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Caminhotto RO, Komino ACM, de Fatima Silva F, et al. Oral β-hydroxybutyrate increases ketonemia, decreases visceral adipocyte volume and improves serum lipid profile in Wistar rats. Nutr Metab (Lond). 2017;14:31doi: 10.1186/s12986-017-0184-4.
Caminhotto, R. O., Komino, A. C. M., de Fatima Silva, F., Andreotti, S., Sertié, R. A. L., Boltes Reis, G., & Lima, F. B. (2017). Oral β-hydroxybutyrate increases ketonemia, decreases visceral adipocyte volume and improves serum lipid profile in Wistar rats. Nutrition & metabolism, 1431. https://doi.org/10.1186/s12986-017-0184-4
Caminhotto, Rennan de Oliveira, et al. "Oral β-hydroxybutyrate increases ketonemia, decreases visceral adipocyte volume and improves serum lipid profile in Wistar rats." Nutrition & metabolism vol. 14 (2017): 31. doi: https://doi.org/10.1186/s12986-017-0184-4
Caminhotto RO, Komino ACM, de Fatima Silva F, Andreotti S, Sertié RAL, Boltes Reis G, Lima FB. Oral β-hydroxybutyrate increases ketonemia, decreases visceral adipocyte volume and improves serum lipid profile in Wistar rats. Nutr Metab (Lond). 2017 Apr 24;14:31. doi: 10.1186/s12986-017-0184-4. eCollection 2017. PMID: 28450882; PMCID: PMC5404327.
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Nutr Metab (Lond). 2017 Apr 24;14:31. doi: 10.1186/s12986-017-0184-4. eCollection 2017.

Oral β-hydroxybutyrate increases ketonemia, decreases visceral adipocyte volume and improves serum lipid profile in Wistar rats.

Nutrition & metabolism

Rennan de Oliveira Caminhotto, Ayumi Cristina Medeiros Komino, Flaviane de Fatima Silva, Sandra Andreotti, Rogério Antônio Laurato Sertié, Gabriela Boltes Reis, Fabio Bessa Lima

Affiliations

  1. Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Av. Prof. Lineu Prestes 1524 - Ed. Biomédicas I sala 131, Butantã, 05508-900 São Paulo Brazil.

PMID: 28450882 PMCID: PMC5404327 DOI: 10.1186/s12986-017-0184-4

Abstract

BACKGROUND: Ketosis can be induced in humans and in animals by fasting or dietary interventions, such as ketogenic diets. However, the increasing interest on the ketogenic state has motivated the development of alternative approaches to rapidly increase ketonemia using less drastic interventions. Here, it was tested whether oral intake of a β-hydroxybutyrate (βHB) mineral salt mixture could increase ketonemia in Wistar rats without any other dietary changes, thereby being a useful model to study ketones effects alone on metabolism.

METHODS: βHB salts were orally administered to provoke elevation in the ketonemia. Effects of this intervention were tested acutely (by gavage) and chronically (4 weeks in drinking water). Acutely, a concomitant glucose overload was used to suppress endogenous ketogenesis and verify whether βHB salts were really absorbed or not. Long-term administration allowed to weekly evaluate the impact on ketonemia, blood glucose and, after 4 weeks, on body weight, visceral fat mass, lipid blood profile, serum lipolysis products and adiponectinemia.

RESULTS: βHB salts increased ketonemia in acute and long-term administrations, improved blood lipid profile by raising HDL-cholesterol concentration and decreasing LDL/HDL ratio, while reduced visceral adipocyte volume. Mean ketonemia correlated positively with HDLc and negatively with adipocyte volume and serum lipolysis products.

CONCLUSIONS: Oral βHB can rapidly increase ketonemia and, therefore, be used as an acute and long-term animal model of ketosis. Long-term treatment points to important beneficial effects of ketone bodies in serum lipid concentrations and visceral fat mass. These results may help to explain the metabolic adaptations following ketogenic diets, such as a better body fat control and a serum lipid profile improvement.

Keywords: Experimental models; HDL-cholesterol; Ketosis; Visceral fat; β-hydroxybutyrate salts

References

  1. Obesity (Silver Spring). 2009 Jul;17(7):1326-31 - PubMed
  2. Lancet. 2003 Apr 26;361(9367):1433-5 - PubMed
  3. Adipocyte. 2013 Oct 1;2(4):217-26 - PubMed
  4. JAMA. 2007 Mar 7;297(9):969-77 - PubMed
  5. Pediatr Res. 2015 Jan;77(1-1):91-8 - PubMed
  6. J Pediatr Endocrinol Metab. 2012;25(7-8):697-704 - PubMed
  7. Am J Cardiol. 2008 Apr 17;101(8A):20B-26B - PubMed
  8. N Engl J Med. 2003 May 22;348(21):2082-90 - PubMed
  9. Obesity (Silver Spring). 2007 Dec;15(12):2875-88 - PubMed
  10. Am J Physiol. 1984 Dec;247(6 Pt 1):E756-64 - PubMed
  11. Nutrition. 2012 Oct;28(10):1016-21 - PubMed
  12. Am J Physiol. 1971 Sep;221(3):850-8 - PubMed
  13. Br J Nutr. 2013 Oct;110(7):1178-87 - PubMed
  14. Am J Physiol Cell Physiol. 2010 Apr;298(4):C961-71 - PubMed
  15. Braz J Med Biol Res. 2014 Feb;47(3):192-205 - PubMed
  16. J Clin Invest. 2004 Jun;113(11):1582-8 - PubMed
  17. Obes Res. 2005 Apr;13(4):703-9 - PubMed
  18. Am J Physiol Endocrinol Metab. 2009 Mar;296(3):E549-58 - PubMed
  19. PLoS Biol. 2013;11(2):e1001485 - PubMed
  20. Nutr Metab (Lond). 2016 Feb 04;13:9 - PubMed
  21. Diabetologia. 2000 Dec;43(12):1498-506 - PubMed
  22. J Biol Chem. 2005 Jul 22;280(29):26649-52 - PubMed
  23. Front Mol Neurosci. 2016 Dec 06;9:137 - PubMed
  24. Extrem Physiol Med. 2014 Oct 29;3:17 - PubMed
  25. FASEB J. 2012 Jun;26(6):2351-62 - PubMed
  26. Am J Physiol Endocrinol Metab. 2007 Jun;292(6):E1724-39 - PubMed
  27. J Intern Med. 2005 Aug;258(2):94-114 - PubMed
  28. Pediatr Res. 2002 Aug;52(2):301-6 - PubMed
  29. J Biol Chem. 1964 Feb;239:375-80 - PubMed
  30. Physiol Rev. 2013 Jan;93(1):359-404 - PubMed

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