Brain leptin reduces liver lipids by increasing hepatic triglyceride secretion and lowering lipogenesis

Martina Theresa Hackl, Clemens Fürnsinn, Christina Maria Schuh, Martin Krssak, Fabrizia Carli, Sara Guerra, Angelika Freudenthaler, Sabina Baumgartner-Parzer, Thomas H. Helbich, Anton Luger, Maximilian Zeyda, Amalia Gastaldelli, Christoph Buettner and Thomas Scherer ()
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Martina Theresa Hackl: Medical University of Vienna
Clemens Fürnsinn: Medical University of Vienna
Christina Maria Schuh: Medical University of Vienna
Martin Krssak: Medical University of Vienna
Fabrizia Carli: National Research Council
Sara Guerra: National Research Council
Angelika Freudenthaler: Medical University of Vienna
Sabina Baumgartner-Parzer: Medical University of Vienna
Thomas H. Helbich: Division of Molecular and Gender Imaging, Medical University of Vienna
Anton Luger: Medical University of Vienna
Maximilian Zeyda: Medical University of Vienna
Amalia Gastaldelli: National Research Council
Christoph Buettner: Obesity and Metabolism Institute (DOMI), Icahn School of Medicine at Mt Sinai, One Gustave L. Levy Pl
Thomas Scherer: Medical University of Vienna

Nature Communications, 2019, vol. 10, issue 1, 1-13

Abstract: Abstract Hepatic steatosis develops when lipid influx and production exceed the liver’s ability to utilize/export triglycerides. Obesity promotes steatosis and is characterized by leptin resistance. A role of leptin in hepatic lipid handling is highlighted by the observation that recombinant leptin reverses steatosis of hypoleptinemic patients with lipodystrophy by an unknown mechanism. Since leptin mainly functions via CNS signaling, we here examine in rats whether leptin regulates hepatic lipid flux via the brain in a series of stereotaxic infusion experiments. We demonstrate that brain leptin protects from steatosis by promoting hepatic triglyceride export and decreasing de novo lipogenesis independently of caloric intake. Leptin’s anti-steatotic effects are generated in the dorsal vagal complex, require hepatic vagal innervation, and are preserved in high-fat-diet-fed rats when the blood brain barrier is bypassed. Thus, CNS leptin protects from ectopic lipid accumulation via a brain-vagus-liver axis and may be a therapeutic strategy to ameliorate obesity-related steatosis.

Date: 2019
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DOI: 10.1038/s41467-019-10684-1

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