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In biochemistry and metabolism, beta oxidation (also β-oxidation) is the catabolic process by which fatty acid molecules are broken down in the cytosol in prokaryotes and in the mitochondria in eukaryotes to generate acetyl-CoA.
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This glossary of biology terms is a list of definitions of fundamental terms and concepts used in biology, the study of life and of living organisms.It is intended as introductory material for novices; for more specific and technical definitions from sub-disciplines and related fields, see Glossary of cell biology, Glossary of genetics, Glossary of evolutionary biology, Glossary of ecology ...
Oxidation by FAD; Hydration; Oxidation by NAD + Thiolysis; Production of acyl-CoA and acetyl-CoA; The final product of β-oxidation of an even-numbered fatty acid is acetyl-CoA, the entry molecule for the citric acid cycle. [3] If the fatty acid is an odd-numbered chain, the final product of β-oxidation will be propionyl-CoA.
The carnitine palmitoyltransferase system is an essential step in the beta-oxidation of long chain fatty acids. This transfer system is necessary because, while fatty acids are activated (in the form of a thioester linkage to coenzyme A) on the outer mitochondrial membrane, the activated fatty acids must be oxidized within the mitochondrial matrix
Schematic demonstrating mitochondrial fatty acid beta-oxidation and effects of long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency, LCHAD deficiency. Mitochondrial trifunctional protein (MTP) is a protein attached to the inner mitochondrial membrane which catalyzes three out of the four steps in beta oxidation. MTP is a hetero-octamer ...
3' untranslated region (3'-UTR). Also three-prime untranslated region, 3' non-translated region (3'-NTR), and trailer sequence.. 3'-end. Also three-prime end.. One of two ends of a single linear strand of DNA or RNA, specifically the end at which the chain of nucleotides terminates at the third carbon atom in the furanose ring of deoxyribose or ribose (i.e. the terminus at which the 3' carbon ...
In humans, defects in the beta-oxidation mechanism result in hypoketotic hyperglycemia, a symptom of starvation, due to the inefficient utilization of fatty acids as a primary source of energy. [9] The metabolic disease was found to be on a genetic level: rats without the genes for enoyl-CoA isomerase also displayed high blood glucose level .