R
Rebecca J. Ford
Researcher at McMaster University
Publications - 33
Citations - 4038
Rebecca J. Ford is an academic researcher from McMaster University. The author has contributed to research in topics: AMPK & AMP-activated protein kinase. The author has an hindex of 23, co-authored 32 publications receiving 2829 citations. Previous affiliations of Rebecca J. Ford include McMaster-Carr.
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Journal ArticleDOI
Single phosphorylation sites in Acc1 and Acc2 regulate lipid homeostasis and the insulin-sensitizing effects of metformin
Morgan D. Fullerton,Sandra Galic,Katarina Marcinko,Sarah Sikkema,Thomas Pulinilkunnil,Zhi-Ping Chen,Hayley M. O'Neill,Rebecca J. Ford,Rengasamy Palanivel,Matthew L. O'Brien,Matthew L. O'Brien,D. Grahame Hardie,S. Lance Macaulay,Jonathan D. Schertzer,Jason R.B. Dyck,Bryce J. W. van Denderen,Bruce E. Kemp,Bruce E. Kemp,Gregory R. Steinberg,Gregory R. Steinberg +19 more
TL;DR: It is established that inhibitory phosphorylation of Acc by Ampk is essential for the control of lipid metabolism and, in the setting of obesity, for metformin-induced improvements in insulin action.
Journal ArticleDOI
AMPK as a Therapeutic Target for Treating Metabolic Diseases
TL;DR: The metabolic phenotypes of transgenic mouse models in which AMPK expression and function have been manipulated are evaluated, and the impact this has on controlling lipid metabolism, glucose homeostasis, and inflammation is evaluated.
Journal ArticleDOI
Inhibiting peripheral serotonin synthesis reduces obesity and metabolic dysfunction by promoting brown adipose tissue thermogenesis
Justin D. Crane,Rengasamy Palanivel,Emilio P. Mottillo,Adam L. Bujak,Huaqing Wang,Rebecca J. Ford,Andrew Collins,Regje M. E. Blümer,Morgan D. Fullerton,Julian M. Yabut,Janice J. Kim,Jean-Eric Ghia,Shereen M. Hamza,Katherine M. Morrison,Jonathan D. Schertzer,Jason R.B. Dyck,Waliul I. Khan,Gregory R. Steinberg +17 more
TL;DR: It is found that Tph1-deficient mice fed a high-fat diet (HFD) are protected from obesity, insulin resistance and nonalcoholic fatty liver disease (NAFLD) while exhibiting greater energy expenditure by BAT.
Journal ArticleDOI
Treatment of nonalcoholic fatty liver disease: role of AMPK.
Brennan K. Smith,Katarina Marcinko,Eric M. Desjardins,James S. V. Lally,Rebecca J. Ford,Gregory R. Steinberg +5 more
TL;DR: Three primary mechanisms by which AMPK activation may improve nonalcoholic fatty liver disease are proposed and 27 studies that have used AMPK activators to reduce NAFLD are identified.
Journal ArticleDOI
Liver-specific ATP-citrate lyase inhibition by bempedoic acid decreases LDL-C and attenuates atherosclerosis.
Stephen L. Pinkosky,Stephen L. Pinkosky,Roger S. Newton,Emily A. Day,Rebecca J. Ford,Šárka Lhoták,Richard C. Austin,Carolyn M. Birch,Brennan K. Smith,Sergey Filippov,Pieter H.E. Groot,Gregory R. Steinberg,Narendra D. Lalwani +12 more
TL;DR: ETC-1002 is a prodrug that requires activation by very long-chain acyl-CoA synthetase-1 (ACSVL1) to modulate both targets, and that inhibition of ACL leads to LDL receptor upregulation, decreased LDL-C and attenuation of atherosclerosis, independently of AMPK.