Fatty Acid Synthesis Process

Questions and Answers

What is the primary function of Acetyl-CoA Carboxylase in fatty acid synthesis?

To catalyze the formation of malonyl-CoA (correct)

To stimulate the citrate cycle

To convert citrate into isocitrate

To inhibit fatty acid breakdown

What is the effect of high ATP levels on the citrate cycle?

It has no effect on the citrate cycle

It inhibits the activity of isocitrate dehydrogenase (correct)

It increases the production of oxaloacetate

It stimulates the activity of isocitrate dehydrogenase

Which of the following hormones inhibits fatty acid synthesis?

Thyroid hormone

Insulin

Glucagon (correct)

Epinephrine (correct)

What is the role of citrate in fatty acid synthesis?

It stimulates Acetyl-CoA Carboxylase Signup and view all the answers

What is the effect of insulin on Acetyl-CoA Carboxylase?

It removes phosphates and stimulates ACC Signup and view all the answers

What is the role of protein kinase A in fatty acid synthesis?

It phosphorylates and inhibits Acetyl-CoA Carboxylase Signup and view all the answers

What is the effect of long-chain fatty acids with CoA on Acetyl-CoA Carboxylase?

They inhibit ACC Signup and view all the answers

What is the primary source of acetyl-CoA in fatty acid synthesis?

Pyruvate Signup and view all the answers

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

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.