Altered tricarboxylic acid cycle flux in primary myotubes from severely obese humans View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2019-04

AUTHORS

Kai Zou, J. Matthew Hinkley, Sanghee Park, Donghai Zheng, Terry E. Jones, Walter J. Pories, Pamela J. Hornby, James Lenhard, G. Lynis Dohm, Joseph A. Houmard

ABSTRACT

BACKGROUND/OBJECTIVE: The partitioning of glucose toward glycolytic end products rather than glucose oxidation and glycogen storage is evident in skeletal muscle with severe obesity and type 2 diabetes. The purpose of the present study was to determine the possible mechanism by which severe obesity alters insulin-mediated glucose partitioning in human skeletal muscle. SUBJECTS/METHODS: Primary human skeletal muscle cells (HSkMC) were isolated from lean (BMI = 23.6 ± 2.6 kg/m2, n = 9) and severely obese (BMI = 48.8 ± 1.9 kg/m2, n = 8) female subjects. Glucose oxidation, glycogen synthesis, non-oxidized glycolysis, pyruvate oxidation, and targeted TCA cycle metabolomics were examined in differentiated myotubes under basal and insulin-stimulated conditions. RESULTS: Myotubes derived from severely obese subjects exhibited attenuated response of glycogen synthesis (20.3%; 95% CI [4.7, 28.8]; P = 0.017) and glucose oxidation (5.6%; 95% CI [0.3, 8.6]; P = 0.046) with a concomitant greater increase (23.8%; 95% CI [5.7, 47.8]; P = 0.004) in non-oxidized glycolytic end products with insulin stimulation in comparison to the lean group (34.2% [24.9, 45.1]; 13.1% [8.6, 16.4], and 2.9% [-4.1, 12.2], respectively). These obesity-related alterations in glucose partitioning appeared to be linked with reduced TCA cycle flux, as 2-[14C]-pyruvate oxidation (358.4 pmol/mg protein/min [303.7, 432.9] vs. lean 439.2 pmol/mg protein/min [393.6, 463.1]; P = 0.013) along with several TCA cycle intermediates, were suppressed in the skeletal muscle of severely obese individuals. CONCLUSIONS: These data suggest that with severe obesity the partitioning of glucose toward anaerobic glycolysis in response to insulin is a resilient characteristic of human skeletal muscle. This altered glucose partitioning appeared to be due, at least in part, to a reduction in TCA cycle flux. More... »

PAGES

895-905

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41366-018-0137-7

DOI

http://dx.doi.org/10.1038/s41366-018-0137-7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1104505249

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29892037


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    "description": "BACKGROUND/OBJECTIVE: The partitioning of glucose toward glycolytic end products rather than glucose oxidation and glycogen storage is evident in skeletal muscle with severe obesity and type 2 diabetes. The purpose of the present study was to determine the possible mechanism by which severe obesity alters insulin-mediated glucose partitioning in human skeletal muscle.\nSUBJECTS/METHODS: Primary human skeletal muscle cells (HSkMC) were isolated from lean (BMI\u2009=\u200923.6\u2009\u00b1\u20092.6\u2009kg/m2, n\u2009=\u20099) and severely obese (BMI\u2009=\u200948.8\u2009\u00b1\u20091.9\u2009kg/m2, n\u2009=\u20098) female subjects. Glucose oxidation, glycogen synthesis, non-oxidized glycolysis, pyruvate oxidation, and targeted TCA cycle metabolomics were examined in differentiated myotubes under basal and insulin-stimulated conditions.\nRESULTS: Myotubes derived from severely obese subjects exhibited attenuated response of glycogen synthesis (20.3%; 95% CI [4.7, 28.8]; P\u2009=\u20090.017) and glucose oxidation (5.6%; 95% CI [0.3, 8.6]; P\u2009=\u20090.046) with a concomitant greater increase (23.8%; 95% CI [5.7, 47.8]; P\u2009=\u20090.004) in non-oxidized glycolytic end products with insulin stimulation in comparison to the lean group (34.2% [24.9, 45.1]; 13.1% [8.6, 16.4], and 2.9% [-4.1, 12.2], respectively). These obesity-related alterations in glucose partitioning appeared to be linked with reduced TCA cycle flux, as 2-[14C]-pyruvate oxidation (358.4\u2009pmol/mg protein/min [303.7, 432.9] vs. lean 439.2\u2009pmol/mg protein/min [393.6, 463.1]; P\u2009=\u20090.013) along with several TCA cycle intermediates, were suppressed in the skeletal muscle of severely obese individuals.\nCONCLUSIONS: These data suggest that with severe obesity the partitioning of glucose toward anaerobic glycolysis in response to insulin is a resilient characteristic of human skeletal muscle. This altered glucose partitioning appeared to be due, at least in part, to a reduction in TCA cycle flux.", 
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279 https://www.grid.ac/institutes/grid.497530.c schema:alternateName Janssen (United States)
280 schema:name Janssen Research & Development LLC, Spring House, PA, USA
281 rdf:type schema:Organization
 




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