Mitochondrial apolipoprotein MIC26 is a metabolic rheostat regulating central cellular fuel pathways

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Mitochondrial apolipoprotein MIC26 is a metabolic rheostat regulating central cellular fuel pathways

Mitochondria play central roles in metabolism and metabolic disorders such as type 2 diabetes. MIC26, a mitochondrial contact site and cristae organising system complex subunit, was linked to diabetes and modulation of lipid metabolism. Yet, the functional role of MIC26 in regulating metabolism under hy-perglycemia is not understood. We used a multi-omics approach combined with functional assays using WT and MIC26 KO cells cultured in normoglycemia or hyperglycemia, mimicking altered nutrient availability. We show that MIC26 has an inhibitory role in glycolysis and cholesterol/lipid metabolism under normo-glycemic conditions. Under hyperglycemia, this inhibitory role is reversed demonstrating that MIC26 is critical for metabolic adaptations. This is partially mediated by alterations of mito-chondrial metabolite transporters. Furthermore, MIC26 deletion led to a major metabolic rewiring of glutamine use and oxidative phosphorylation. We propose that MIC26 acts as a metabolic � ��rheostat," that modulates mitochondrial metabolite exchange via regulating mitochondrial cristae, allowing cells to cope with nutrient overload. © 2024, Life Science Alliance, LLC. All rights reserved.

Authors : Damiecki M.; Naha R.; Schaumkessel Y.; Westhoff P.; Atanelov N.; Stefanski A.; Petzsch P.; Stühler K.; Köhrer K.; Weber A.P.M.; Anand R.; Reichert A.S.; Kondadi A.K.

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