C
Christopher J. Lynch
Researcher at Old Dominion University
Publications - 174
Citations - 9608
Christopher J. Lynch is an academic researcher from Old Dominion University. The author has contributed to research in topics: Phosphorylation & Adipose tissue. The author has an hindex of 50, co-authored 166 publications receiving 8379 citations. Previous affiliations of Christopher J. Lynch include Pennsylvania State University & Suffolk University.
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Journal ArticleDOI
Branched-chain amino acids in metabolic signalling and insulin resistance
TL;DR: Whether and how impaired BCAA metabolism might occur in obesity is discussed in this Review, and a BCAA dysmetabolism model proposes that the accumulation of mitotoxic metabolites promotes β-cell mitochondrial dysfunction, stress signalling and apoptosis associated with T2DM.
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Obesity-related elevations in plasma leucine are associated with alterations in enzymes involved in branched-chain amino acid metabolism
Pengxiang She,Cynthia G. Van Horn,Tanya Reid,Susan M. Hutson,Robert N. Cooney,Christopher J. Lynch +5 more
TL;DR: The results are consistent with the idea that tissue-specific alterations in BCAA metabolism, in liver and adipose tissue but not in muscle, may contribute to the rise in plasma BCAAs in obesity.
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Catabolic defect of branched-chain amino acids promotes heart failure
Haipeng Sun,Haipeng Sun,Kristine C. Olson,Chen Gao,Domenick A. Prosdocimo,Meiyi Zhou,Zhihua Wang,Darwin Jeyaraj,Ji Youn Youn,Shuxun Ren,Yunxia Liu,Christoph Rau,Svati H. Shah,Olga Ilkayeva,Wen Jun Gui,Noelle S. William,R. Max Wynn,Christopher B. Newgard,Hua Cai,Xinshu Xiao,David T. Chuang,Paul Christian Schulze,Paul Christian Schulze,Christopher J. Lynch,Mukesh K. Jain,Yibin Wang,Yibin Wang +26 more
TL;DR: BCAA catabolic defect is a metabolic hallmark of failing heart resulting from Krüppel-like factor 15–mediated transcriptional reprogramming, and pharmacological enhancement of branched-chain &agr;-keto acid dehydrogenase activity significantly blunted cardiac dysfunction after pressure overload.
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Disruption of BCATm in Mice Leads to Increased Energy Expenditure Associated with the Activation of a Futile Protein Turnover Cycle
Pengxiang She,Tanya Reid,Sarah K. Bronson,Thomas C. Vary,Andras Hajnal,Christopher J. Lynch,Susan M. Hutson +6 more
TL;DR: Highlights from disrupted BCATm mice suggest that elevated BCAAs and/or loss of BCAA catabolism in peripheral tissues play an important role in regulating insulin sensitivity and energy expenditure.
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Adipose Tissue Branched Chain Amino Acid (BCAA) Metabolism Modulates Circulating BCAA Levels
TL;DR: The capacity of adipose tissue to catabolize circulating BCAAs in vivo is demonstrated for the first time and coordinate regulation of adipOSE-tissue BCAA enzymes may modulate circulating BCAA levels are confirmed.