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Дата последнего поиска статьи во внешних источниках: 1 апреля 2026 г.
Аннотация:For a long time, glycolysis and mitochondrial oxidative phosphorylation were opposedto each other. Glycolysis works when there is a lack of oxygen; the mitochondria supplyATP in an oxygen environment. In recent decades, it has been discovered that glycolysisin vivo always works and the final product is lactate. Lactate can accumulate and is thetransport form for pyruvate. In this review, we look at how obligate lactate formationduring glycolysis affects the tricarboxylic acid (TCA) cycle and mitochondrial respiration.We conclude that fatty acid β-oxidation is a prerequisite for obligate lactate formationduring glycolysis, which in turn promotes and enhances the anaplerotic functions of theTCA cycle. In this way, a supply of two types of substrates for mitochondria is formed:fatty acids as the basic energy substrates, and lactate as an emergency substrate for theheart, skeletal muscles, and brain. High steady-state levels of lactate and ATP, supported byβ-oxidation, stimulate gluconeogenesis and thus support the lactate cycle. It is concludedthat mitochondrial fatty acids β-oxidation and glycolysis constitute a single interdependentsystem of energy metabolism of the human body.Keywords: beta-oxidation of fatty acids; energy metabolism; fatty acids; glycolysis; lactate;lactate cycle; mitochondria; pyruvate; respirasome; tricarboxylic acid cycle