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Biochem Self Study > Lipids & Lipid Catabolism > Flashcards

Lipids & Lipid Catabolism Flashcards

1
Q

Lipid Digestion Overview

A

Digestion Site: Lipids are digested at the lipid-water interface.

Rate Determinant: Digestion rate depends on the surface area of the interface.

Bile Acids: Secreted into the small intestine, increasing surface area through detergent activities.

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1
Q

Role of Bile Acids

A

Function: Bile acids increase lipid-water surface area.

Mechanism: Detergent activities induce formation of lipid micelles.

Location: Bile acids are secreted into the small intestine for digestion.

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2
Q

Triacylglyceride Degradation

A

Process: Triacylglycerides broken down by lipases.

Pancreatic Lipase: Catalyzes sequential hydrolysis of triacylglycerols.

Products: Generates free fatty acids and 2-monoglyceride.

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3
Q

Phospholipid Degradation

A

Pancreatic Phospholipase A2: Degrades phospholipids.

Cleavage: Cleaves C2 fatty acid, yielding lysophospholipids.

Detergent Nature: Lysophospholipids act as detergents, emulsifying fat similar to bile acids.

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4
Q

Lipolysis Process in Adipose Cells

A

Definition: Lipolysis is the process of releasing fatty acids from triacylglycerols stored in adipose cells.

Regulation: Hormone-dependent, primarily regulated by adrenaline (epinephrine).

Hormone Action: Adrenaline activates G-protein, leading to cyclic AMP (cAMP) production through adenyl cyclase.

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5
Q

Protein Kinase A (PKA) Activation

A

cAMP Activation: Increasing cAMP levels activate Protein Kinase A (PKA).

PKA Substrates: PKA targets glycogen phosphorylase kinase, perilipin, and hormone-sensitive triacylglycerol lipase.

Perilipin Function: Phosphorylation of perilipin by PKA opens lipid droplets, allowing lipase access.

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6
Q

Lipase Activation

A

Hormone-Sensitive Lipase (HSL): Activated by PKA phosphorylation.

Triacylglycerol Breakdown: HSL degrades triacylglycerols into fatty acids.

Perilipin Role: Phosphorylation of perilipin facilitates access for lipase to lipid droplet.

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7
Q

Fatty Acid Transport and Utilization

A

Fatty Acid Release: Fatty acids are released from adipocytes.

Transport: Fatty acids bind to serum albumin in the blood for solubilization and transport.

Target Tissues: Fatty acids enter target tissues via specific transporters for energy production.

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8
Q

Mobilization Trigger

A

Trigger: Low glucose levels stimulate glucagon release.

Glucagon Action: Binds to adipocyte receptor, activates adenylyl cyclase, and increases cAMP.

PKA Activation: cAMP activates PKA, initiating phosphorylation of lipase and perilipin for triacylglycerol breakdown.

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9
Q

Fatty Acid Activation

A

Process: Fatty acid activation involves converting fatty acids into fatty-acyl-CoA.

Location: Takes place outside the mitochondria.

Purpose: Preparation for fatty acid degradation to generate energy.

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10
Q

Enzymatic Process

A

Enzyme: Catalyzed by fatty acyl–CoA synthetase.

Steps: Conjugation of fatty acid with CoA.

Energy Cost: Requires one ATP, yielding AMP and pyrophosphate.

Delta G: Reaction has a positive delta G, overcome by immediate hydrolysis of pyrophosphate.

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11
Q

High Energy CoA Molecules

A

Product: Formation of high-energy CoA molecules.

Hydrolysis: Immediate hydrolysis of pyrophosphate is crucial.

Net Delta G: Achieves a net negative delta G for the reaction.

Purpose: Provides energy for the subsequent steps in fatty acid metabolism.

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12
Q

Conversion Steps

A

Catalyst: Fatty acyl–CoA synthetase and inorganic pyrophosphatase catalyze the conversion.

Exergonic Reaction: The overall process is highly exergonic.

Preparation: Converts free fatty acids into activated fatty-acyl-CoA for efficient degradation.

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13
Q

Carnitine Shuttle System

A

Function: Transports long-chain acyl CoA through mitochondrial membranes.

Conversion: Acyl CoA is converted to acyl carnitine by carnitine acyltransferase I.

Transport: Acyl carnitine travels through the intermembrane space to the inner mitochondrial membrane.

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14
Q

Mitochondrial Entry

A

Transporter: Specific transporter facilitates the entry of acyl carnitine into the mitochondrial matrix.

Enzyme: Carnitine acyltransferase II converts acyl carnitine back to acyl CoA inside the mitochondria.

Utilization: Acyl CoA is utilized for beta-oxidation, a process in fatty acid metabolism.

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15
Q

Fatty Acid Entry

A

Process: Fatty acid entry into mitochondria via the acyl-carnitine/carnitine transporter.

Diffusion: Acyl-carnitine moves through the transporter in the inner mitochondrial membrane.

Matrix Reaction: Acyl group is transferred to mitochondrial coenzyme A in the matrix.

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16
Q

Inhibition Mechanism

A

Inhibition: Acyltransferase I is inhibited by malonyl-CoA.

Prevention: Inhibition prevents simultaneous synthesis and degradation of fatty acids.

Regulation: Malonyl-CoA regulates the balance between fatty acid synthesis and degradation.

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17
Q

Beta-Oxidation Overview

A

Stage 1: Fatty acid oxidation to acetyl-CoA.

Stage 2: Acetyl-CoA oxidation to CO2 via the citric acid cycle.

Stage 3: Electrons from Stages 1 and 2 drive ATP synthesis in oxidative phosphorylation.

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18
Q

Beta-Oxidation Pathway

A

Steps: Four-step sequence - Oxidation, Hydration, Oxidation, and Cleavage.

Acetyl-CoA Formation: One acetyl residue is removed as acetyl-CoA from the carboxyl end.

Repetition: Six more passes yield 7 additional acetyl-CoA molecules.

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19
Q

Acetyl-CoA Generation

A

Total Acetyl-CoA: Eight molecules of acetyl-CoA are formed.

Sequence: Acetyl residues removed from the fatty acyl chain in successive passes.

Carbon Source: The 7th acetyl-CoA arises from the last two carbon atoms of the 16-carbon chain.

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20
Q

Ketone Bodies as Fuels

A

Utilization: Important fuels for heart, skeletal muscle, kidney cortex, and brain during starvation.

Exclusion: Not utilized by the liver.

20
Q

Ketone Bodies Overview

A

Fate of Acetyl-CoA: Besides citric acid cycle oxidation, undergoes ketogenesis in liver mitochondria.

Products: Acetoacetate, -hydroxybutyrate, and acetone are collectively known as ketone bodies.

21
Q

Properties of Ketone Bodies

A

Water Solubility: Ketone bodies are water-soluble equivalents of short fatty acids.

Synthesis Location: Synthesized in the mitochondrial matrix.

22
Q

Acetone in Ketone Bodies

A

Metabolism: Acetone is not metabolized; it is “blown off” in the lungs.

Conditions: Produced in excess during ketosis, untreated diabetes, or high protein-low carbohydrate diets.

23
Q

Ketosis and Acidosis

A

Ketosis Causes: More ketone bodies produced than metabolized, seen in untreated diabetes or specific diets.

Acidosis Risk: Ketone bodies are acidic; high levels, especially in untreated diabetes, can lead to blood acidosis.

23
Q

Ketone Body Formation Overview

A

Normal Levels: Ketone body formation is typically low under normal conditions.

Trigger: Increases during acetyl-CoA accumulation, such as in starvation or untreated diabetes

24
Q

Steps in Ketone Body Formation

A

Enzymatic Catalysis: Thiolase catalyzes the condensation of two acetyl-CoA molecules.

Intermediates: Formation of acetoacetyl-CoA and then HMG-CoA, the precursor of the three ketone bodies.

Location: Process occurs in the matrix of liver mitochondria.

25
Q

Reasons for Liver Ketone Body Formation

A

Oxaloacetate Limitation: Occurs when oxaloacetate is limited due to its utilization in gluconeogenesis.

High NADH Levels: PDC, isocitrate dehydrogenase, and alpha-ketoglutarate DeH are inhibited due to elevated NADH levels during starvation.

26
Q

Citric Acid Cycle Inhibition

A

Oxaloacetate Depletion: Limited availability for citric acid cycle due to oxaloacetate being consumed in gluconeogenesis.

Enzyme Shutdown: PDC, isocitrate dehydrogenase, and alpha-ketoglutarate DeH are inhibited under high NADH levels.

27
Q

Significance of Ketone Bodies in Liver

A

Alternative Energy Source: During starvation, ketone bodies serve as an alternative energy source when glucose is scarce.

Maintaining Energy Balance: Allows the liver to continue producing energy-efficient ketone bodies when glucose supply is limited.

28
Q

Storage Lipids

A

Fatty acids, akin to low oxidation state hydrocarbons, undergo highly exergonic cellular oxidation to CO2 and H2O, resembling burning fossil fuels.

29
Q

Structural Lipids in Membranes

A

Biological Membranes: Composed of lipid bilayers forming cell barriers preventing the passage of polar molecules.

Amphipathic Nature: Lipids in bilayers are amphipathic, with hydrophobic fatty acids interacting internally and hydrophilic parts interacting externally and with the cytoplasm.

Diversity: Enormous diversity in membrane lipids due to various combinations of hydrophilic head groups and fatty acids.

30
Q

Trans Fatty Acids

A

Purpose: Improve shelf life and stability, commonly used in deep frying and baking.

Sources: Found in partially hydrogenated oils like Crisco and margarine.

Natural Occurrence: Present in low amounts (2-5% of total fat) in milk and meat from ruminants (cows and sheep).

Health Impact: Associated with increased heart disease; FDA banned their use in 2018.

31
Q

Triacylglycerol

A

Major Fat Storage Form

Energy Content: More reduced than carbohydrates, containing twice as much energy per gram.

Hydrophobic Nature: Does not require carrying the weight of water (2g water/g carbohydrate) necessary for hydration.

32
Q

Fluid Mosaic Model for Membrane Structure

A

Composition: Membranes consist of lipids (phospholipids and cholesterol) and proteins.

Hydrophobic Region: Interior fatty acyl chains form a fluid, hydrophobic region.

Protein Movement: Proteins and lipids can move laterally in the plane of the bilayer, but movement between leaflets is restricted.

Carbohydrate Moieties: Some extracellular proteins have attached carbohydrate moieties.

33
Q

Sphingolipids

A

Sphingosine
Ceramide
Sphingomyelin
Glycosphingolipids:

34
Q

Sphingosine

A

18C amino alcohol with trans configuration of C4=C5 double bond.

35
Q

Ceramide

A

Sphingosine with fatty acid via amide linkage.

36
Q

Sphingomyelin

A

Second most common lipid in the plasma membrane; ~85% of all sphingolipids in humans.

37
Q

Glycosphingolipids

A

Ceramide with one or more sugar residues; examples include cerebroside and ganglioside.

38
Q

Lipids as Signaling Molecules

A

Steroids
Eicosanoids
COX Inhibition

39
Q

Steroids

A

Derived from cholesterol; examples include testosterone, estradiol, cortisol, and aldosterone.

40
Q

Eicosanoids

A

Produced from arachidonic acid by COX enzymes; includes prostaglandins, thromboxanes, and leukotrienes.

41
Q

COX Inhibition

A

Nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin and ibuprofen block the formation of prostaglandins and thromboxanes by inhibiting cyclooxygenase (COX).

42
Q

Aspirin Mechanism

A

Acetylation of COX 1 and 2: Aspirin (acetylsalicylic acid) acetylates and inactivates both COX 1 and 2.

Thromboxane Inhibition: Blocks the production of thromboxane, a lipid-based signaling factor.

Platelet Aggregation: Thromboxane increases platelet aggregation, forming clots; aspirin inhibits this, reducing clot formation.

43
Q

Aspirin and Cardiovascular Disease

A

Heart Attack and Stroke: Thromboxane increases blood clots, leading to heart attacks and strokes.

Cardiovascular Risk Reduction: Aspirin inhibits thromboxane, decreasing cardiovascular disease risk.

44
Q

Specific COX2 Inhibitors and Issues

A

COX1 and COX2 Inhibition

Vioxx Withdrawal:

Prostacyclin and Thromboxane Balance

Need for Selectivity: Specific COX2 inhibitors sought for treating osteoarthritis and pain without stomach bleeding.

45
Q

COX1 and COX2 Inhibition:

A

Aspirin and ibuprofen inhibit both COX1 and COX2, protecting the stomach lining but causing bleeding.

46
Q

Vioxx Withdrawal:

A

FDA-approved Vioxx withdrawn in 2004 due to increased heart attack and stroke risks; associated with 88,000 to 140,000 cases of serious heart disease.

47
Q

Prostacyclin and Thromboxane Balance:

A

Inhibition of COX2 alone reduces prostacyclin production, altering the prostacyclin to thromboxane ratio, increasing cardiovascular disease risk.

Biochem Self Study (7 decks)

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