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Adipocyte. 2015 Jul 15;5(1):11-21. doi: 10.1080/21623945.2015.1061723. eCollection 2016.

High-fat diet-induced obesity Rat model: a comparison between Wistar and Sprague-Dawley Rat.

Adipocyte

Cláudia Marques, Manuela Meireles, Sónia Norberto, Joana Leite, Joana Freitas, Diogo Pestana, Ana Faria, Conceição Calhau

Affiliations

  1. Departamento de Bioquímica; Faculdade de Medicina; Universidade do Porto; Porto, Portugal; CINTESIS; Centro de Investigação em Tecnologias e Sistemas de Informação em Saúde; Porto, Portugal.
  2. Departamento de Bioquímica; Faculdade de Medicina; Universidade do Porto ; Porto, Portugal.
  3. Departamento de Bioquímica; Faculdade de Medicina; Universidade do Porto; Porto, Portugal; Universidade de Trás-os-Montes e Alto Douro; Vila Real, Portugal.
  4. Departamento de Bioquímica; Faculdade de Medicina; Universidade do Porto; Porto, Portugal; Faculdade de Ciências da Nutrição e da Alimentação; Universidade do Porto; Porto, Portugal; Faculdade de Ciências; Universidade do Porto; Porto, Portugal.

PMID: 27144092 PMCID: PMC4836488 DOI: 10.1080/21623945.2015.1061723

Abstract

In the past decades, obesity and associated metabolic complications have reached epidemic proportions. For the study of these pathologies, a number of animal models have been developed. However, a direct comparison between Wistar and Sprague-Dawley (SD) Rat as models of high-fat (HF) diet-induced obesity has not been adequately evaluated so far. Wistar and SD rats were assigned for 2 experimental groups for 17 weeks: standard (St) and high-fat (HF) diet groups. To assess some of the features of the metabolic syndrome, oral glucose tolerance tests, systolic blood pressure measurements and blood biochemical analysis were performed throughout the study. The gut microbiota composition of the animals of each group was evaluated at the end of the study by real-time PCR. HF diet increased weight gain, body fat mass, mesenteric adipocyte's size, adiponectin and leptin plasma levels and decreased oral glucose tolerance in both Wistar and SD rats. However, the majority of these effects were more pronounced or earlier detected in Wistar rats. The gut microbiota of SD rats was less abundant in Bacteroides and Prevotella but richer in Bifidobacterium and Lactobacillus comparatively to the gut microbiota of Wistar rats. Nevertheless, the modulation of the gut microbiota by HF diet was similar in both strains, except for Clostridium leptum that was only reduced in Wistar rats fed with HF diet. In conclusion, both Wistar and SD Rat can be used as models of HF diet-induced obesity although the metabolic effects caused by HF diet seemed to be more pronounced in Wistar Rat. Differences in the gut microbial ecology may account for the worsened metabolic scenario observed in Wistar Rat.

Keywords: animal models; diet-induced obesity; high-fat diet; metabolic syndrome; microbiota; obesity

References

  1. J Proteome Res. 2007 Apr;6(4):1364-70 - PubMed
  2. Microbiol Res. 2008;163(6):663-70 - PubMed
  3. Rev Endocr Metab Disord. 2014 Jun;15(2):157-67 - PubMed
  4. Lancet. 2005 Apr 16-22;365(9468):1415-28 - PubMed
  5. Obes Rev. 2007 Jan;8(1):21-34 - PubMed
  6. Mol Nutr Food Res. 2014 Jul;58(7):1513-8 - PubMed
  7. Appl Environ Microbiol. 2002 Nov;68(11):5445-51 - PubMed
  8. Diabetes. 2002 Mar;51(3):662-8 - PubMed
  9. Am J Physiol Renal Physiol. 2003 Oct;285(4):F619-28 - PubMed
  10. FASEB J. 2005 Jan;19(1):136-8 - PubMed
  11. Obesity (Silver Spring). 2009 Nov;17(11):1994-2002 - PubMed
  12. Future Microbiol. 2012 Jan;7(1):91-109 - PubMed
  13. Appl Environ Microbiol. 2004 Dec;70(12):7220-8 - PubMed
  14. Obesity (Silver Spring). 2013 Dec;21(12):E607-15 - PubMed
  15. Gut. 2013 Aug;62(8):1112-21 - PubMed
  16. Nahrung. 1978;22(1):85-8 - PubMed
  17. Lab Anim. 1998 Jan;32(1):65-71 - PubMed
  18. Clin Exp Hypertens. 2006 Jan;28(1):57-72 - PubMed
  19. PLoS One. 2014 Jan 24;9(1):e86117 - PubMed
  20. J Biomed Biotechnol. 2011;2011:351982 - PubMed
  21. J Appl Microbiol. 2004;97(6):1166-77 - PubMed
  22. Obesity (Silver Spring). 2014 Mar;22(3):763-71 - PubMed
  23. J Cardiovasc Pharmacol. 2011 May;57(5):611-24 - PubMed
  24. Circulation. 2009 Oct 20;120(16):1640-5 - PubMed
  25. Am J Physiol Endocrinol Metab. 2009 Nov;297(5):E1023-9 - PubMed
  26. Diabetes. 2008 Jun;57(6):1470-81 - PubMed
  27. Inflammation. 1986 Mar;10(1):59-66 - PubMed
  28. Nat Med. 1995 Dec;1(12):1311-4 - PubMed
  29. Obesity (Silver Spring). 2007 Apr;15(4):798-808 - PubMed
  30. Gut Microbes. 2012 May-Jun;3(3):186-202 - PubMed
  31. Nat Rev Endocrinol. 2013 Jan;9(1):13-27 - PubMed
  32. Lancet. 2014 Aug 30;384(9945):766-81 - PubMed
  33. Clin Nutr. 2013 Dec;32(6):1017-22 - PubMed
  34. Gut Pathog. 2013 Apr 30;5(1):10 - PubMed
  35. J Obes. 2011;2011:null - PubMed
  36. Diabetes. 1996 Jul;45(7):984-7 - PubMed
  37. Hypertension. 2000 Apr;35(4):1009-15 - PubMed
  38. Diabetes Metab Res Rev. 2010 May;26(4):306-18 - PubMed
  39. Acta Pharmacol Sin. 2012 Feb;33(2):173-81 - PubMed
  40. Diabetes. 2007 Jul;56(7):1761-72 - PubMed
  41. PLoS One. 2013 May 28;8(5):e65465 - PubMed
  42. Mol Metab. 2014 Jun 27;3(6):595-607 - PubMed

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