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Questions and Answers
What is the primary function of Acetyl-CoA Carboxylase in fatty acid synthesis?
What is the primary function of Acetyl-CoA Carboxylase in fatty acid synthesis?
What is the effect of high ATP levels on the citrate cycle?
What is the effect of high ATP levels on the citrate cycle?
Which of the following hormones inhibits fatty acid synthesis?
Which of the following hormones inhibits fatty acid synthesis?
What is the role of citrate in fatty acid synthesis?
What is the role of citrate in fatty acid synthesis?
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What is the effect of insulin on Acetyl-CoA Carboxylase?
What is the effect of insulin on Acetyl-CoA Carboxylase?
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What is the role of protein kinase A in fatty acid synthesis?
What is the role of protein kinase A in fatty acid synthesis?
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What is the effect of long-chain fatty acids with CoA on Acetyl-CoA Carboxylase?
What is the effect of long-chain fatty acids with CoA on Acetyl-CoA Carboxylase?
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What is the primary source of acetyl-CoA in fatty acid synthesis?
What is the primary source of acetyl-CoA in fatty acid synthesis?
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Study Notes
Fatty Acid Synthesis
- Occurs in various tissues, particularly in the liver, when blood glucose levels are high (fed state)
- Regulated by insulin, which stimulates fatty acid synthesis
- Other hormones like glucagon, epinephrine, and norepinephrine inhibit fatty acid synthesis
- Process occurs when there is excess ATP production or high blood glucose levels
- Glucose is converted into pyruvate, then into acetyl-CoA, which enters the citrate cycle
- In the citrate cycle, acetyl-CoA combines with oxaloacetate to form citrate
- Citrate is converted into isocitrate, then into α-ketoglutarate, producing ATP, NADH, and FADH2
- High ATP levels allosterically inhibit isocitrate dehydrogenase, causing citrate to accumulate
- Citrate can pass through the mitochondrial membrane and is converted back into oxaloacetate and acetyl-CoA
- Acetyl-CoA is then converted into malonyl-CoA, a precursor for fatty acid synthesis
Regulation of Acetyl-CoA Carboxylase (ACC)
- ACC is the key enzyme in fatty acid synthesis
- Exists in two forms: active (polymerized) and inactive (dimeric)
- Citrate stimulates ACC, causing it to polymerize and become active
- Long-chain fatty acids with CoA inhibit ACC, causing it to dimerize and become inactive
- Insulin stimulates ACC, promoting fatty acid synthesis
- Glucagon and epinephrine inhibit ACC, promoting fatty acid breakdown
Phospho Protein Phosphatases and Protein Kinase A
- Insulin activates phospho protein phosphatases, which remove phosphates from ACC, stimulating its activity
- Glucagon and epinephrine activate protein kinase A, which phosphorylates and inhibits ACC
- Phospho protein phosphatases counteract protein kinase A, allowing ACC to become active and promote fatty acid synthesis
Fatty Acid Synthesis
- Fatty acid synthesis occurs in various tissues, especially in the liver, when blood glucose levels are high and insulin levels are elevated
- Insulin stimulates fatty acid synthesis by regulating key enzymes in the process
- In contrast, glucagon, epinephrine, and norepinephrine inhibit fatty acid synthesis
- The process begins with the conversion of glucose into pyruvate, then into acetyl-CoA, which enters the citrate cycle
- In the citrate cycle, acetyl-CoA combines with oxaloacetate to form citrate, which is then converted into isocitrate and α-ketoglutarate, producing ATP, NADH, and FADH2
- High ATP levels inhibit isocitrate dehydrogenase, causing citrate to accumulate
- Citrate can then leave the mitochondria and be converted back into oxaloacetate and acetyl-CoA
- Acetyl-CoA is then converted into malonyl-CoA, a crucial precursor for fatty acid synthesis
Regulation of Acetyl-CoA Carboxylase (ACC)
- Acetyl-CoA carboxylase (ACC) is the key enzyme in fatty acid synthesis
- ACC exists in two forms: active (polymerized) and inactive (dimeric)
- Citrate stimulates ACC, causing it to polymerize and become active, promoting fatty acid synthesis
- In contrast, long-chain fatty acids with CoA inhibit ACC, causing it to dimerize and become inactive, inhibiting fatty acid synthesis
- Insulin stimulates ACC, promoting fatty acid synthesis, while glucagon and epinephrine inhibit ACC, promoting fatty acid breakdown
Phospho Protein Phosphatases and Protein Kinase A
- Insulin activates phospho protein phosphatases, which remove phosphates from ACC, stimulating its activity and promoting fatty acid synthesis
- Glucagon and epinephrine activate protein kinase A, which phosphorylates and inhibits ACC, inhibiting fatty acid synthesis
- Phospho protein phosphatases counteract protein kinase A, allowing ACC to become active and promote fatty acid synthesis
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Description
This quiz covers the process of fatty acid synthesis, including its regulation, steps, and conditions. It occurs in tissues like the liver when blood glucose levels are high and is regulated by hormones like insulin and glucagon.
