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    Reversing diet-induced metabolic dysregulation by diet switching leads to altered hepatic de novo lipogenesis and glycerolipid synthesis

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    Author
    Kowalski, GM; Hamley, S; Selathurai, A; Kloehn, J; De Souza, DP; O'Callaghan, S; Nijagal, B; Tull, DL; McConville, MJ; Bruce, CR
    Date
    2016-06-07
    Source Title
    Scientific Reports
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    McConville, Malcolm; KLOEHN, JOACHIM; O'Callaghan, Sean; de Souza, David; Nijagal, Brunda; Tull, Dedreia
    Affiliation
    Biochemistry and Molecular Biology
    Bio21
    Metadata
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    Document Type
    Journal Article
    Citations
    Kowalski, G. M., Hamley, S., Selathurai, A., Kloehn, J., De Souza, D. P., O'Callaghan, S., Nijagal, B., Tull, D. L., McConville, M. J. & Bruce, C. R. (2016). Reversing diet-induced metabolic dysregulation by diet switching leads to altered hepatic de novo lipogenesis and glycerolipid synthesis. SCIENTIFIC REPORTS, 6 (1), https://doi.org/10.1038/srep27541.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259325
    DOI
    10.1038/srep27541
    NHMRC Grant code
    NHMRC/1059530
    Abstract
    In humans, low-energy diets rapidly reduce hepatic fat and improve/normalise glycemic control. Due to difficulties in obtaining human liver, little is known about changes to the lipid species and pathway fluxes that occur under these conditions. Using a combination of stable isotope, and targeted metabolomic approaches we investigated the acute (7-9 days) hepatic effects of switching high-fat high-sucrose diet (HFD) fed obese mice back to a chow diet. Upon the switch, energy intake was reduced, resulting in reductions of fat mass and hepatic triacyl- and diacylglycerol. However, these parameters were still elevated compared to chow fed mice, thus representing an intermediate phenotype. Nonetheless, glucose intolerance and hyperinsulinemia were completely normalized. The diet reversal resulted in marked reductions in hepatic de novo lipogenesis when compared to the chow and HFD groups. Compared with HFD, glycerolipid synthesis was reduced in the reversal animals, however it remained elevated above that of chow controls, indicating that despite experiencing a net loss in lipid stores, the liver was still actively esterifying available fatty acids at rates higher than that in chow control mice. This effect likely promotes the re-esterification of excess free fatty acids released from the breakdown of adipose depots during the weight loss period.

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