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Thomas M. O’Connell

Researcher at Indiana University

Publications -  83
Citations -  4049

Thomas M. O’Connell is an academic researcher from Indiana University. The author has contributed to research in topics: Cachexia & Metabolome. The author has an hindex of 28, co-authored 81 publications receiving 3172 citations. Previous affiliations of Thomas M. O’Connell include Beaumont Health & Harvard University.

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The microbiome and butyrate regulate energy metabolism and autophagy in the mammalian colon

TL;DR: It is demonstrated that microbiota have a strong effect on energy homeostasis in the colon compared to other tissues and this tissue specificity is due to colonocytes utilizing bacterially produced butyrate as their primary energy source.
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A Class of Reactive Acyl-CoA Species Reveals the Non-enzymatic Origins of Protein Acylation

TL;DR: The tricarboxylic acid cycle is identified as a pathway commonly regulated by acylation and validated malate dehydrogenase as a key target and data uncover a fundamental relationship between reactive acyl-CoA species and proteins and define a new regulatory paradigm in metabolism.
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Use of Pharmaco‐Metabonomics for Early Prediction of Acetaminophen‐Induced Hepatotoxicity in Humans

TL;DR: It is demonstrated that the pattern of endogenous metabolites in urine could predict susceptibility to acetaminophen‐induced liver injury in rats, and this “early‐intervention pharmaco‐metabonomics” approach should now be tested in clinical trials of other potentially hepatotoxic drugs.
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Cachexia induced by cancer and chemotherapy yield distinct perturbations to energy metabolism

TL;DR: A comprehensive and systems level metabolomics approach is applied to characterize the metabolic perturbations in murine models of cancer‐induced and chemotherapy‐induced cachexia.
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Metabolomic Profiling Reveals Mitochondrial-Derived Lipid Biomarkers That Drive Obesity-Associated Inflammation

TL;DR: Compared to a traditional HFD model, the CAF diet provides a robust model for diet-induced human obesity, which models Metabolic Syndrome-related mitochondrial dysfunction in serum, muscle, and adipose, along with pro-inflammatory metabolite alterations, and suggest that modifying the availability or metabolism of saturated fatty acids may limit the inflammation associated with obesity leading to Metabolic syndrome.