so you can see that we have all of these reactions here and notice that most of these reactions are being catalyzed by Michaelis Menten enzymes. But here we do have one enzyme that is displaying allosteric kinetics. And so, notice here that we have a final product f and if the concentration of f happens to get way too high, then f can actually come back and inhibit the allosteric enzyme number 1 here. And we know that it's inhibiting because, again, we have a minus sign here, that represents inhibition. And so if f comes all the way back to inhibit enzyme number 1, then that's going to prevent the conversion from a to b. And, ultimately, that's going to lead to the decrease of the concentration of product f. And so when the final concentration of the product f over here is returned back to normal or lower levels, then, the feedback inhibition that is caused by product f here is essentially going to stop, and that's going to allow the metabolic pathway to proceed once again. And so, clearly here we're talking about negative feedback inhibition. And you can see how really through negative feedback inhibition, molecules such as product f here are able to regulate their own production. And so, by coming back and inhibiting enzyme number 1, product f can influence the decrease or the lowering of its concentration. And so, it turns out again that negative feedback inhibition is an efficient and a common means for biochemical regulation. So later in our course we're going to talk about many different examples of negative feedback. And in our next lesson video, we'll specifically talk about one particular example. And so, I'll see you guys in that video.
- 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
Negative Feedback - Online Tutor, Practice Problems & Exam Prep
Negative feedback, or feedback inhibition, is a crucial mechanism for regulating biochemical reactions in cells. It prevents overproduction and waste by allowing a final product to inhibit an earlier step in its metabolic pathway. This process involves an allosteric enzyme, where the product binds to an allosteric site, effectively slowing down the pathway and decreasing the product's concentration. Once levels normalize, inhibition ceases, allowing the pathway to resume. This efficient regulation is vital for maintaining homeostasis in cellular metabolism.
Negative Feedback
Video transcript
Negative Feedback Example 1
Video transcript
So now that we've covered the basics of negative feedback or feedback inhibition, in this video we're going to cover an example of feedback regulation in glycolysis. And so recall from your previous biology courses that glycolysis is just a process in cellular respiration that breaks down glucose to generate energy in the form of ATP. Notice in the image below, we're showing you a snippet of the glycolysis process or metabolic pathway. Over here on the far left, notice we are starting with a glucose molecule. One of the final products of glycolysis is the net generation of ATP. We're not showing the full glycolysis metabolic pathway here, but we will cover it later in our course. For now, we just want to emphasize that the cell already has plenty of ATP. And in that scenario, the cell would not want to be breaking down glucose to generate even more ATP. In this scenario, ATP can act as a negative feedback regulator to inhibit one of the enzymes that act in glycolysis, and this enzyme is known as phosphofructokinase, abbreviated as PFK. Phosphofructokinase or PFK is an allosteric enzyme that catalyzes a particular reaction in glycolysis. If we look below, notice that PFK catalyzes the conversion of fructose 6-phosphate into fructose 1,6-bisphosphate, essentially adding an extra phosphate group at this position. It needs to utilize ATP here as a co-substrate to catalyze this reaction. Again, PFK is going to be regulated via negative feedback by ATP. ATP can come back and negatively regulate PFK to inhibit it, essentially leading to the decrease of ATP or preventing the production of ATP. Because ATP is also utilized as a co-substrate for PFK, and ATP also acts as a negative allosteric regulator of PFK, that actually makes ATP a homotrophic allosteric effector. And that's because ATP is used as a substrate as well as an allosteric effector. Because the substrate is the same as the allosteric effector, that makes the allosteric effector homotrophic. This is just one example of negative feedback in glycolysis, but later in our course, we'll talk about a lot more examples of negative feedback throughout all of cellular respiration. But for now, this concludes our example of feedback regulation in glycolysis, and in our next video, we will be able to get some practice utilizing the concepts that we've learned. So I'll see you guys in that video.
The scheme below represents a hypothetical metabolic pathway for the synthesis of compound Y. The pathway is regulated by feedback inhibition. If S → T is the rate-limiting step, circle what the most likely inhibitor is and indicate with an arrow where the inhibition most likely occurs:
S → T → U → V → W → X → Y
Problem Transcript
Which of the following is TRUE about feedback inhibition?
Here’s what students ask on this topic:
What is negative feedback in biochemical reactions?
Negative feedback, also known as feedback inhibition, is a regulatory mechanism in biochemical reactions where the final product of a metabolic pathway inhibits an earlier step in the same pathway. This process helps prevent the overproduction and wasteful accumulation of the product. The inhibition typically occurs through the binding of the product to an allosteric site on an enzyme, which slows down the pathway and decreases the product's concentration. Once the product levels return to normal, the inhibition ceases, allowing the pathway to resume. This efficient regulation is crucial for maintaining cellular homeostasis.
How does negative feedback prevent overproduction in cells?
Negative feedback prevents overproduction in cells by allowing the final product of a metabolic pathway to inhibit an earlier step in the same pathway. When the concentration of the product becomes too high, it binds to an allosteric site on an enzyme involved in the pathway, reducing the enzyme's activity. This slows down the entire pathway, decreasing the production of the product. Once the product levels normalize, the inhibition stops, and the pathway can proceed again. This mechanism ensures that cells produce only the necessary amount of a product, avoiding waste and maintaining balance.
What role do allosteric enzymes play in negative feedback?
Allosteric enzymes play a crucial role in negative feedback by serving as the target for inhibition by the final product of a metabolic pathway. These enzymes have allosteric sites, distinct from their active sites, where the product can bind. When the product binds to the allosteric site, it induces a conformational change in the enzyme, reducing its activity. This decrease in enzyme activity slows down the metabolic pathway, leading to a reduction in the product's concentration. Once the product levels return to normal, the inhibition ceases, allowing the enzyme to regain its activity and the pathway to resume.
Can you provide an example of negative feedback in a metabolic pathway?
An example of negative feedback in a metabolic pathway is the regulation of the synthesis of isoleucine from threonine in bacteria. In this pathway, the final product, isoleucine, inhibits the activity of the first enzyme, threonine deaminase, by binding to its allosteric site. When isoleucine levels are high, it binds to threonine deaminase, reducing its activity and slowing down the pathway. This prevents the overproduction of isoleucine. Once isoleucine levels decrease, the inhibition is lifted, and threonine deaminase becomes active again, allowing the pathway to proceed and produce more isoleucine as needed.
Why is negative feedback important for cellular homeostasis?
Negative feedback is important for cellular homeostasis because it helps maintain the balance of biochemical reactions within the cell. By preventing the overproduction and wasteful accumulation of metabolic products, negative feedback ensures that cells produce only the necessary amounts of substances. This regulation is crucial for conserving energy and resources, avoiding toxic buildup of intermediates, and maintaining optimal conditions for cellular functions. Without negative feedback, cells could experience imbalances that disrupt metabolic processes and overall cellular health, leading to potential dysfunction or disease.