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Brian T. O’Neill
Researcher at Roy J. and Lucille A. Carver College of Medicine
Publications - 186
Citations - 5878
Brian T. O’Neill is an academic researcher from Roy J. and Lucille A. Carver College of Medicine. The author has contributed to research in topics: Internal medicine & Medicine. The author has an hindex of 37, co-authored 157 publications receiving 5132 citations. Previous affiliations of Brian T. O’Neill include Veterans Health Administration & Harvard University.
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Journal ArticleDOI
Varenicline: An α4β2 Nicotinic Receptor Partial Agonist for Smoking Cessation
Jotham Wadsworth Coe,Paige Roanne Palmer Brooks,Michael G. Vetelino,Michael C. Wirtz,Eric P. Arnold,Huang Jianhua,Steven B. Sands,Thomas I. Davis,Lorraine A. Lebel,Carol B. Fox,Alka Shrikhande,James Heym,Eric Schaeffer,Hans Rollema,Yi Lu,Robert S. Mansbach,Leslie K. Chambers,Charles C. Rovetti,David W. Schulz,and F. David Tingley,Brian T. O’Neill +20 more
TL;DR: Varenicline displays high α4β2 nAChR affinity and the desired in vivo dopaminergic profile and provides relief from the craving and withdrawal syndrome that accompanies cessation attempts.
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Reduced Mitochondrial Oxidative Capacity and Increased Mitochondrial Uncoupling Impair Myocardial Energetics in Obesity
TL;DR: Reduced mitochondrial oxidative capacity may contribute to cardiac dysfunction in ob/ob mice and fatty acid but not glucose-induced mitochondrial uncoupling reduces CE in obese mice by limiting ATP production and increasing M&OV0312;o2.
Journal ArticleDOI
Impaired cardiac efficiency and increased fatty acid oxidation in insulin-resistant ob/ob mouse hearts.
Pradip K. Mazumder,Brian T. O’Neill,Matthew W. Roberts,Jonathan Buchanan,Ui Jeong Yun,Robert C. Cooksey,Sihem Boudina,E. Dale Abel +7 more
TL;DR: The data indicate that although the hearts of glucose-intolerant ob/ob mice are capable of maintaining their function under conditions of increased fatty acid supply and hyperinsulinemia, they are insulin-resistant, metabolically inefficient, and unable to modulate substrate utilization in response to changes in insulin and fatty acids supply.
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Contribution of Impaired Myocardial Insulin Signaling to Mitochondrial Dysfunction and Oxidative Stress in the Heart
Sihem Boudina,Heiko Bugger,Sandra Sena,Brian T. O’Neill,Vlad G. Zaha,Olesya Ilkun,Jordan J. Wright,Pradip K. Mazumder,Eric Palfreyman,Timothy Tidwell,Heather A. Theobald,Oleh Khalimonchuk,Benjamin Wayment,Xiaoming Sheng,Kenneth J. Rodnick,Ryan Centini,Dong Chen,Sheldon E. Litwin,Bart E. Weimer,E. Dale Abel +19 more
TL;DR: In this paper, the authors tested the hypothesis that perinatal loss of insulin signaling in the heart impairs mitochondria function and found that the contribution of altered myocardial insulin action independent of associated changes in systemic metabolism is incompletely understood.
Journal ArticleDOI
Sirt3 Regulates Metabolic Flexibility of Skeletal Muscle through Reversible Enzymatic Deacetylation
Enxuan Jing,Brian T. O’Neill,Matthew J. Rardin,André Kleinridders,Olga R. Ilkeyeva,Siegfried Ussar,James R. Bain,Kevin Y. Lee,Eric Verdin,Christopher B. Newgard,Bradford W. Gibson,C. Ronald Kahn +11 more
TL;DR: Sirt3 plays an important role in skeletal muscle mitochondrial substrate choice and metabolic flexibility in part by regulating PDH function through deacetylation, which induces a switch of skeletal muscle substrate utilization from carbohydrate oxidation toward lactate production and fatty acid utilization even in the fed state.