Hungry for your alanine: when liver depends on muscle proteolysis
Theresia Sarabhai1,2 and Michael Roden1,2,3
1Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University, Düsseldorf, Germany.
2German Center for Diabetes Research, München-Neuherberg, Germany.
3Division of Endocrinology and Diabetology, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.
Address correspondence to: Michael Roden, Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University, Auf’m Hennekamp 65, 40225, Düsseldorf, Germany. Phone: 49.211.33.82.201; Email: michael.roden@ddz.de.
Find articles by Sarabhai, T. in: JCI | PubMed | Google Scholar
1Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University, Düsseldorf, Germany.
2German Center for Diabetes Research, München-Neuherberg, Germany.
3Division of Endocrinology and Diabetology, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.
Address correspondence to: Michael Roden, Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University, Auf’m Hennekamp 65, 40225, Düsseldorf, Germany. Phone: 49.211.33.82.201; Email: michael.roden@ddz.de.
Find articles by Roden, M. in: JCI | PubMed | Google Scholar
First published September 23, 2019 - More info
J Clin Invest. 2019;129(11):4563–4566. https://doi.org/10.1172/JCI131931.
© 2019 American Society for Clinical Investigation
Fasting requires complex endocrine and metabolic interorgan crosstalk, which involves shifting from glucose to fatty acid oxidation, derived from adipose tissue lipolysis, in order to preserve glucose for the brain. The glucose-alanine (Cahill) cycle is critical for regenerating glucose. In this issue of JCI, Petersen et al. report on their use of an innovative stable isotope tracer method to show that skeletal muscle–derived alanine becomes rate controlling for hepatic mitochondrial oxidation and, in turn, for glucose production during prolonged fasting. These results provide new insight into skeletal muscle–liver metabolic crosstalk during the fed-to-fasting transition in humans.
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