puc-header

Hepatic JARID1a Ablation Disrupts the Transcription Adaptation to Feeding and Alters Systemic Metabolism

26 Pages Posted: 30 Dec 2018 Publication Status: Published

See all articles by Kacee A. DiTacchio

Kacee A. DiTacchio

University of Kansas, University of Kansas Medical Center, Department of Pharmacology, Toxicology, and Therapeutics

Diana Kalinowska

University of Kansas, University of Kansas Medical Center, Department of Pharmacology, Toxicology, and Therapeutics

Anand Saran

University of Kansas, University of Kansas Medical Center, Department of Pharmacology, Toxicology, and Therapeutics

Ashley Byrne

University of California, Santa Cruz, Jack Baskin School of Engineering, Department of Biomedical Engineering

Christopher Vollmers

University of California, Santa Cruz, Jack Baskin School of Engineering, Department of Biomedical Engineering

Luciano DiTacchio

University of Kansas, University of Kansas Medical Center, Department of Pharmacology, Toxicology, and Therapeutics

More...

Abstract

The liver is a key regulator of systemic energy homeostasis whose proper function is dependent on the circadian clock. Here, we show that livers deficient in the oscillator component JARID1a exhibit a dysregulation of genes involved in energy metabolism. Importantly, we find that mice that lack hepatic JARID1a have decreased lean body mass, decreased respiratory exchange ratios, faster production of ketones and increased glucose production in response to fasting. Finally, we find that JARID1a loss compromises the response of the hepatic transcriptome to nutrient availability. In all, ablation of hepatic JARID1a disrupts the coordination of hepatic metabolic programs with whole-body consequences.

Suggested Citation

DiTacchio, Kacee A. and Kalinowska, Diana and Saran, Anand and Byrne, Ashley and Vollmers, Christopher and DiTacchio, Luciano, Hepatic JARID1a Ablation Disrupts the Transcription Adaptation to Feeding and Alters Systemic Metabolism (December 28, 2018). Available at SSRN: https://ssrn.com/abstract=3307378 or http://dx.doi.org/10.2139/ssrn.3307378
This version of the paper has not been formally peer reviewed.

Kacee A. Ditacchio

University of Kansas, University of Kansas Medical Center, Department of Pharmacology, Toxicology, and Therapeutics

Kansas City, KS
United States

Diana Kalinowska

University of Kansas, University of Kansas Medical Center, Department of Pharmacology, Toxicology, and Therapeutics

Kansas City, KS
United States

Anand Saran

University of Kansas, University of Kansas Medical Center, Department of Pharmacology, Toxicology, and Therapeutics

Kansas City, KS
United States

Ashley Byrne

University of California, Santa Cruz, Jack Baskin School of Engineering, Department of Biomedical Engineering

Santa Cruz, CA 95064
United States

Christopher Vollmers

University of California, Santa Cruz, Jack Baskin School of Engineering, Department of Biomedical Engineering

Santa Cruz, CA 95064
United States

Luciano Ditacchio (Contact Author)

University of Kansas, University of Kansas Medical Center, Department of Pharmacology, Toxicology, and Therapeutics ( email )

Kansas City, KS
United States