Journal
JOURNAL OF PHYSIOLOGY-LONDON
Volume 597, Issue 1, Pages 121-136Publisher
WILEY
DOI: 10.1113/JP276386
Keywords
Exercise; Fetal Programming; Skeletal muscle; Insulin release; Mitochondria; High fat diet; Pancreas
Categories
Funding
- Australian Collaborative Research Network (CRN)
- Australian Institute for Musculoskeletal Science (AIMSS)
- International Postgraduate Research Scholarship (2013-2016)
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A paternal high-fat diet (HFD) impairs female rat offspring glucose tolerance, pancreatic morphology and insulin secretion. We examined whether only 4 weeks of exercise early in life could reprogram these negative effects. Male Sprague-Dawley rats consumed a HFD for 10 weeks before mating with chow-fed dams. Female offspring remained sedentary or performed moderate intensity treadmill exercise (5 days week(-1), 60 min day(-1), 20 m min(-1)) from 5 to 9 weeks of age. Paternal HFD impaired (P < 0.05) adult offspring whole body insulin sensitivity (i.p. insulin sensitivity test), as well as skeletal muscle ex vivo insulin sensitivity and TBC1D4 phosphorylation. It also lowered beta-cell mass and reduced in vivo insulin secretion in response to an i.p. glucose tolerance test. Early-life exercise in offspring reprogrammed the negative effects of a paternal HFD on whole body insulin sensitivity, skeletal muscle ex vivo insulin-stimulated glucose uptake and TBC1D4 phosphorylation and also increased glucose transporter 4 protein. However, early exercise did not normalize the reduced pancreatic beta-cell mass or insulin secretion. In conclusion, only 4 weeks of exercise early in life in female rat offspring reprograms reductions in insulin sensitivity in adulthood caused by a paternal HFD without affecting pancreatic beta-cell mass or insulin secretion.
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