Pathways

The degradation of fatty acids occurs is many ways, but for the most part in most species it occurs mainly through the beta-oxidation cycle. Take mammals for example, in this subset of species we find that beta-oxidation takes place not only in mitochondria, but in peroxisomes as well. In contrast, it tends to be the case that in plants and fungi beta-oxidation is only seen in peroxisomes. The reason the beta-oxidation cycle is found to occur in both mitochondria and peroxisomes in mammals is thought to be that extremely long chain fatty acids will in fact undergo oxidation in both locations, an initial or first oxidation in peroxisomes and second oxidation in the mitochondria. There is however a difference between the oxidation cycle which occurs in both these organelles. Namely, that the oxidation undergone in peroxisomes does not have any coupling to ATP synthesis, unlike the corresponding oxidation which occurs in the mitochondria. We find rather that electrons are passed to molecules of oxygen, which produces hydrogen peroxide. Moreover, there is an enzyme which is found only peroxisomes which ties into this process. It can turn hydrogen peroxide back into water and oxygen and is catalase. To expound further the differences between the oxidation cycle found in the peroxisomes and the mitchondria consider the following three key differences. One, in the peroxisome the beta-oxidation cycle takes as a necessary input a special enzyme called, peroxisomal carnitine acyltransferase, which is needed to move an activated acyl group from outside the peroxisome to inside it. In mitochondrial oxidation similar but different enzymes are used called carnitine acyltransferase I and II. Difference number two is that oxidation in the peroxisome commences with catalysis induced by an enzyme called acyl CoA oxidase. Also, it should be noted that another enzyme called beta-ketothiolase which aids in peroxisomal beta-oxidation has a substrate specificity which differs from that of the mitochondrial beta-ketothiolase. Turning now to how the oxidation cycle function in mitochondria, note that the mitochondrial beta-oxidation pathway is composed of four repeating reactions that take place with each fatty acid molecule. The oxidation of fatty acid chains is a process of progress through repetition. With each turn of the cycle two carbons are removed from the fatty acid chain and the energy of the chemical bonds once housed by the molecule is captured by the reduced energy carriers NADH and FADH2. Acetyl-CoA is created in this 4 step reaction beta-oxidation process and is sent to the TCA cycle. Once inside the TCA cycle, the process of oxidation continues until even the acetyl-CoA is oxidized to CO2. More NADH and FADH2 result.

The degradation of fatty acids occurs is many ways, but for the most part in most species it occurs mainly through the beta-oxidation cycle. Take mammals for example, in this subset of species we find that beta-oxidation takes place not only in mitochondria, but in peroxisomes as well. In contrast, it tends to be the case that in plants and fungi beta-oxidation is only seen in peroxisomes. The reason the beta-oxidation cycle is found to occur in both mitochondria and peroxisomes in mammals is thought to be that extremely long chain fatty acids will in fact undergo oxidation in both locations, an initial or first oxidation in peroxisomes and second oxidation in the mitochondria. There is however a difference between the oxidation cycle which occurs in both these organelles. Namely, that the oxidation undergone in peroxisomes does not have any coupling to ATP synthesis, unlike the corresponding oxidation which occurs in the mitochondria. We find rather that electrons are passed to molecules of oxygen, which produces hydrogen peroxide. Moreover, there is an enzyme which is found only peroxisomes which ties into this process. It can turn hydrogen peroxide back into water and oxygen and is catalase. To expound further the differences between the oxidation cycle found in the peroxisomes and the mitchondria consider the following three key differences. One, in the peroxisome the beta-oxidation cycle takes as a necessary input a special enzyme called, peroxisomal carnitine acyltransferase, which is needed to move an activated acyl group from outside the peroxisome to inside it. In mitochondrial oxidation similar but different enzymes are used called carnitine acyltransferase I and II. Difference number two is that oxidation in the peroxisome commences with catalysis induced by an enzyme called acyl CoA oxidase. Also, it should be noted that another enzyme called beta-ketothiolase which aids in peroxisomal beta-oxidation has a substrate specificity which differs from that of the mitochondrial beta-ketothiolase. Turning now to how the oxidation cycle function in mitochondria, note that the mitochondrial beta-oxidation pathway is composed of four repeating reactions that take place with each fatty acid molecule. The oxidation of fatty acid chains is a process of progress through repetition. With each turn of the cycle two carbons are removed from the fatty acid chain and the energy of the chemical bonds once housed by the molecule is captured by the reduced energy carriers NADH and FADH2. Acetyl-CoA is created in this 4 step reaction beta-oxidation process and is sent to the TCA cycle. Once inside the TCA cycle, the process of oxidation continues until even the acetyl-CoA is oxidized to CO2. More NADH and FADH2 result.

The degradation of fatty acids occurs is many ways, but for the most part in most species it occurs mainly through the beta-oxidation cycle. Take mammals for example, in this subset of species we find that beta-oxidation takes place not only in mitochondria, but in peroxisomes as well. In contrast, it tends to be the case that in plants and fungi beta-oxidation is only seen in peroxisomes. The reason the beta-oxidation cycle is found to occur in both mitochondria and peroxisomes in mammals is thought to be that extremely long chain fatty acids will in fact undergo oxidation in both locations, an initial or first oxidation in peroxisomes and second oxidation in the mitochondria. There is however a difference between the oxidation cycle which occurs in both these organelles. Namely, that the oxidation undergone in peroxisomes does not have any coupling to ATP synthesis, unlike the corresponding oxidation which occurs in the mitochondria. We find rather that electrons are passed to molecules of oxygen, which produces hydrogen peroxide. Moreover, there is an enzyme which is found only peroxisomes which ties into this process. It can turn hydrogen peroxide back into water and oxygen and is catalase. To expound further the differences between the oxidation cycle found in the peroxisomes and the mitchondria consider the following three key differences. One, in the peroxisome the beta-oxidation cycle takes as a necessary input a special enzyme called, peroxisomal carnitine acyltransferase, which is needed to move an activated acyl group from outside the peroxisome to inside it. In mitochondrial oxidation similar but different enzymes are used called carnitine acyltransferase I and II. Difference number two is that oxidation in the peroxisome commences with catalysis induced by an enzyme called acyl CoA oxidase. Also, it should be noted that another enzyme called beta-ketothiolase which aids in peroxisomal beta-oxidation has a substrate specificity which differs from that of the mitochondrial beta-ketothiolase. Turning now to how the oxidation cycle function in mitochondria, note that the mitochondrial beta-oxidation pathway is composed of four repeating reactions that take place with each fatty acid molecule. The oxidation of fatty acid chains is a process of progress through repetition. With each turn of the cycle two carbons are removed from the fatty acid chain and the energy of the chemical bonds once housed by the molecule is captured by the reduced energy carriers NADH and FADH2. Acetyl-CoA is created in this 4 step reaction beta-oxidation process and is sent to the TCA cycle. Once inside the TCA cycle, the process of oxidation continues until even the acetyl-CoA is oxidized to CO2. More NADH and FADH2 result.

The degradation of fatty acids occurs is many ways, but for the most part in most species it occurs mainly through the beta-oxidation cycle. Take mammals for example, in this subset of species we find that beta-oxidation takes place not only in mitochondria, but in peroxisomes as well. In contrast, it tends to be the case that in plants and fungi beta-oxidation is only seen in peroxisomes. The reason the beta-oxidation cycle is found to occur in both mitochondria and peroxisomes in mammals is thought to be that extremely long chain fatty acids will in fact undergo oxidation in both locations, an initial or first oxidation in peroxisomes and second oxidation in the mitochondria. There is however a difference between the oxidation cycle which occurs in both these organelles. Namely, that the oxidation undergone in peroxisomes does not have any coupling to ATP synthesis, unlike the corresponding oxidation which occurs in the mitochondria. We find rather that electrons are passed to molecules of oxygen, which produces hydrogen peroxide. Moreover, there is an enzyme which is found only peroxisomes which ties into this process. It can turn hydrogen peroxide back into water and oxygen and is catalase. To expound further the differences between the oxidation cycle found in the peroxisomes and the mitchondria consider the following three key differences. One, in the peroxisome the beta-oxidation cycle takes as a necessary input a special enzyme called, peroxisomal carnitine acyltransferase, which is needed to move an activated acyl group from outside the peroxisome to inside it. In mitochondrial oxidation similar but different enzymes are used called carnitine acyltransferase I and II. Difference number two is that oxidation in the peroxisome commences with catalysis induced by an enzyme called acyl CoA oxidase. Also, it should be noted that another enzyme called beta-ketothiolase which aids in peroxisomal beta-oxidation has a substrate specificity which differs from that of the mitochondrial beta-ketothiolase. Turning now to how the oxidation cycle function in mitochondria, note that the mitochondrial beta-oxidation pathway is composed of four repeating reactions that take place with each fatty acid molecule. The oxidation of fatty acid chains is a process of progress through repetition. With each turn of the cycle two carbons are removed from the fatty acid chain and the energy of the chemical bonds once housed by the molecule is captured by the reduced energy carriers NADH and FADH2. Acetyl-CoA is created in this 4 step reaction beta-oxidation process and is sent to the TCA cycle. Once inside the TCA cycle, the process of oxidation continues until even the acetyl-CoA is oxidized to CO2. More NADH and FADH2 result.

The degradation of fatty acids occurs is many ways, but for the most part in most species it occurs mainly through the beta-oxidation cycle. Take mammals for example, in this subset of species we find that beta-oxidation takes place not only in mitochondria, but in peroxisomes as well. In contrast, it tends to be the case that in plants and fungi beta-oxidation is only seen in peroxisomes. The reason the beta-oxidation cycle is found to occur in both mitochondria and peroxisomes in mammals is thought to be that extremely long chain fatty acids will in fact undergo oxidation in both locations, an initial or first oxidation in peroxisomes and second oxidation in the mitochondria. There is however a difference between the oxidation cycle which occurs in both these organelles. Namely, that the oxidation undergone in peroxisomes does not have any coupling to ATP synthesis, unlike the corresponding oxidation which occurs in the mitochondria. We find rather that electrons are passed to molecules of oxygen, which produces hydrogen peroxide. Moreover, there is an enzyme which is found only peroxisomes which ties into this process. It can turn hydrogen peroxide back into water and oxygen and is catalase. To expound further the differences between the oxidation cycle found in the peroxisomes and the mitchondria consider the following three key differences. One, in the peroxisome the beta-oxidation cycle takes as a necessary input a special enzyme called, peroxisomal carnitine acyltransferase, which is needed to move an activated acyl group from outside the peroxisome to inside it. In mitochondrial oxidation similar but different enzymes are used called carnitine acyltransferase I and II. Difference number two is that oxidation in the peroxisome commences with catalysis induced by an enzyme called acyl CoA oxidase. Also, it should be noted that another enzyme called beta-ketothiolase which aids in peroxisomal beta-oxidation has a substrate specificity which differs from that of the mitochondrial beta-ketothiolase. Turning now to how the oxidation cycle function in mitochondria, note that the mitochondrial beta-oxidation pathway is composed of four repeating reactions that take place with each fatty acid molecule. The oxidation of fatty acid chains is a process of progress through repetition. With each turn of the cycle two carbons are removed from the fatty acid chain and the energy of the chemical bonds once housed by the molecule is captured by the reduced energy carriers NADH and FADH2. Acetyl-CoA is created in this 4 step reaction beta-oxidation process and is sent to the TCA cycle. Once inside the TCA cycle, the process of oxidation continues until even the acetyl-CoA is oxidized to CO2. More NADH and FADH2 result.

The degradation of fatty acids occurs is many ways, but for the most part in most species it occurs mainly through the beta-oxidation cycle. Take mammals for example, in this subset of species we find that beta-oxidation takes place not only in mitochondria, but in peroxisomes as well. In contrast, it tends to be the case that in plants and fungi beta-oxidation is only seen in peroxisomes. The reason the beta-oxidation cycle is found to occur in both mitochondria and peroxisomes in mammals is thought to be that extremely long chain fatty acids will in fact undergo oxidation in both locations, an initial or first oxidation in peroxisomes and second oxidation in the mitochondria. There is however a difference between the oxidation cycle which occurs in both these organelles. Namely, that the oxidation undergone in peroxisomes does not have any coupling to ATP synthesis, unlike the corresponding oxidation which occurs in the mitochondria. We find rather that electrons are passed to molecules of oxygen, which produces hydrogen peroxide. Moreover, there is an enzyme which is found only peroxisomes which ties into this process. It can turn hydrogen peroxide back into water and oxygen and is catalase. To expound further the differences between the oxidation cycle found in the peroxisomes and the mitchondria consider the following three key differences. One, in the peroxisome the beta-oxidation cycle takes as a necessary input a special enzyme called, peroxisomal carnitine acyltransferase, which is needed to move an activated acyl group from outside the peroxisome to inside it. In mitochondrial oxidation similar but different enzymes are used called carnitine acyltransferase I and II. Difference number two is that oxidation in the peroxisome commences with catalysis induced by an enzyme called acyl CoA oxidase. Also, it should be noted that another enzyme called beta-ketothiolase which aids in peroxisomal beta-oxidation has a substrate specificity which differs from that of the mitochondrial beta-ketothiolase. Turning now to how the oxidation cycle function in mitochondria, note that the mitochondrial beta-oxidation pathway is composed of four repeating reactions that take place with each fatty acid molecule. The oxidation of fatty acid chains is a process of progress through repetition. With each turn of the cycle two carbons are removed from the fatty acid chain and the energy of the chemical bonds once housed by the molecule is captured by the reduced energy carriers NADH and FADH2. Acetyl-CoA is created in this 4 step reaction beta-oxidation process and is sent to the TCA cycle. Once inside the TCA cycle, the process of oxidation continues until even the acetyl-CoA is oxidized to CO2. More NADH and FADH2 result.

Beta-alanine, 3-aminopropanoic acid, is a non-essential amino acid. Beta-Alanine is formed by the proteolytic degradation of beta-alanine containing dipeptides: carnosine, anserine, balenine, and pantothenic acid (vitamin B5). These dipeptides are consumed from protein-rich foods such as chicken, beef, pork, and fish. Beta-Alanine can also be formed in the liver from the breakdown of pyrimidine nucleotides into uracil and dihydrouracil and then metabolized into beta-alanine and beta-aminoisobutyrate. Beta-Alanine can also be formed via the action of aldehyde dehydrogenase on beta-aminoproionaldehyde which is generated from various aliphatic polyamines. Under normal conditions, beta-alanine is metabolized to aspartic acid through the action of glutamate decarboxylase. It addition, it can be converted to malonate semialdehyde and thereby participate in propanoate metabolism. Beta-Alanine is not a proteogenic amino acid. This amino acid is a common athletic supplementation due to its belief to improve performance by increased muscle carnosine levels.

Beta-alanine, 3-aminopropanoic acid, is a non-essential amino acid. Beta-Alanine is formed by the proteolytic degradation of beta-alanine containing dipeptides: carnosine, anserine, balenine, and pantothenic acid (vitamin B5). These dipeptides are consumed from protein-rich foods such as chicken, beef, pork, and fish. Beta-Alanine can also be formed in the liver from the breakdown of pyrimidine nucleotides into uracil and dihydrouracil and then metabolized into beta-alanine and beta-aminoisobutyrate. Beta-Alanine can also be formed via the action of aldehyde dehydrogenase on beta-aminoproionaldehyde which is generated from various aliphatic polyamines. Under normal conditions, beta-alanine is metabolized to aspartic acid through the action of glutamate decarboxylase. It addition, it can be converted to malonate semialdehyde and thereby participate in propanoate metabolism. Beta-Alanine is not a proteogenic amino acid. This amino acid is a common athletic supplementation due to its belief to improve performance by increased muscle carnosine levels.