Holzner 2019 MitoFit Preprint Arch EA

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Holzner 2019 MitoFit Preprint Arch EA

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Holzner Lorenz MW, Sowton AP, Murray AJ (2019) Evidence of altered mitochondrial function in glycolytic, but not oxidative skeletal muscle in mice after one month of high fat, high sucrose feeding. MitoFit Preprint Arch doi:10.26124/mitofit:ea19.MiPSchool.0004.
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Evidence of altered mitochondrial function in glycolytic but not oxidative skeletal muscle in mice after one month of high fat high sucrose feeding

Holzner Lorenz MW, Sowton AP, Murray AJ (2019) MitoFit Preprint Arch

Abstract: Version 1 (v1) 2019-06-11 doi:10.26124/mitofit:ea19.MiPSchool.0004

Rates of obesity and the metabolic syndrome, which are strongly associated with type 2 diabetes (T2D) and cardiovascular disease, continue to rise worldwide. Skeletal muscle is an important tissue in the development of these disorders, as it serves as the major “glucose sink” in the body, and skeletal muscle mitochondrial dysfunction occurs in both metabolic syndrome and T2D [1]. Understanding of the early processes involved in skeletal muscle dysfunction, including changes in mitochondrial function, is currently lacking. It has been proposed that greater mitochondrial oxidation capacity, as is the case in oxidative muscles such as the soleus, can allay the onset of mitochondrial dysfunction induced by high fat, high sugar (HFHS) feeding. Previous studies in fructose fed rats appear to support this view [2]. If this is the case, soleus muscle may be less likely to develop mitochondrial dysfunction than a more glycolytic muscle, such as the gastrocnemius, when exposed to short term HFHS feeding. Here we investigated effect of HFHS feeding over one month on skeletal muscle oxidative capacity, comparing respiration in soleus and gastrocnemius fibres.

Keywords: [[has publicationkeywords::Diabetes & [1]] Bioblast editor: Iglesias-Gonzalez J O2k-Network Lab: UK Cambridge Murray AJ


Holzner Lorenz MW(1), Sowton AP(2), Murray AJ(1)

  1. Institute of Metabolic Science, Metabolic Research Laboratories, University of Cambridge - lmwh2@cam.ac.uk
  2. Department of Physiology, Development and Neuroscience, University of Cambridge


Holzner 2019 MitoFit Preprint Arch EA Figure 1.png
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  1. Thyfault JP, Kraus RM, Hickner RC, Howell AW, Wolfe RR, Dohm GL (2004) "Impaired plasma fatty acid oxidation in extremely obese women," Am J Physiol Endocrinol Metab 287(6):1076-81
  2. Warren BE, Lou PH, Lucchinetti E, Zhang L, Clanachan AS, Affolter A, Hersberger M, Zaugg M, Lemieux H (2014), "Early mitochondrial dysfunction in glycolytic muscle, but not oxidative muscle, of the fructose-fed insulin-resistant rat," Am J Physiol Endocrinol Metab, 306(6):658-67
  3. Horscroft JA, O'Brien KA, Clark AD, Lindsay RT, Steel AS, Procter NEK, Devaux J, Frenneaux M, Harridge SDR, Murray AJ (2019) "Inorganic nitrate, hypoxia, and the regulation of cardiac mitochondrial respiration—probing the role of PPARα," FASEB J, 33

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