G
Golam M. Uddin
Researcher at University of Alberta
Publications - 25
Citations - 976
Golam M. Uddin is an academic researcher from University of Alberta. The author has contributed to research in topics: Mitochondrion & Cardiac function curve. The author has an hindex of 11, co-authored 23 publications receiving 557 citations. Previous affiliations of Golam M. Uddin include Alberta Children's Hospital & Korea Institute of Science and Technology.
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Journal ArticleDOI
Empagliflozin Increases Cardiac Energy Production in Diabetes: Novel Translational Insights Into the Heart Failure Benefits of SGLT2 Inhibitors.
Subodh Verma,Sonia Rawat,Kim L. Ho,Cory S. Wagg,Liyan Zhang,Hwee Teoh,John E. Dyck,Golam M. Uddin,Gavin Y. Oudit,Eric Mayoux,Michael Lehrke,Nikolaus Marx,Gary D. Lopaschuk +12 more
TL;DR: In this article, the authors evaluated cardiac energy production and bioenergetics in an experimental model of diabetes treated with the SGLT2 inhibitor empagliflozin.
Journal ArticleDOI
Loss of Metabolic Flexibility in the Failing Heart.
TL;DR: An increasing body of evidence shows that increasing cardiac ATP production and/or modulating cardiac energy substrate preference positively correlates with heart function and can lead to better outcomes.
Journal ArticleDOI
Impaired branched chain amino acid oxidation contributes to cardiac insulin resistance in heart failure
Golam M. Uddin,Liyan Zhang,Saumya Shah,Arata Fukushima,Cory S. Wagg,Keshav Gopal,Rami Al Batran,Simran Pherwani,Kim L. Ho,Jamie Boisvenue,Qutuba G. Karwi,Qutuba G. Karwi,Tariq R. Altamimi,David S. Wishart,Jason R.B. Dyck,John R. Ussher,Gavin Y. Oudit,Gary D. Lopaschuk +17 more
TL;DR: It is concluded that impaired cardiac BCAA catabolism and insulin signaling occur in human heart failure, while enhancing BCAA oxidation can improve cardiac function in the failing mouse heart.
Journal ArticleDOI
Head to Head Comparison of Short-Term Treatment with the NAD+ Precursor Nicotinamide Mononucleotide (NMN) and 6 Weeks of Exercise in Obese Female Mice
TL;DR: The data suggest that while exercise and NMN-supplementation can induce similar reversal of the glucose intolerance induced by obesity, they are associated with tissue-specific effects and differential alterations to mitochondrial function in muscle and liver.
Journal ArticleDOI
Nicotinamide mononucleotide (NMN) supplementation ameliorates the impact of maternal obesity in mice: comparison with exercise
Golam M. Uddin,Neil A. Youngson,Bronte M. Doyle,David A. Sinclair,David A. Sinclair,Margaret J. Morris +5 more
TL;DR: Both interventions reduced adiposity, and showed a modest improvement in glucose tolerance and improved markers of mitochondrial function, and the interventions appeared to exert the most global benefit in mice that were most metabolically challenged (HFD-consuming offspring of obese mothers).