Editing Metabolism (section)

===Energy from organic compounds===
{{further|Cellular respiration|Fermentation (biochemistry)|Carbohydrate catabolism|Fat catabolism|Protein catabolism}}

Carbohydrate catabolism is the breakdown of carbohydrates into smaller units. Carbohydrates are usually taken into cells after they have been digested into [[monosaccharide]]s such as [[glucose]] and [[fructose]].<ref>{{cite journal | vauthors = Bell GI, Burant CF, Takeda J, Gould GW | title = Structure and function of mammalian facilitative sugar transporters | journal = The Journal of Biological Chemistry | volume = 268 | issue = 26 | pages = 19161–4 | date = September 1993 | doi = 10.1016/S0021-9258(19)36489-0 | pmid = 8366068 | doi-access = free }}</ref> Once inside, the major route of breakdown is [[glycolysis]], in which glucose is converted into [[pyruvic acid|pyruvate]]. This process generates the energy-conveying molecule [[NADH]] from NAD<sup>+</sup>, and generates [[Adenosine triphosphate|ATP]] from [[Adenosine diphosphate|ADP]] for use in powering many processes within the cell.<ref name="Bouché-2004">{{cite journal | vauthors = Bouché C, Serdy S, Kahn CR, Goldfine AB | title = The cellular fate of glucose and its relevance in type 2 diabetes | journal = Endocrine Reviews | volume = 25 | issue = 5 | pages = 807–30 | date = October 2004 | pmid = 15466941 | doi = 10.1210/er.2003-0026 | df = dmy-all | doi-access = free }}</ref> Pyruvate is an intermediate in several metabolic pathways, but the majority is converted to [[acetyl-CoA]] and fed into the [[citric acid cycle]], which enables more ATP production by means of [[oxidative phosphorylation]]. This oxidation consumes molecular oxygen and releases water and the waste product carbon dioxide. When oxygen is lacking, or when pyruvate is temporarily produced faster than it can be consumed by the citric acid cycle (as in intense muscular exertion), pyruvate is converted to [[lactic acid|lactate]] by the enzyme [[lactate dehydrogenase]], a process that also oxidizes NADH back to NAD<sup>+</sup> for re-use in further glycolysis, allowing energy production to continue.<ref>{{cite journal | vauthors = Alfarouk KO, Verduzco D, Rauch C, Muddathir AK, Adil HH, Elhassan GO, Ibrahim ME, David Polo Orozco J, Cardone RA, Reshkin SJ, Harguindey S | display-authors = 6 | title = Glycolysis, tumor metabolism, cancer growth and dissemination. A new pH-based etiopathogenic perspective and therapeutic approach to an old cancer question | journal = Oncoscience | volume = 1 | issue = 12 | pages = 777–802 | date = 18 December 2014 | pmid = 25621294 | pmc = 4303887 | doi = 10.18632/oncoscience.109 | doi-access = free }}</ref> The lactate is later converted back to pyruvate for ATP production where energy is needed, or back to glucose in the [[Cori cycle]]. An alternative route for glucose breakdown is the [[pentose phosphate pathway]], which produces less energy but supports [[#Anabolism|anabolism]] (biomolecule synthesis). This pathway reduces the coenzyme [[NADP+|NADP<sup>+</sup>]] to NADPH and produces [[pentose]] compounds such as [[ribose 5-phosphate]] for synthesis of many biomolecules such as [[nucleotide]]s and [[aromatic amino acid]]s.<ref name="Kruger-2003">{{cite journal |last1=Kruger |first1=Nicholas J |last2=von Schaewen |first2=Antje |title=The oxidative pentose phosphate pathway: structure and organisation |journal=Current Opinion in Plant Biology |volume=6 |date=2003 |issue=3 |doi=10.1016/S1369-5266(03)00039-6 |pages=236–246|pmid=12753973 |bibcode=2003COPB....6..236K }}</ref>

[[File:Carbon Catabolism.png|thumb|500px|Carbon Catabolism pathway map for free energy including carbohydrate and lipid sources of energy]]

Fats are catabolized by [[hydrolysis]] to free fatty acids and glycerol. The glycerol enters glycolysis and the fatty acids are broken down by [[beta oxidation]] to release acetyl-CoA, which then is fed into the citric acid cycle. Fatty acids release more energy upon oxidation than carbohydrates. Steroids are also broken down by some bacteria in a process similar to beta oxidation, and this breakdown process involves the release of significant amounts of acetyl-CoA, propionyl-CoA, and pyruvate, which can all be used by the cell for energy. ''M. tuberculosis'' can also grow on the lipid [[cholesterol]] as a sole source of carbon, and genes involved in the cholesterol-use pathway(s) have been validated as important during various stages of the infection lifecycle of ''M. tuberculosis''.<ref>{{cite journal | vauthors = Wipperman MF, Sampson NS, Thomas ST | title = Pathogen roid rage: cholesterol utilization by Mycobacterium tuberculosis | journal = Critical Reviews in Biochemistry and Molecular Biology | volume = 49 | issue = 4 | pages = 269–93 | date = 2014 | pmid = 24611808 | pmc = 4255906 | doi = 10.3109/10409238.2014.895700 }}</ref>

[[Amino acid]]s are either used to synthesize proteins and other biomolecules, or oxidized to [[urea]] and carbon dioxide to produce energy.<ref>{{cite journal | vauthors = Sakami W, Harrington H | title = Amino Acid Metabolism | journal = [[Annual Review of Biochemistry]] | volume = 32 | pages = 355–98 | year = 1963 | pmid = 14144484 | doi = 10.1146/annurev.bi.32.070163.002035 }}</ref> The oxidation pathway starts with the removal of the amino group by a [[transaminase]]. The amino group is fed into the [[urea cycle]], leaving a deaminated carbon skeleton in the form of a [[keto acid]]. Several of these keto acids are intermediates in the citric acid cycle, for example α-[[alpha-Ketoglutaric acid|ketoglutarate]] formed by deamination of [[glutamate]].<ref>{{cite journal | vauthors = Brosnan JT | title = Glutamate, at the interface between amino acid and carbohydrate metabolism | journal = The Journal of Nutrition | volume = 130 | issue = 4S Suppl | pages = 988S–90S | date = April 2000 | pmid = 10736367 | doi = 10.1093/jn/130.4.988S | doi-access = free }}</ref> The [[glucogenic amino acid]]s can also be converted into glucose, through [[gluconeogenesis]].<ref>{{cite journal | vauthors = Young VR, Ajami AM | title = Glutamine: the emperor or his clothes? | journal = The Journal of Nutrition | volume = 131 | issue = 9 Suppl | pages = 2449S–59S; discussion 2486S–7S | date = September 2001 | pmid = 11533293 | doi = 10.1093/jn/131.9.2449S | doi-access = free }}</ref>