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37 Cards in this Set
- Front
- Back
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What is TRIACYGLYCEROLS (TAG)? |
Esters of glycerol with three fatty acids; called "Triglycerides" Main constituents of body fat. |
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TRIACYGLYCEROLS (TAG) consists of |
Glycerol & three fatty acids |
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Bond of TRIACYGLYCEROLS (TAG) |
Ester bond |
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Lipogenesis is |
Synthesis of TAG from fatty acid and glycerol |
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Site of lipogenesis |
Liver, adipose tissues, muscles, kidney, intestine, and lactating mammary glands |
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How many steps are in lipogenesis? What are they? |
1. Activation of glycerol to glycerol-3-phosphate by glycerol kinase. 2. Activation of fatty acid to acyl CoA by acyl CoA synthetase (thiokinase) 3. Synthesis of 1-monoacylglycerol phosphate by transfer of active saturated fatty acids to glycerol-3-phosphate. 4. Synthesis of diacylglycerol phosphate (phosphatic acid) by transfer of another molecule of unsaturated acyl CoA to 1-monoacylglycerol phosphate. 5. Synthesis of diacylglycerol (DAG) by removal of phosphate from diacylglycerol phosphate. 6. Synthesis of triacylglycerol (TAG) by transfer of a third molecule of saturated or unsaturated acyl CoA to DAG |
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Activation of glycerol to glycerol-3-phosphate by |
Glycerol kinase with the help of ATP |
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Where is Glycerol kinase present? |
Mainly in the liver and kidney. Low activity in adipose tissues and muscles. |
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If Glycerol kinase is low in adipose tissues and muscles, where can they get an enzyme to activate Glycerol to Glycerol-3-phosphate? |
Both muscles and adipose tissue depend on glycolysis to get glycerol-3-phosphate from dihydroxyacetone phosphate by glycerol-3-phosphate dehydrogenase. |
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The second step of lipogenesis |
Activation of fatty acid to Acyl CoA by acyl CoA synthase (thiokinase) |
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Enzyme responsible for activation of fatty acid to acyl CoA |
Thiokinase / acy CoA synthase |
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Product of transfer of activated saturated fatty acid to glycerol-3-phosphate |
1-monoacylglycerol phosphate |
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The addition/transfer of another molecule of unsaturated acyl CoA to 1-monoacylglycerol phosphate, produces what? |
Diacylglycerol phosphate / Phosphatidic acid |
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How does the synthesis of diacylglycerol from diacylglycerol phosphate occur? |
By removal of phosphate |
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Synthesis of triacylglycerol (TAG) occurs due to |
Transfer of third molecule of saturated/unsaturated acyl CoA to DAG |
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Does unsaturated fat or saturated fat have a double bond? |
Unsaturated |
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What is the use of lipogenesis? |
Storing your food as fat (TAG) |
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Regulation of lipogenesis |
1. After a meal, insulin is released. 2. Increasing glycolysis 3. Increasing dihydroxyacetone phosphate (DHAP) 4. Increasing production of glycerol-3-phosphate 5. Stimulating lipogenesis |
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What happened to lipogenesis during fasting? |
Lipogenesis is inhibited and lipolysis is stimulated |
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Why is lipogenesis inhibited during fasting? |
During fasting, anti-insulin hormones are secreted; epinephrine & glucagon, which inhibit lipogenesis and stimulate lipolysis (to form ATP). |
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Definition of Lipolysis |
Hydrolysis of TAG into fatty acids and glycerol in adipose tissue |
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Site of lipolysis |
Adipose tissue |
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Enzymes used in Lipogenesis |
1. Glycerol kinase 2. Glycerol-3-dehydrogenase 3. Thiokinase / Acyl CoA synthase
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Enzymes used in lipolysis |
1. Hormone-sensitive lipase (HSL) 2. Monoacylglycerol lipase (MAG) |
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When does Lipolysis occurs? |
It starts after 8 hours of fasting or during exercise |
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Key regulatory enzyme of Lipolysis |
Hormone-sensitive lipase (HSL) |
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Form of Hormone-sensitive lipase (HSL) |
1. Active (phosphorylated) 2. Inactive (dephosphorylated) |
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What happened during fasting? |
Anti-insulin hormones activate adenylyl cyclase, which increases the production of cAMP, leading to the phosphorylation of active hormone-sensitive lipase (HSL) |
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Anti-insulin hormones or lipolytic hormones |
1. Epinephrine and norepinephrine 2. Glucagon hormone (activates adenylyl cyclase) 3. Glucorticoids (increase synthesis of HSL) 4. Thyroxin (facilitate action of epinephrine by increasing number of its receptors or G-protein) |
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What happened to patients with hyperthyroidism in relation to lipolysis? |
Patients will lose a lot of weight |
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Effect of eating on the mechanism of lipolysis |
1. Insulin activates both phosphodiesterase (converts cAMP to AMP) and phosphatase enzyme (removal of phosphate from phosphorylated HSL). 2. Decreasing cAMP and inactivation of HSL occurs |
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What happened to diabetes mellitus for having low insulin production? |
Patients will suffer from extreme loss of weights due to high lipolysis |
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Effect of caffeine and Theophylline on lipolysis |
It inhibits phosphodiesterase, which increases cAMP. Hence, increasing lipolysis. |
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Cause of excessive lipolysis |
1. Starvation 2. Uncontrolled diabetes mellitus 3. Low carbohydrate meal 4. Excessive catabolic states (ex. fever, hyperthyroidism) |
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Fate of fatty acids after lipolysis |
1. Transported to peripheral tissues such as muscles for oxidation and energy production. 2. Reuse for synthesis of TAG. (Over 50% of fatty acids released from lipolysis in adipose tissue are re-esterified with glycerol-3-phosphate to form TAG) |
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Why doesn't the brain use fatty acids for energy? |
Because a long chain of fatty acids can't pass the blood-brain barrier. The brain uses glucose /lactate instead. |
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Fate of glycerol |
1. Glycerol released during TAG degradation can't be metabolized by adipocytes (it lacks glycerol kinase) 2. Glycerol is brought back to the blood, then to the liver, and reused back for the formation of glycerol-3-phosphate 3. Converted to Dihydroxyacetone phosphate (DHAP) by glycerol phosphate dehydrogenase (can participate in glycolysis to give pyruvate or glucogenesis to give glucose) |
