Sensing Mitochondrial Acetyl-CoA to Tune Respiration

Christine A Mills; Alec G Trub; Matthew D Hirschey

doi:10.1016/j.tem.2018.10.003

Sensing Mitochondrial Acetyl-CoA to Tune Respiration

Trends Endocrinol Metab. 2019 Jan;30(1):1-3. doi: 10.1016/j.tem.2018.10.003. Epub 2018 Nov 12.

Authors

Christine A Mills¹, Alec G Trub², Matthew D Hirschey³

Affiliations

¹ Duke Molecular Physiology Institute and Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27701, USA.
² Duke Molecular Physiology Institute and Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27701, USA; Department of Pharmacology & Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA.
³ Duke Molecular Physiology Institute and Sarah W. Stedman Nutrition and Metabolism Center, Duke University Medical Center, Durham, NC 27701, USA; Department of Pharmacology & Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA; Department of Medicine, Division of Endocrinology, Metabolism, and Nutrition, Duke University Medical Center, Durham, NC 27710, USA. Electronic address: matthew.hirschey@duke.edu.

Abstract

Fatty acid synthesis (FAS) in mitochondria produces a key metabolite called lipoic acid. However, a new study by Van Vranken et al.[1] (Mol. Cell 2018;71:567-580) shows that mitochondrial FAS regulates the assembly of oxidative phosphorylation complexes, thereby functioning as a nutrient sensor for mitochondrial respiration.

Keywords: acetyl-coA; acyl-carrier protein (ACP); fatty acid synthesis; mitochondria; nutrient sensing.

Publication types

Review

MeSH terms

Acetyl Coenzyme A / metabolism*
Acyl Carrier Protein / metabolism*
Eukaryota / metabolism*
Fatty Acids / metabolism*
Mitochondria / metabolism*
Respiration*

Substances

Acyl Carrier Protein
Fatty Acids
Acetyl Coenzyme A

Abstract

Publication types

MeSH terms

Substances

Grants and funding