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- Malate-anaplerotic pathway control state + ([[File:M.jpg|left|200px|M]] '''M''': [[Mal … [[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 (α-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. However, 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 pyruvate&malate or glutamate&malate substrate combinations ([[PM-pathway control state]], [[GM-pathway control state]]).[GM-pathway control state]]).)
