Display options
Share it on

Sci Pharm. 2017 Mar 20;85(1). doi: 10.3390/scipharm85010013.

Dehydroepiandrosterone (DHEA) Feeding Protects Liver Steatosis in Obese Breast Cancer Rat Model.

Scientia pharmaceutica

Reza Hakkak, Andrea Bell, Soheila Korourian

Affiliations

  1. Department of Dietetics and Nutrition, 4301 W. Markham St., Mail Slot 627, Little Rock, AR 72205, USA. [email protected].
  2. Pediatrics, University of Arkansas for Medical Sciences, 4301 W. Markham St., Little Rock, AR 72205, USA. [email protected].
  3. Arkansas Children's Research Institute, 13 Children's Way, Little Rock, AR 72202, USA. [email protected].
  4. Department of Dietetics and Nutrition, 4301 W. Markham St., Mail Slot 627, Little Rock, AR 72205, USA. [email protected].
  5. Department of Pathology, University of Arkansas for Medical Sciences, W. Markham St., Little Rock, AR 72205, USA. [email protected].

PMID: 28335515 PMCID: PMC5388150 DOI: 10.3390/scipharm85010013

Abstract

Obesity is a major health problem in the US and globally. Obesity is associated with the risk of cardiovascular disease, type 2 diabetes, cancers, hyperlipidemia, and liver steatosis development. Dehydroepiandrosterone (DHEA) is a dietary supplement used as an anti-obesity supplement. Previously, we reported that DHEA feeding protects 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary tumors. The objectives of this study were to investigate the effects of obesity and DHEA feeding on liver steatosis, body weight gain, and serum DHEA, DHEA sulfate (DHEA-S), insulin-like growth factor-1 (IGF-1), and insulin-like growth factor binding protein-3 (IGFBP-3) levels. Female Zucker rats were randomly assigned to either a control diet or a control diet with DHEA supplementation for 155 days. Livers were collected for histological examination. Serum was collected to measure DHEA, DHEA-S, IGF-1, and IGFBP-3. Our results show that DHEA-fed rats had significantly less liver steatosis (

Keywords: DHEA; liver steatosis; obesity; weight loss

References

  1. Lipids. 2000 Jun;35(6):613-20 - PubMed
  2. Am J Epidemiol. 2013 Jul 1;178(1):38-45 - PubMed
  3. Am J Physiol. 1984 Feb;246(2 Pt 1):E123-8 - PubMed
  4. J Gastroenterol Hepatol. 2014 Mar;29(3):589-96 - PubMed
  5. Hypertension. 2012 Mar;59(3):680-93 - PubMed
  6. Genes Nutr. 2012 Oct;7(4):549-58 - PubMed
  7. Toxicol Sci. 1999 Jan;47(1):110-7 - PubMed
  8. Oncol Lett. 2011 Jan;2(1):29-36 - PubMed
  9. J Gerontol A Biol Sci Med Sci. 1998 Jan;53(1):B19-24 - PubMed
  10. Int J Obes. 1986;10(3):193-204 - PubMed
  11. J Clin Endocrinol Metab. 2011 Oct;96(10 ):E1640-4 - PubMed
  12. Int J Obes Relat Metab Disord. 1993 Nov;17(11):643-9 - PubMed
  13. Clin Liver Dis. 2007 Feb;11(1):1-16, vii - PubMed
  14. JAMA. 2003 Jan 1;289(1):76-9 - PubMed
  15. Am J Clin Nutr. 2009 Feb;89(2):663S-7S - PubMed
  16. Biochem Biophys Res Commun. 2000 Oct 22;277(2):361-7 - PubMed
  17. Toxicol Sci. 2006 Oct;93(2):348-56 - PubMed
  18. J Clin Endocrinol Metab. 1988 Jan;66(1):57-61 - PubMed
  19. Int J Mol Sci. 2014 Apr 11;15(4):6184-223 - PubMed
  20. Hepatology. 2004 Dec;40(6):1387-95 - PubMed
  21. JAMA. 2014 Feb 26;311(8):806-14 - PubMed
  22. Endocrinology. 1997 Mar;138(3):1066-71 - PubMed
  23. Biochem Pharmacol. 1999 Sep 15;58(6):925-33 - PubMed
  24. Oncol Rep. 2010 Aug;24(2):357-62 - PubMed
  25. J Clin Endocrinol Metab. 1996 Jan;81(1):59-64 - PubMed
  26. J Med Food. 2015 Nov;18(11):1274-80 - PubMed
  27. Metabolism. 1994 May;43(5):599-603 - PubMed
  28. J Hepatol. 2008 Oct;49(4):608-12 - PubMed
  29. Am J Physiol. 1997 Nov;273(5 Pt 2):R1704-8 - PubMed

Publication Types