Amino acid degradation

Amino acid degradation produces cytosolic acetyl-CoA. 

The acetyl-CoA derived from amino acid degradation is normally insufficient for fatty acid biosynthesis, and the acetyl-CoA produced by pyruvate dehydrogenase and by fatty acid oxidation cannot cross the mitochondrial membrane to participate directly in fatty acid synthesis. Instead, acetyl-CoA is linked with oxaloacetate to form citrate, which is transported from the mitochondrial matrix to the cytosol (Figure 25.1). Here it can be converted back into acetyl-CoA and oxaloacetate by ATP-citrate lyase. In this manner, mitochondrial acetyl-CoA becomes the substrate for cytosolic fatty acid synthesis. (Oxaloacetate returns to the mitochondria in the form of either pyruvate or malate, which is then reconverted to acetyl-CoA and oxaloacetate, respectively.)... 

Barker HA (1981) Amino acid degradation by anaerobic bacteria. Annu Rev Biochem 50 23-40. 

To amino acid degradation through acetyl-CoA and various intermediates of the cycle. 

Nonessential Amino Acid Synthesis Essential Amino Acids Amino Acid Degradation Generalities of Amino Acid Catabolism Products of Amino Acid Degradation... 

Figure 8.6 The three dehydrogenase (oxidase) reactions in amino acid degradation. The enzymes are D-amino acid oxidase, glutamate dehydrogenase and proline oxidase (dehydrogenase). Biochemical details are given in Appendix 8.4.

Glucocorticoids—mainly cortisol (see p. 374)—induce all of the key enzymes involved in gluconeogenesis [4, 6, 8, 9]. At the same time, they also induce enzymes involved in amino acid degradation and thereby provide precursors for gluconeogenesis. Regulation of the expression of PEP carbo>Q -kinase, a key enzyme in gluconeogenesis, is discussed in detail on p. 244. 

A large number of metabolic pathways are available for amino acid degradation, and an overview of these is presented here. Further details are given on pp. 414 and 415. 

The kidneys main function is excretion of water and water-soluble substances (1). This is closely associated with their role in regulating the body s electrolyte and acid-base balance (homeostasis, 2 see pp.326 and 328). Both excretion and homeostasis are subject to hormonal control. The kidneys are also involved in synthesizing several hormones (3 see p. 315). Finally, the kidneys also play a role in the intermediary metabolism (4), particularly in amino acid degradation and gluconeo-genesis (see p. 154). 

B. The mechanisms of amino acid degradation are grouped according to the ways their carbon skeletons are subsequently metabolized. 

Simple amino acid degradation products aldehydes, sulphur compounds (e.g. hydrogen sulphide, methanethiol), nitrogen compounds (e.g. ammonia, amines)... 

The pathways of amino acid catabolism are quite similar in most organisms. The focus of this chapter is on the pathways in vertebrates, because these have received the most research attention. As in carbohydrate and fatty acid catabolism, the processes of amino acid degradation converge on the central catabolic pathways, with the carbon skeletons of most amino acids finding their way to the citric acid cycle. In some cases the reaction pathways of amino acid breakdown closely parallel steps in the catabolism of fatty acids (Chapter 17). 

Amino acid degradation amino acids-----> acetyl-CoA, citric acid cycle intermediates... 

Reorganizes coverage of amino acid degradation to focus on the big picture Adds new material on the relative importance of several degradative pathways Includes a new description of the interplay of the pyridoxal phosphate and tetrahydrofolate cofactors in serine and glycine metabolism... 

Equilibrium of transamination reactions For most transamina tion reactions, the equilibrium constant is near one, allowing the reaction to function in both amino acid degradation through removal of a-amino groups (for example, after consumption of a protein-rich meal), and biosynthesis through addition of amino groups to the carbon skeletons of a-keto acids (for example, when the supply of amino acids from the diet is not adequate to meet the synthetic needs of cells). 

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