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Difference between revisions of "Malate-anaplerotic pathway control state"

From Bioblast
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{{MitoPedia
{{MitoPedia
|abbr=M
|abbr=M
|description=[[File:M.jpg|left|200px|M]] '''M''': [[Malate]] alone does not support respiration of mt-preparations if [[oxaloacetate]] cannot be metabolized further in the absence of a source of acetyl-CoA. Transport of oxaloacetate across the inner mt-membrane is restricted particularly in liver. Mitochondrial citrate and 2-oxoglutarate (Ξ±-ketoglutarate) are depleted by antiport with malate. [[Succinate]] is lost from the mitochondria through the dicarboxylate carrier. OXPHOS capacity with malate alone is only 1.3% of that with [[PM |Pyruvate&Malate]] in isolated rat skeletal muscle mitochondria. Many mammalian and non-mammalian mitochondria have a mt-isoform of NADP<sup>+-</sup> or NAD(P)<big>+</big>-dependent [[malic enzyme]] (mtME), the latter being particularly active in proliferating cells. Then the [[anaplerotic pathway control state]] with malate alone supports high respiratory activities.
|description=[[File:M.jpg|left|200px|M]] '''M''': [[Malate]] alone does not support respiration of mt-preparations if [[oxaloacetate]] cannot be metabolized further in the absence of a source of acetyl-CoA. Transport of oxaloacetate across the inner mt-membrane is restricted particularly in liver. Mitochondrial citrate and 2-oxoglutarate (Ξ±-ketoglutarate) are depleted by antiport with malate. [[Succinate]] is lost from the mitochondria through the dicarboxylate carrier. OXPHOS capacity with malate alone is only 1.3% of that with [[PM |Pyruvate&Malate]] in isolated rat skeletal muscle mitochondria. Many mammalian and non-mammalian mitochondria have a mt-isoform of NADP<sup>+-</sup> or NAD(P)<big>+</big>-dependent [[malic enzyme]] (mtME), the latter being particularly active in proliferating cells. Then the [[anaplerotic pathway control state]] with malate alone (aN) supports high respiratory activities comparable to the NADH-linked pathway control states (N) with with pyruvate&malate or glutamate&malate substrate combinations ([[PM pathway control state]], [[GM pathway control state]]).
|info=[[Gnaiger 2014 MitoPathways]] - Chapter 3.1
|info=[[Gnaiger 2014 MitoPathways]] - Chapter 3.1
}}
}}
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|mitopedia concept=SUIT state
|mitopedia concept=SUIT state
}}
}}
Communicated by [[Gnaiger E]] 2016-01-24, edited 2016-11-30.
[[File:M-malic enzyme.jpg|right|300px|M and malic enzyme]]
[[File:M-malic enzyme.jpg|right|300px|M and malic enzyme]]



Revision as of 10:01, 30 November 2016


high-resolution terminology - matching measurements at high-resolution


Malate-anaplerotic pathway control state

Description

M

M: Malate alone does not support respiration of mt-preparations if oxaloacetate cannot be metabolized further in the absence of a source of acetyl-CoA. Transport of oxaloacetate across the inner mt-membrane is restricted particularly in liver. Mitochondrial citrate and 2-oxoglutarate (Ξ±-ketoglutarate) are depleted by antiport with malate. Succinate is lost from the mitochondria through the dicarboxylate carrier. OXPHOS capacity with malate alone is only 1.3% of that with Pyruvate&Malate in isolated rat skeletal muscle mitochondria. Many mammalian and non-mammalian mitochondria have a mt-isoform of NADP+- or NAD(P)+-dependent malic enzyme (mtME), the latter being particularly active in proliferating cells. Then the anaplerotic pathway control state with malate alone (aN) supports high respiratory activities comparable to the NADH-linked pathway control states (N) with with pyruvate&malate or glutamate&malate substrate combinations (PM pathway control state, GM pathway control state).

Abbreviation: M

Reference: Gnaiger 2014 MitoPathways - Chapter 3.1


MitoPedia concepts: SUIT state 

Communicated by Gnaiger E 2016-01-24, edited 2016-11-30.
M and malic enzyme

M(L)

M(P)

M(E)