Scripps Florida Logo

The Butler Lab

Publications

Melanocortin-3 receptors are involved in adaptation to restricted feeding.
Begriche K, Marston OJ, Rossi J, Burke LK, McDonald P, Heisler LK, Butler AA.
Genes Brain Behav. 2012 Apr;11(3):291-302. doi: 10.1111/j.1601-183X.2012.00766.x. Epub 2012 Feb 6.
PubMed Link

Adropin Deficiency Is Associated With Increased Adiposity and Insulin Resistance.
Ganesh Kumar K, Zhang J, Gao S, Rossi J, McGuinness OP, Halem HH, Culler MD, Mynatt RL, Butler AA.
Obesity (Silver Spring). 2012 Feb 9. doi: 10.1038/oby.2012.31. [Epub ahead of print]
PubMed Link

Genetic dissection of the functions of the melanocortin-3 receptor, a seven-transmembrane G-protein-coupled receptor, suggests roles for central and peripheral receptors in energy homeostasis.
Begriche K, Levasseur PR, Zhang J, Rossi J, Skorupa D, Solt LA, Young B, Burris TP, Marks DL, Mynatt RL, Butler AA.
J Biol Chem. 2011 Nov 25;286(47):40771-81. Epub 2011 Oct 7.
PubMed Link

Homeostastic and non-homeostatic functions of melanocortin-3 receptors in the control of energy balance and metabolism.
Begriche K, Sutton GM, Butler AA.
Physiol Behav. 2011 Sep 26;104(4):546-54. Epub 2011 Apr 13. Review.
PubMed Link

A recurring problem with the analysis of energy expenditure in genetic models expressing lean and obese phenotypes.
Butler AA, Kozak LP. 
Diabetes 2010 Feb;59(2):323-9.

Central nervous system melanocortin-3 receptors are required for synchronizing metabolism during entrainment to restricted feeding during the light cycle.
Sutton GM, Begriche K, Kumar KG, Gimble JM, Perez-Tilve D, Nogueiras R, McMillan RP, Hulver MW, Tschöp MH, Butler AA.
FASEB J. 2010 Mar;24(3):862-72.

Protein malnutrition during pregnancy in C57BL/6J mice results in offspring with altered circadian physiology before obesity.
Sutton GM, Centanni AV, Butler AA.
Endocrinology 2010 Apr;151(4):1570-80.

Discussed by Reyes TM and Simmons RA - Setting the “Clock”: Importance of Maternal Diet (Editorial). Endocrinology 2010 151(4), 1385-1386.

Melanocortin signaling in the CNS directly regulates circulating cholesterol.
Perez-Tilve D, Hofmann SM, Basford J, Nogueiras R, Pfluger PT, Patterson JT, Grant E, Wilson-Perez HE, Granholm NA, Arnold M, Trevaskis JL, Butler AA, Davidson WS, Woods SC, Benoit SC, Sleeman MW, DiMarchi RD, Hui DY, Tschöp MH.
Nat Neurosci. 2010 Jul;13(7):877-82.

Discussed by Yi-Chun Loraine Tung and Giles SH Yeo. Central melanocortin signaling regulates cholesterol  (News and Views). Nature Neuroscience 2010 Jul; 13(7), 779-780.
Faculty of 1000 selection - must read.

 

Yang H, Youm YH, Vandanmagsar B, Rood J, Kumar KG, Butler AA, Dixit VD.
Obesity accelerates thymic aging.
Blood 2009 Oct 29;114(18):3803-12.

 

Identification of adropin as a secreted factor linking dietary macronutrient intake with energy homeostasis and lipid metabolism.
Kumar KG, Trevaskis JL, Lam DD, Sutton GM, Koza RA, Chouljenko VN, Kousoulas KG, Rogers PM, Kesterson RA, Thearle M, Ferrante AW Jr, Mynatt RL, Burris TP, Dong JZ, Halem HA, Culler MD, Heisler LK, Stephens JM, Butler AA.
Cell Metab. 2008 Dec;8(6):468-81.
Faculty of 1000 selection - recommended.

Serotonin 2C receptor agonists improve type 2 diabetes via melanocortin-4 receptor signaling pathways.
Zhou L, Sutton GM, Rochford JJ, Semple RK, Lam DD, Oksanen LJ, Thornton-Jones ZD, Clifton PG, Yueh CY, Evans ML, McCrimmon RJ, Elmquist JK*, Butler AA*, Heisler LK*.
Cell Metab. 2007 Nov;6(5):398-405. * corresponding authors.

Discussed by Pissios P and Maratos-Flier E - More Then Satiety: Central Serotonin Signaling And Glucose Homeostasis (News and Views).
Cell Metabolism 2007 Nov; 6(5):345-347, and in Miller KJ and Azzara AV - An Old Dog Leans A New Trick: Regulation Of Peripheral Glucose Homeostasis By The Serotonin (5-HT)2C receptor. Molecular Interventions 2008 8:73-77, and in Crunkhorn S - Metabolic Disease: New Opportunity for Serotonin Receptor Agonists. Nature Reviews Drug Discovery
Faculty of 1000 - must read.

___________

Overview
___________

Research
___________

Lab Personnel
___________

Publications
___________

Contact
___________

Support Us
___________