Faculty

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Lily C. Chao, MD
Clinical Assistant Professor of Pediatrics (Clinician Educator)
Pediatrics
CHL Mail Stop 61 Off Campus Los Angeles
+1 323 361 7116

Overview

My research interest centers on mechanisms that regulate muscle metabolism and growth. As the largest organ in the human body, skeletal muscle plays an indispensible function in glucose utilization and metabolism. In addition to its metabolic function, coordinated contractility of skeletal muscle powers body movement and exercise performance.

The nuclear receptor Nur77 (also known as NR4A1) integrates glucose metabolism in multiple tissues. We previously demonstrated that in skeletal muscle, Nur77 directs the transcription of a number of genes linked to glucose utilization. More recently, we identified Nur77 as a regulator of muscle mass and myofiber size in mice. These findings have led us to examine the crosstalk between muscle metabolism and growth. To address this question, we have active research projects investigation the function of Nur77 expression in muscle development, regeneration, and diabetic myopathy. Findings from these studies will broaden our fundamental knowledge of the signaling pathways that integrate metabolism and muscle mass, and may have translational applications in conditions such as diabetes, muscular dystrophy, cancer, cachexia, as well as other forms of muscle wasting.

Awards

Endocrine Society: Early Investigator Award, 2014

Pediatric Endocrine Society: Clinical Research Scholar, 2013

Pasadena Magazine's Top Doctors

Society of Pediatric Research: Fellow's Basic Research Award, 2007

Howard Hughes Medical Institute-National Institutes of Health: Research Scholar, 1999

Publications

Nur77 deletion impairs muscle growth during developmental myogenesis and muscle regeneration in mice. PLoS One. 2017; 12(2):e0171268. View in: PubMed

The orphan nuclear receptor Nur77 is a determinant of myofiber size and muscle mass in mice. Mol Cell Biol. 2015 Apr; 35(7):1125-38. View in: PubMed

The orphan nuclear receptor nur77 is a determinant of myofiber size and muscle mass in mice. Mol Cell Biol. 2015 Apr 1; 35(7):1125-38. View in: PubMed

The macrophage LBP gene is an LXR target that promotes macrophage survival and atherosclerosis. J Lipid Res. 2014 Jun; 55(6):1120-30. View in: PubMed

Nkx6. 1 regulates islet ß-cell proliferation via Nr4a1 and Nr4a3 nuclear receptors. Proc Natl Acad Sci U S A. 2014 Apr 8; 111(14):5242-7. View in: PubMed

Nkx6. 1 regulates islet ß-cell proliferation via Nr4a1 and Nr4a3 nuclear receptors. Proc Natl Acad Sci U S A. 2014 Apr 08; 111(14):5242-7. View in: PubMed

The macrophage LBP gene is an LXR target that promotes macrophage survival and atherosclerosis. J Lipid Res. 2014 Mar 26; 55(6):1120-1130. View in: PubMed

Progesterone receptor in the vascular endothelium triggers physiological uterine permeability preimplantation. Cell. 2014 Jan 30; 156(3):549-62. View in: PubMed

Reciprocal regulation of hepatic and adipose lipogenesis by liver X receptors in obesity and insulin resistance. Cell Metab. 2013 Jul 2; 18(1):106-17. View in: PubMed

Reciprocal regulation of hepatic and adipose lipogenesis by liver X receptors in obesity and insulin resistance. Cell Metab. 2013 Jul 02; 18(1):106-17. View in: PubMed

Bone marrow NR4A expression is not a dominant factor in the development of atherosclerosis or macrophage polarization in mice. J Lipid Res. 2013 Mar; 54(3):806-15. View in: PubMed

Skeletal muscle Nur77 expression enhances oxidative metabolism and substrate utilization. J Lipid Res. 2012 Dec; 53(12):2610-9. View in: PubMed

SIRT1 regulation-it ain't all NAD. Mol Cell. 2012 Jan 13; 45(1):9-11. View in: PubMed

TLE3 is a dual-function transcriptional coregulator of adipogenesis. Cell Metab. 2011 Apr 06; 13(4):413-427. View in: PubMed

TLE3 is a dual-function transcriptional coregulator of adipogenesis. Cell Metab. 2011 Apr 6; 13(4):413-27. View in: PubMed

Insulin resistance and altered systemic glucose metabolism in mice lacking Nur77. Diabetes. 2009 Dec; 58(12):2788-96. View in: PubMed

Preserved glucose tolerance in high-fat-fed C57BL/6 mice transplanted with PPARgamma-/-, PPARdelta-/-, PPARgammadelta-/-, or LXRalphabeta-/- bone marrow. J Lipid Res. 2009 Feb; 50(2):214-24. View in: PubMed

Inhibition of adipocyte differentiation by Nur77, Nurr1, and Nor1. Mol Endocrinol. 2008 Dec; 22(12):2596-608. View in: PubMed

Nur77 coordinately regulates expression of genes linked to glucose metabolism in skeletal muscle. Mol Endocrinol. 2007 Sep; 21(9):2152-63. View in: PubMed

Liver X receptors are regulators of adipocyte gene expression but not differentiation: identification of apoD as a direct target. J Lipid Res. 2004 Apr; 45(4):616-25. View in: PubMed

Differential effects of rosiglitazone on skeletal muscle and liver insulin resistance in A-ZIP/F-1 fatless mice. Diabetes. 2003 Jun; 52(6):1311-8. View in: PubMed

Activation of liver X receptor improves glucose tolerance through coordinate regulation of glucose metabolism in liver and adipose tissue. Proc Natl Acad Sci U S A. 2003 Apr 29; 100(9):5419-24. View in: PubMed

Adipose tissue is required for the antidiabetic, but not for the hypolipidemic, effect of thiazolidinediones. J Clin Invest. 2000 Nov; 106(10):1221-8. View in: PubMed

Suppression of food intake and growth by amino acids in Drosophila: the role of pumpless, a fat body expressed gene with homology to vertebrate glycine cleavage system. Development. 1999 Dec; 126(23):5275-84. View in: PubMed

Assembly of the cleavage and polyadenylation apparatus requires about 10 seconds in vivo and is faster for strong than for weak poly(A) sites. Mol Cell Biol. 1999 Aug; 19(8):5588-600. View in: PubMed

Poly(A)-driven and poly(A)-assisted termination: two different modes of poly(A)-dependent transcription termination. Mol Cell Biol. 1998 Jan; 18(1):276-89. View in: PubMed

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