Resolution of glucose intolerance in long-term high-fat, high-sucrose-fed mice
- 1Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, Geelong, Victoria, Australia
- 2Haematopoiesis and Leukocyte Biology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia
- 3Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York, USA
- Correspondence should be addressed to C R Bruce; Email: clinton.bruce{at}deakin.edu.au
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Figure 2
The effect of 42 weeks of high-fat, high-sucrose diet (HFSD) on body mass (A), liver mass (B), heart mass (C), epididymal fat pad (D) and inguinal fat pad (E) mass, glucose tolerance (F and G), plasma insulin (H) and FFA levels (I) during the OGTT, triglyceride content in the liver (J), muscle (K) and heart (L), and glycogen content in liver (M) and muscle (N). Data are mean ± s.e.m. **P < 0.01; **P < 0.001; ****P < 0.0001 vs chow at specified time point. N = 7 for chow; N = 17 for HFSD.
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Figure 3
Comparison of the effects of 22 vs 42 weeks of HFSD or chow feeding on body mass (A, D) and glucose tolerance (B, C, E and F). These data are also presented in Figs 1 and 2. Data are mean ± s.e.m. **P < 0.01; **P < 0.001; ****P < 0.0001 at specified time point. N = 7 for chow; N = 17 for HFSD.
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Figure 4
Body composition (A), blood glucose (B and C), plasma insulin (D), FFAs (E), endogenous glucose levels (F), disposal of 2-[2H]glucose (G and H) and 6,6-[2H]glucose (I and J) and hepatic futile glucose cycling (K) during the stable isotope-labelled OGTT. Data are mean ± s.e.m. **P < 0.01; **P < 0.001; ****P < 0.0001 vs chow at a specified time point. N = 6 for chow; N = 10 for HFSD.
- © 2017 Society for Endocrinology
