Display options
Share it on

Antioxidants (Basel). 2019 Dec 13;8(12). doi: 10.3390/antiox8120643.

Effects of Very Low Calorie Ketogenic Diet on the Orexinergic System, Visceral Adipose Tissue, and ROS Production.

Antioxidants (Basel, Switzerland)

Anna Valenzano, Rita Polito, Valentina Trimigno, Antonella Di Palma, Fiorenzo Moscatelli, Gaetano Corso, Francesco Sessa, Monica Salerno, Angelo Montana, Nunzio Di Nunno, Marinella Astuto, Aurora Daniele, Marco Carotenuto, Giovanni Messina, Giuseppe Cibelli, Vincenzo Monda

Affiliations

  1. Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy.
  2. Department of Medical, Surgical and Advanced Technologies "G.F. Ingrassia", University of Catania, 95123 Catania, Italy.
  3. Department of History, Society and Studies on Humanity, University of Salento, 73100 Lecce, Italy.
  4. Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy.
  5. CEINGE Biotecnologie Avanzate S.C. a r.l., 80131 Napoli, Italy.
  6. Clinic of Child and Adolescent Neuropsychiatry, Department of Mental Health, Physical and Preventive Medicine, Università degli Studi della Campania "Luigi Vanvitelli", 80100 Naples, Italy.
  7. Department of Experimental Medicine, Section of Human Physiology and Unit of Dietetics and Sports Medicine, Università degli Studi della Campania "Luigi Vanvitelli", 80100 Naples, Italy.

PMID: 31847149 PMCID: PMC6943716 DOI: 10.3390/antiox8120643

Abstract

BACKGROUND: Caloric restriction is a valid strategy to reduce the visceral adipose tissue (VAT) content in obese persons. Hypocretin-1 (orexin-A) is a neuropeptide synthesized in the lateral hypothalamus that strongly modulates food intake, thus influencing adipose tissue accumulation. Therapeutic diets in obesity treatment may combine the advantages of caloric restriction and dietary ketosis. The current study aimed to evaluate the effect of a very low calorie ketogenic diet (VLCKD) in a population of obese patients.

METHODS: Adiposity parameters and orexin-A serum profiling were quantified over an 8 week period. The effect of the VLCKD on reactive oxygen species (ROS) production and cell viability was evaluated, in vitro, by culturing Hep-G2 cells in the presence of VLCKD sera.

RESULTS: Dietary intervention induced significant effects on body weight, adiposity, and blood chemistry parameters. Moreover, a selective reduction in VAT was measured by dual-energy X-ray absorptiometry. Orexin-A levels significantly increased after dietary treatment. Hep-G2 cell viability was not affected after 24, 48, and 72 h incubation with patients' sera, before and after the VLCKD. In the same model system, ROS production was not significantly influenced by dietary treatment.

CONCLUSION: The VLCKD exerts a positive effect on VAT decrease, ameliorating adiposity and blood chemistry parameters. Furthermore, short-term mild dietary ketosis does not appear to have a cytotoxic effect, nor does it represent a factor capable of increasing oxidative stress. Finally, to the best of our knowledge, this is the first study that shows an effect of the VLCKD upon the orexinergic system, supporting the usefulness of such a therapeutic intervention in promoting obesity reduction in the individual burden of this disease.

Keywords: VLCK diet; orexin-A; visceral adipose tissue

References

  1. Br J Nutr. 2013 Oct;110(7):1178-87 - PubMed
  2. FASEB J. 2004 Nov;18(14):1657-69 - PubMed
  3. J Transl Med. 2016 Oct 13;14(1):290 - PubMed
  4. J Endocrinol. 2006 Oct;191(1):129-36 - PubMed
  5. J Nutr. 2001 Dec;131(12):3208-11 - PubMed
  6. Ann Intern Med. 2010 Sep 7;153(5):289-98 - PubMed
  7. Am J Physiol Endocrinol Metab. 2010 Nov;299(5):E808-15 - PubMed
  8. Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14960-5 - PubMed
  9. Obes Rev. 2010 Jan;11(1):11-8 - PubMed
  10. Curr Opin Neurol. 2017 Apr;30(2):187-192 - PubMed
  11. Front Physiol. 2018 Jul 24;9:982 - PubMed
  12. Afr Health Sci. 2017 Mar;17(1):99-107 - PubMed
  13. Nutrients. 2019 May 07;11(5):null - PubMed
  14. Obes Res. 2003 Sep;11(9):1147-54 - PubMed
  15. J Clin Invest. 2004 Dec;114(12):1752-61 - PubMed
  16. JAMA. 2003 Aug 20;290(7):912-20 - PubMed
  17. Endocrinol Metab Clin North Am. 2008 Sep;37(3):753-68, x-xi - PubMed
  18. World Health Organ Tech Rep Ser. 2003;916:i-viii, 1-149, backcover - PubMed
  19. Obesity (Silver Spring). 2009 Mar;17(3):439-46 - PubMed
  20. Obesity (Silver Spring). 2012 May;20(5):1109-14 - PubMed
  21. Endocrine. 2016 Dec;54(3):681-690 - PubMed
  22. Diabetes. 2005 Aug;54(8):2277-86 - PubMed
  23. Physiol Behav. 2018 Jun 1;190:71-81 - PubMed
  24. Front Psychol. 2014 Sep 08;5:997 - PubMed
  25. Atherosclerosis. 2014 Mar;233(1):104-12 - PubMed
  26. Eur J Clin Nutr. 2015 Mar;69(3):329-36 - PubMed
  27. Neurochem Res. 2003 Dec;28(12):1793-7 - PubMed
  28. J Cereb Blood Flow Metab. 2008 Dec;28(12):1907-16 - PubMed
  29. Int J Obes Relat Metab Disord. 2002 Feb;26(2):274-6 - PubMed
  30. Front Neurol. 2019 Aug 27;10:932 - PubMed
  31. Pharmacol Rev. 2009 Jun;61(2):162-76 - PubMed
  32. Int J Mol Sci. 2013 Feb 11;14(2):3834-59 - PubMed
  33. Proc Nutr Soc. 2005 May;64(2):163-9 - PubMed
  34. Nutrients. 2017 May 19;9(5):null - PubMed
  35. Cell Metab. 2009 Dec;10(6):466-80 - PubMed
  36. PLoS One. 2017 Jan 13;12(1):e0169908 - PubMed
  37. Obes Rev. 2006 Feb;7(1):49-58 - PubMed
  38. Int J Obes (Lond). 2017 Aug;41(8):1256-1262 - PubMed
  39. Proc Natl Acad Sci U S A. 2008 Aug 19;105(33):11975-80 - PubMed
  40. Front Physiol. 2017 May 31;8:357 - PubMed
  41. J Cereb Blood Flow Metab. 2016 Sep;36(9):1603-13 - PubMed
  42. Front Physiol. 2018 Mar 22;9:261 - PubMed
  43. Obes Rev. 2017 Jul;18(7):715-723 - PubMed
  44. Horm Mol Biol Clin Investig. 2015 Feb;21(2):125-36 - PubMed
  45. J Physiol. 2005 Mar 1;563(Pt 2):569-82 - PubMed

Publication Types