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Surplus fat rapidly increases fat oxidation and insulin resistance in lipodystrophic mice

Girousse, Amandine, Virtue, Samuel, Hart, Dan, Vidal-Puig, Antonio, Murgatroyd, Peter R., Mouisel, Etienne, Sengenès, Coralie, Savage, David B.·2018·Molecular Metabolism
DOI 10.1016/j.molmet.2018.05.006PMC PMC6026316
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Figure 1 Energetic response to acute high fat feeding in lipodystrophic (AZIP) mice. (A) 24 h macronutrient (protein (Prot), carbohydrate (CHO), fat (Fat)) specific – and total energy intake and disposal in wild type (WT) littermates and AZIP lipodystrophic mice fed either a low fat chow diet (LFD) or after acutely switching from a LFD to a high fat diet (HFD). The estimated (based on measured blood triglycerides (TG) and estimated circulation volume) energy contained in circulating TGs is included in the AZIP data. This measurement is negligible in WT mice. The graph presents the average of the second 24 h period for each diet. (B) Continuous respiratory quotient (RQ) curves assessed by indirect calorimetry in a thermoneutral environment. Arrows represent the daily opening of the calorimetry chambers for animal/food/water weighing. Grey columns represent dark (night-time) periods. (C) Respiratory quotient averages over the second 24 h period. (D) Changes in respiratory quotient, represented as a delta between the LFD and HFD values. (E) Changes in body weight, measured as a delta between the LFD and HFD. (F) Insulin tolerance tests (ITT) performed after a 5 h fast in WT and AZIP mice maintained on a chow (ND) or high fat diet (HFD). Blood glucose concentrations are shown at baseline and following an insulin injection (0.5 U/kg). (G) Area under the curve representation of the data in (F). WT n = 10–14, AZIP n = 8–14; except for ITT data where n = 4–6; AZIP, red bars/squares, WT, black bars/squares. *p < 0.05, **p < 0.01, ***p < 0.001 (2-ways ANOVA and t-test).
Figure 1 Energetic response to acute high fat feeding in lipodystrophic (AZIP) mice. (A) 24 h macronutrient (protein (Prot), carbohydrate (CHO), fat (Fat)) specific – and total energy intake and disposal in wild type (WT) littermates and AZIP lipodystrophic mice fed either a low fat chow diet (LFD) or after acutely switching from a LFD to a high fat diet (HFD). The estimated (based on measured blood triglycerides (TG) and estimated circulation volume) energy contained in circulating TGs is included in the AZIP data. This measurement is negligible in WT mice. The graph presents the average of the second 24 h period for each diet. (B) Continuous respiratory quotient (RQ) curves assessed by indirect calorimetry in a thermoneutral environment. Arrows represent the daily opening of the calorimetry chambers for animal/food/water weighing. Grey columns represent dark (night-time) periods. (C) Respiratory quotient averages over the second 24 h period. (D) Changes in respiratory quotient, represented as a delta between the LFD and HFD values. (E) Changes in body weight, measured as a delta between the LFD and HFD. (F) Insulin tolerance tests (ITT) performed after a 5 h fast in WT and AZIP mice maintained on a chow (ND) or high fat diet (HFD). Blood glucose concentrations are shown at baseline and following an insulin injection (0.5 U/kg). (G) Area under the curve representation of the data in (F). WT n = 10–14, AZIP n = 8–14; except for ITT data where n = 4–6; AZIP, red bars/squares, WT, black bars/squares. *p < 0.05, **p < 0.01, ***p < 0.001 (2-ways ANOVA and t-test).CC BY · PubMed Central
Figure 2 Tissue specific fat disposal in lipodystrophic (AZIP) mice fed with HFD for 48 h. (A-D-G) Ex vivo palmitate oxidation measured in Soleus muscle (A), Extensor digitorum longus (EDL) muscle (D) and liver (G) in the presence or absence of a CPT1 (carnitine palmitoyltransferase 1) inhibitor, Etomoxir. Hatched and solid parts respectively represent complete and incomplete oxidation. (B-E-H) Microarray-based heat maps of mRNA gene expression of Soleus (B), EDL (E) and liver (H) from WT and AZIP mice fed a HFD. The log ratios illustrate relative expression levels of genes involved in the fatty acid oxidation pathway. (C-F-I) Quantitative real-time PCR (qPCR) analysis of genes involved in fatty acid oxidation in the Soleus (C), EDL (F) and liver (I) of WT and AZIP mice fed with a HFD. (J) Triglyceride and glycogen quantification in the liver of WT and Azip animals fed a LFD or HFD for 48 h, measurements done in the fed state. WT, black bars n = 4–6; AZIP, red bars n = 4–6. *p < 0.05, **p < 0.01, ***p < 0.001 (2-ways ANOVA and t-test).
Figure 2 Tissue specific fat disposal in lipodystrophic (AZIP) mice fed with HFD for 48 h. (A-D-G) Ex vivo palmitate oxidation measured in Soleus muscle (A), Extensor digitorum longus (EDL) muscle (D) and liver (G) in the presence or absence of a CPT1 (carnitine palmitoyltransferase 1) inhibitor, Etomoxir. Hatched and solid parts respectively represent complete and incomplete oxidation. (B-E-H) Microarray-based heat maps of mRNA gene expression of Soleus (B), EDL (E) and liver (H) from WT and AZIP mice fed a HFD. The log ratios illustrate relative expression levels of genes involved in the fatty acid oxidation pathway. (C-F-I) Quantitative real-time PCR (qPCR) analysis of genes involved in fatty acid oxidation in the Soleus (C), EDL (F) and liver (I) of WT and AZIP mice fed with a HFD. (J) Triglyceride and glycogen quantification in the liver of WT and Azip animals fed a LFD or HFD for 48 h, measurements done in the fed state. WT, black bars n = 4–6; AZIP, red bars n = 4–6. *p < 0.05, **p < 0.01, ***p < 0.001 (2-ways ANOVA and t-test).CC BY · PubMed Central

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Citations

Cites

Research works printed but not linked: 13

  1. Shulman, 2000, Cellular mechanisms of insulin resistance, The Journal of Clinical Investigation, 106, 171, 10.1172/JCI10583 · DOI · Paper page
  2. Unger, 2003, Lipid overload and overflow: metabolic trauma and the metabolic syndrome, Trends in Endocrinology and Metabolism, 14, 398, 10.1016/j.tem.2003.09.008 · DOI
  3. Muoio, 2014, Metabolic inflexibility: when mitochondrial indecision leads to metabolic gridlock, Cell, 159, 1253, 10.1016/j.cell.2014.11.034 · DOI · Paper page
  4. Perry, 2014, The role of hepatic lipids in hepatic insulin resistance and type 2 diabetes, Nature, 510, 84, 10.1038/nature13478 · DOI
  5. Virtue, 2008, It's not how fat you are, it's what you do with it that counts, PLoS Biology, 6, e237, 10.1371/journal.pbio.0060237 · DOI
  6. Frayn, 2002, Adipose tissue as a buffer for daily lipid flux, Diabetologia, 45, 1201, 10.1007/s00125-002-0873-y · DOI · Paper page
  7. Garg, 2004, Acquired and inherited lipodystrophies, New England Journal of Medicine, 350, 1220, 10.1056/NEJMra025261 · DOI
  8. Huang-Doran, 2010, Lipodystrophy: metabolic insights from a rare disorder, Journal of Endocrinology, 207, 245, 10.1677/JOE-10-0272 · DOI · Paper page
  9. Moitra, 1998, Life without white fat: a transgenic mouse, Genes & Development, 12, 3168, 10.1101/gad.12.20.3168 · DOI
  10. Savage, 2009, Mouse models of inherited lipodystrophy, Disease Models & Mechanisms, 2, 554, 10.1242/dmm.002907 · DOI
  11. Randle, 1966, Carbohydrate metabolism and lipid storage and breakdown in diabetes, Diabetologia, 2, 237, 10.1007/BF01268180 · DOI
  12. Randle, 1963, The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus, The Lancet, 1, 785, 10.1016/S0140-6736(63)91500-9 · DOI · Paper page
  13. Boden, 2002, Free fatty acids in obesity and type 2 diabetes: defining their role in the development of insulin resistance and beta-cell dysfunction, European Journal of Clinical Investigation, 32, 14, 10.1046/j.1365-2362.32.s3.3.x · DOI · Paper page

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Metadata

Authors
Girousse, A., Virtue, S., Hart, D., Vidal-Puig, A., Murgatroyd, P. R., Mouisel, E., Sengenès, C., & Savage, D. B.
Venue
Molecular Metabolism
Publisher
Elsevier BV
Published
2018-07
Volume
13
Pages
24-29
ISSN
2212-8778
DOI
10.1016/j.molmet.2018.05.006
PMC
PMC6026316
Cited by
26
References
2
Language
en
Licence
Funders
Wellcome Trust (DBS 107064)

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