POSTER PRESENTATION Open Access Metabolic defects induced by high-fat feeding in mice are rapidly reversed by a low-fat diet Nigel Turner * , Simon J Leslie, Nicole L Hallahan, Gregory J Cooney From Metabolism, diet and disease Washington, DC, USA. 29-31 May 2012 Background It is well established that high-fat feeding increases adiposity and impairs glucose metabolism in mice. The aim of this study was to determine the extent to which these changes are reversible if the high-fat diet (HFD) is removed. Materials and methods C57BI6 mice were fed a low-fat chow diet (LFD) or a HFD (45% calories as fat) for 9 weeks and body compo- sition, glucose tolerance and tissue triglycerides were assessed. A group of fat-fed animals were then switched to a LFD (HFD-LFD) and after 4-5 days their body com- position and glucose tolerance were reassessed. Results Mice fed the HFD displayed a 73% increase (P<0.01) in whole-body fat mass, an 80% elevation (P<0.01) in muscle and liver triglyceride levels and a substantial impair- ment in glucose tolerance compared to animals fed the LFD (area under curve during GTT: 1166 ± 76 vs. 506 ± 47 mM.min, P<0.001). The switch to a LFD resulted in a transient decrease in total caloric intake, but only a small drop in body weight (31.3 ± 0.8 vs. 30.3 ± 0.5g, pre vs. post, P=0.06). Despite the minimal change in body weight, whole-body fat mass in the HFD-LFD group was reduced almost to the level of LFD controls (12.7% vs. 14.2% by DXA, LFD vs. HFD-LFD). Consistent with the reduction in whole-body adiposity, glucose tolerance (AUC during GTT: 510 ± 49 mM.min) and muscle and liver triglycerides in the HFD-LFD animals were also restored to the level of LFD animals. Intriguingly, a sepa- rate group of mice that were pair-fed HFD to match the drop in caloric intake in the HFD-LFD group, displayed no improvements in glucose tolerance or tissue triglyceride levels. Conclusions Our findings suggest that the metabolic defects induced by high-fat feeding in mice are rapidly reversible if animals are switched to a LFD. Published: 1 June 2012 doi:10.1186/1753-6561-6-S3-P49 Cite this article as: Turner et al.: Metabolic defects induced by high-fat feeding in mice are rapidly reversed by a low-fat diet. BMC Proceedings 2012 6(Suppl 3):P49. Submit your next manuscript to BioMed Central and take full advantage of: • Convenient online submission • Thorough peer review • No space constraints or color ﬁgure charges • Immediate publication on acceptance • Inclusion in PubMed, CAS, Scopus and Google Scholar • Research which is freely available for redistribution Submit your manuscript at www.biomedcentral.com/submit Diabetes & Obesity Research Program, Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, NSW 2010, Australia Turner et al. BMC Proceedings 2012, 6(Suppl 3):P49 http://www.biomedcentral.com/1753-6561/6/S3/P49 © 2012 Turner et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Metabolic defects induced by high-fat feeding in mice are rapidly reversed by a low-fat diet

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Page 1: Metabolic defects induced by high-fat feeding in mice are rapidly reversed by a low-fat diet

POSTER PRESENTATION Open Access

Metabolic defects induced by high-fat feeding inmice are rapidly reversed by a low-fat dietNigel Turner*, Simon J Leslie, Nicole L Hallahan, Gregory J Cooney

From Metabolism, diet and diseaseWashington, DC, USA. 29-31 May 2012

BackgroundIt is well established that high-fat feeding increases adip-osity and impairs glucose metabolism in mice. The aimof this study was to determine the extent to which thesechanges are reversible if the high-fat diet (HFD) isremoved.

Materials and methodsC57BI6 mice were fed a low-fat chow diet (LFD) or aHFD (45% calories as fat) for 9 weeks and body compo-sition, glucose tolerance and tissue triglycerides wereassessed. A group of fat-fed animals were then switchedto a LFD (HFD-LFD) and after 4-5 days their body com-position and glucose tolerance were reassessed.

ResultsMice fed the HFD displayed a 73% increase (P<0.01) inwhole-body fat mass, an 80% elevation (P<0.01) in mus-cle and liver triglyceride levels and a substantial impair-ment in glucose tolerance compared to animals fed theLFD (area under curve during GTT: 1166 ± 76 vs. 506 ±47 mM.min, P<0.001). The switch to a LFD resulted in atransient decrease in total caloric intake, but only a smalldrop in body weight (31.3 ± 0.8 vs. 30.3 ± 0.5g, pre vs.post, P=0.06). Despite the minimal change in bodyweight, whole-body fat mass in the HFD-LFD group wasreduced almost to the level of LFD controls (12.7% vs.14.2% by DXA, LFD vs. HFD-LFD). Consistent with thereduction in whole-body adiposity, glucose tolerance(AUC during GTT: 510 ± 49 mM.min) and muscle andliver triglycerides in the HFD-LFD animals were alsorestored to the level of LFD animals. Intriguingly, a sepa-rate group of mice that were pair-fed HFD to match thedrop in caloric intake in the HFD-LFD group, displayed

no improvements in glucose tolerance or tissue triglycer-ide levels.

ConclusionsOur findings suggest that the metabolic defects inducedby high-fat feeding in mice are rapidly reversible if ani-mals are switched to a LFD.

Published: 1 June 2012

doi:10.1186/1753-6561-6-S3-P49Cite this article as: Turner et al.: Metabolic defects induced by high-fatfeeding in mice are rapidly reversed by a low-fat diet. BMC Proceedings2012 6(Suppl 3):P49.

Submit your next manuscript to BioMed Centraland take full advantage of:

• Convenient online submission

• Thorough peer review

• No space constraints or color figure charges

• Immediate publication on acceptance

• Inclusion in PubMed, CAS, Scopus and Google Scholar

• Research which is freely available for redistribution

Submit your manuscript at www.biomedcentral.com/submitDiabetes & Obesity Research Program, Garvan Institute of Medical Research,

384 Victoria St, Darlinghurst, NSW 2010, Australia

Turner et al. BMC Proceedings 2012, 6(Suppl 3):P49http://www.biomedcentral.com/1753-6561/6/S3/P49

© 2012 Turner et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative CommonsAttribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction inany medium, provided the original work is properly cited.

http://creativecommons.org/licenses/by/2.0