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Human skeletal muscle metabolic responses to 6 days of high-fat overfeeding are associated with dietary n-3PUFA content and muscle oxidative capacity

Wardle, SL, Macnaughton, LS, McGlory, C, Witard, OC, Dick, JR, Whitfield, PD, Ferrando, AA, Wolfe, RR, Kim, IY, Hamilton, DL, Moran, CN, Tipton, KD and Galloway, SDR 2020, Human skeletal muscle metabolic responses to 6 days of high-fat overfeeding are associated with dietary n-3PUFA content and muscle oxidative capacity, Physiological Reports, vol. 8, no. 16, pp. 1-15, doi: 10.14814/phy2.14529.

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Title Human skeletal muscle metabolic responses to 6 days of high-fat overfeeding are associated with dietary n-3PUFA content and muscle oxidative capacity
Author(s) Wardle, SL
Macnaughton, LS
McGlory, C
Witard, OC
Dick, JR
Whitfield, PD
Ferrando, AA
Wolfe, RR
Kim, IY
Hamilton, DLORCID iD for Hamilton, DL orcid.org/0000-0002-5620-4788
Moran, CN
Tipton, KD
Galloway, SDR
Journal name Physiological Reports
Volume number 8
Issue number 16
Article ID e14529
Start page 1
End page 15
Total pages 15
Publisher Wiley
Place of publication Hoboken, NJ
Publication date 2020-08
ISSN 2051-817X
2051-817X
Keyword(s) Science & Technology
Life Sciences & Biomedicine
Physiology
exercise
fish oil
insulin resistance
omega-3
overfeeding
type 2 diabetes
INSULIN-RESISTANCE
SHORT-TERM
DIABETES-MELLITUS
WEIGHT-GAIN
SENSITIVITY
GLUCOSE
HEALTHY
ACIDS
RISK
LIPOPROTEINS
Summary Understanding human physiological responses to high‐fat energy excess (HFEE) may help combat the development of metabolic disease. We aimed to investigate the impact of manipulating the n‐3PUFA content of HFEE diets on whole‐body and skeletal muscle markers of insulin sensitivity. Twenty healthy males were overfed (150% energy, 60% fat, 25% carbohydrate, 15% protein) for 6 d. One group (n = 10) received 10% of fat intake as n‐3PUFA rich fish oil (HF‐FO), and the other group consumed a mix of fats (HF‐C). Oral glucose tolerance tests with stable isotope tracer infusions were conducted before, and following, HFEE, with muscle biopsies obtained in basal and insulin‐stimulated states for measurement of membrane phospholipids, ceramides, mitochondrial enzyme activities, and PKB and AMPKα2 activity. Insulin sensitivity and glucose disposal did not change following HFEE, irrespective of group. Skeletal muscle ceramide content increased following HFEE (8.5 ± 1.2 to 12.1 ± 1.7 nmol/mg, p = .03), irrespective of group. No change in mitochondrial enzyme activity was observed following HFEE, but citrate synthase activity was inversely associated with the increase in the ceramide content (r=−0.52, p = .048). A time by group interaction was observed for PKB activity (p = .003), with increased activity following HFEE in HF‐C (4.5 ± 13.0mU/mg) and decreased activity in HF‐FO (−10.1 ± 20.7 mU/mg) following HFEE. Basal AMPKα2 activity increased in HF‐FO (4.1 ± 0.6 to 5.3 ± 0.7mU/mg, p = .049), but did not change in HF‐C (4.6 ± 0.7 to 3.8 ± 0.9mU/mg) following HFEE. We conclude that early skeletal muscle signaling responses to HFEE appear to be modified by dietary n‐3PUFA content, but the potential impact on future development of metabolic disease needs exploring.
Language eng
DOI 10.14814/phy2.14529
Indigenous content off
Field of Research 0606 Physiology
1103 Clinical Sciences
1116 Medical Physiology
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2020, The Authors
Free to Read? Yes
Use Rights Creative Commons Attribution licence
Persistent URL http://hdl.handle.net/10536/DRO/DU:30143589

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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.