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Effect of neonatal orally administered S-allyl cysteine in high-fructose diet fed Wistar rats

Published online by Cambridge University Press:  20 November 2017

B. W. Lembede ,
K. H. Erlwanger ,
P. Nkomozepi  and
E. Chivandi
B. W. Lembede*
Affiliation:
School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Parktown, Johannesburg, Republic of South Africa
K. H. Erlwanger
Affiliation:
School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Parktown, Johannesburg, Republic of South Africa
P. Nkomozepi
Affiliation:
Department of Human Anatomy and Physiology, Faculty of Health Sciences, University of Johannesburg, Doornfontein, Johannesburg, Republic of South Africa
E. Chivandi
Affiliation:
School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, Parktown, Johannesburg, Republic of South Africa
*
*Address for correspondence: B. W. Lembede, School of Physiology, Faculty of Health Sciences, University of the Witwatersrand, 7 York Road, Parktown, Johannesburg, Republic of South Africa. (Email Busisani.Lembede@wits.ac.za)
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Abstract

S-allyl cysteine (SAC) has antioxidant, antidiabetic and antiobesity properties. We hypothesized that neonatal oral administration of SAC would protect rats against neonatal and adulthood high-fructose diet-induced adverse metabolic outcomes in adulthood. In total, 112 (males=56; females=56), 4-day-old Wistar rat pups were randomly allocated to groups and administered the following treatment regimens daily for 15 days from postnatal day (PND) 6–20: group I – 10 ml/kg distilled water, group II – 10 ml/kg 20% fructose solution (FS), group III – 150 mg/kg SAC and group IV – SAC+FS. On PND 21, the pups were weaned and allowed to grow on a standard rat chow (SRC) until PND 56. The rats from each treatment regimen were then randomly split into two subgroups: one on a SRC and plain drinking water and another on SRC and 20% FS as drinking fluid and then subjected to these treatment regimens for 8 weeks after which they were euthanized and tissues collected for analyzes. Neonatal oral administration of SAC attenuated the neonatal high-fructose diet-induced programming for hepatic lipid accretion in adulthood but not against adulthood high-fructose diet-induced visceral obesity. Neonatal oral administration of SAC programmes for protection against neonatal fructose-induced programming for hepatic lipid accumulation thus could potentially protect against fat-mediated liver derangements in adult life.

Keywords

hepatic lipidhigh-fructose dietneonatalS-allyl cysteinevisceral adiposity
Type
Original Article
Information
Journal of Developmental Origins of Health and Disease , Volume 9 , Issue 2 , April 2018 , pp. 160 - 171
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Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2017 

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References

1. Smith, KB, Smith, MS. Obesity statistics. Prim Care Clin Office Pract. 2016; 43, 121–135.CrossRefGoogle ScholarPubMed
2. Reinehr, T. Metabolic syndrome in children and adolescents: a critical approach considering the interaction between pubertal stage and insulin resistance. Curr Diab Rep. 2016; 16, 8.CrossRefGoogle ScholarPubMed
3. Alisi, A, Nobili, V. Overlapping clinical features between NAFLD and metabolic syndrome in children. EMJ Hepatol. 2014; 1, 55–61.CrossRefGoogle Scholar
4. Pandita, A, Sharma, D, Pandita, D, et al. Childhood obesity: prevention is better than cure. Diabetes Metab Syndr Obes. 2016; 9, 83–89.CrossRefGoogle ScholarPubMed
5. Nomura, K, Yamanouchi, T. The role of fructose-enriched diets in mechanisms of nonalcoholic fatty liver disease. J Nutr Biochem. 2012; 23, 203–208.CrossRefGoogle ScholarPubMed
6. Vickers, MH, Clayton, ZE, Yap, C, Sloboda, DM. Maternal fructose intake during pregnancy and lactation alters placental growth and leads to sex-specific changes in fetal and neonatal endocrine function. Endocrinology. 2011; 152, 1378–1387.CrossRefGoogle ScholarPubMed
7. Laker, RC, Wlodek, ME, Connelly, JJ, Yan, Z. Epigenetic origins of metabolic disease: the impact of the maternal condition to the offspring epigenome and later health consequences. Food Sci Hum Wellness. 2013; 2, 1–11.CrossRefGoogle Scholar
8. Almond, D, Currie, J. Killing Me Softly: the fetal origins hypothesis. J Econ Perspect. 2011; 25, 153–172.CrossRefGoogle ScholarPubMed
9. Tamashiro, KLK, Moran, TH. Perinatal environment and its influences on metabolic programming of offspring. Physiol Behav. 2010; 100, 560–566.CrossRefGoogle ScholarPubMed
10. Stewart, MS, Heerwagen, MJR, Friedman, JE. Developmental programming of pediatric nonalcoholic fatty liver disease: redefining the’first hit. Clin Obstet Gynecol. 2013; 56, 577–590.CrossRefGoogle ScholarPubMed
11. Huynh, M, Luiken, JJJP, Coumans, W, Bell, RC. Dietary fructose during the suckling period increases body weight and fatty acid uptake into skeletal muscle in adult rats. Obesity (Silver Spring). 2008; 16, 1755–1762.CrossRefGoogle ScholarPubMed
12. Chowdhury, S, Lecomte, V, Erlich, J, Maloney, C, Morris, M. Paternal high fat diet in rats leads to renal accumulation of lipid and tubular changes in adult offspring. Nutrients. 2016; 8, 521.CrossRefGoogle ScholarPubMed
13. Chen, W-P, Tang, J-L, Bao, J-P, et al. Effects of diallyl sulphide in chondrocyte and cartilage in experimental osteoarthritis in rabbit. Phytother Res. 2011; 25, 351–356.CrossRefGoogle ScholarPubMed
14. Ching, RHH, Yeung, LOY, Tse, IMY, Sit, W-H, Li, ETS. Supplementation of bitter melon to rats fed a high-fructose diet during gestation and lactation ameliorates fructose-induced dyslipidemia and hepatic oxidative stress in male offspring. J Nutr. 2011; 141, 1664–1672.CrossRefGoogle ScholarPubMed
15. Tanaka, M, Kita, T, Yamasaki, S, et al. Maternal resveratrol intake during lactation attenuates hepatic triglyceride and fatty acid synthesis in adult male rat offspring. Biochem Biophys Rep. 2017; 9, 173–179.Google ScholarPubMed
16. Amagase, H, Petesch, BL, Matsuura, H, et al. Recent advances on the nutritional effects associated with the use of garlic as a supplement. Am Soc Nutr Sci. 2001; 1, 1118–1119.Google Scholar
17. Asdaq, SMB. Antioxidant and hypolipidemic potential of aged garlic extract and its constituent, S-allyl cysteine, in rats. Evid Based Complement Alternat Med. 2015; 2015, 1–7.CrossRefGoogle ScholarPubMed
18. Saravanan, G, Ponmurugan, P. S-allylcysteine improves streptozotocin-induced alterations of blood glucose, liver cytochrome P450 2E1, plasma antioxidant system, and adipocytes hormones in diabetic rats. Int J Endocrinol Metab. 2013; 11, 1–8.CrossRefGoogle ScholarPubMed
19. Loxham, SJG, Teague, J, Poucher, SM, et al. Glucagon challenge in the rat: a robust method for the in vivo assessment of Glycogen phosphorlyase inhibitor efficacy. J Pharmacol Toxicol Methods. 2007; 55, 71–77.CrossRefGoogle Scholar
20. Sakaguchi, K, Hirota, Y, Hashimoto, N, et al. A minimally invasive system for glucose area under the curve measurement using interstitial fluid extraction technology: evaluation of the accuracy and usefulness with oral glucose tolerance tests in subjects with and without diabetes. Diabetes Technol Ther. 2012; 14, 485–491.CrossRefGoogle ScholarPubMed
21. Matthews, DR, Hosker, JR, Rudenski, AS, et al. Homeostasis model assessment: insulin resistance and fl-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985; 28, 412–419.CrossRefGoogle Scholar
22. Reyes-Gordillo, K, Segovia, J, Shibayama, M, et al. Curcumin protects against acute liver damage in the rat by inhibiting NF-κB, proinflammatory cytokines production and oxidative stress. Biochim Biophys Acta Gen Subj. 2007; 1770, 989–996.CrossRefGoogle ScholarPubMed
23. Kleiner, DE, Brunt, EM, Van Natta, M, et al. Design and validation of a histological scoring system for nonalcoholic fatty liver disease. Hepatology. 2005; 41, 1313–1321.CrossRefGoogle ScholarPubMed
24. AOAC International. Official Methods of Analysis of AOAC International, 18th edn (ed. Horwitz WLG), 2005. AOAC International: Gaithersburg, MD.Google Scholar
25. Liu, X, Xue, R, Ji, L, et al. Activation of farnesoid X receptor (FXR) protects against fructose-induced liver steatosis via inflammatory inhibition and ADRP reduction. Biochem Biophys Res Commun. 2014; 450, 117–123.CrossRefGoogle ScholarPubMed
26. Ferreira de Moura, R, Ribeiro, C, Aparecida de Oliveira, J, Stevanato, E, Rostom de Mello, MA. Metabolic syndrome signs in Wistar rats submitted to different high-fructose ingestion protocols. Br J Nutr. 2009; 101, 1178–1184.CrossRefGoogle Scholar
27. Sanchez-Lozada, LG, Tapia, E, Jimenez, A, et al. Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats. Am J Physiol Renal Physiol. 2006; 292, f423–f429.CrossRefGoogle ScholarPubMed
28. Clayton, ZE, Vickers, MH, Bernal, A, Yap, C, Sloboda, DM. Early life exposure to fructose alters maternal, fetal and neonatal hepatic gene expression and leads to sex-dependent changes in lipid metabolism in rat offspring. PLoS One. 2015; 10, e0141962.CrossRefGoogle ScholarPubMed
29. Kadowaki, T. Adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome. J Clin Invest. 2006; 116, 1784–1792.CrossRefGoogle ScholarPubMed
30. Kim, S, Kwon, H, Park, J-H, et al. A low level of serum total testosterone is independently associated with nonalcoholic fatty liver disease. BMC Gastroenterol. 2012; 12, 69.CrossRefGoogle ScholarPubMed
31. Carulli, L, Lonardo, A, Lombardini, S, Marchesini, G, Loria, P. Gender, fatty liver and GGT. Hepatology. 2006; 44, 278–279.CrossRefGoogle ScholarPubMed
32. Sakuma, Y. Gonadal steroid action and brain sex differentiation in the rat. J Neuroendocrinol. 2009; 21, 410–414.CrossRefGoogle ScholarPubMed
33. Viveros, MP, Llorente, R, López-Gallardo, M, et al. Sex-dependent alterations in response to maternal deprivation in rats. Psychoneuroendocrinology. 2009; 34, S217–S226.CrossRefGoogle ScholarPubMed
34. Tandra, S, Yeh, MM, Brunt, EM, et al. Presence and significance of microvesicular steatosis in nonalcoholic fatty liver disease. J Hepatol. 2011; 55, 654–659.CrossRefGoogle ScholarPubMed
35. Rabinowich, L, Shibolet, O. Drug induced steatohepatitis: an uncommon culprit of a common disease. Biomed Res Int. 2015; 2015, 168905.CrossRefGoogle ScholarPubMed
36. Gaggini, M, Morelli, M, Buzzigoli, E, et al. Non-alcoholic fatty liver disease (NAFLD) and its connection with insulin resistance, dyslipidemia, atherosclerosis and coronary heart disease. Nutrients. 2013; 5, 1544–1560.CrossRefGoogle ScholarPubMed
37. Esser, N, Legrand-Poels, S, Piette, J, Scheen, AJ, Paquot, N. Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes. Diabetes Res Clin Pract. 2014; 105, 141–150.CrossRefGoogle ScholarPubMed
38. DeBoer, MD. Obesity, systemic inflammation, and increased risk for cardiovascular disease and diabetes among adolescents: a need for screening tools to target interventions. Nutrition. 2013; 29, 379–386.CrossRefGoogle ScholarPubMed
39. Katib, A. Mechanisms linking obesity with male infertility. Cent Eur J Urol. 2015; 68, 437–447.CrossRefGoogle ScholarPubMed
40. El-Wakf, AM, Hassan, HA, Mahmoud, AZ, Habza, MN. Fenugreek potent activity against nitrate-induced diabetes in young and adult male rats. Cytotechnology. 2015; 67, 437–447.CrossRefGoogle Scholar
41. Pektaş, MB, Sadi, G, Akar, F. Long-term dietary fructose causes gender-different metabolic and vascular dysfunction in rats: modulatory effects of resveratrol. Cell Physiol Biochem. 2015; 37, 1407–1420.CrossRefGoogle ScholarPubMed
42. Tran, LT, Yuen, VG, McNeill, JH. The fructose-fed rat: a review on the mechanisms of fructose-induced insulin resistance and hypertension. Mol Cell Biochem. 2009; 332, 145–159.CrossRefGoogle Scholar
43. Horst, KW. Fructose consumption, lipogenesis, and non-alcoholic fatty liver disease. Nutrients. 2017; 9, 981.CrossRefGoogle ScholarPubMed
44. Vos, MB, Lavine, JE. Dietary fructose in nonalcoholic fatty liver disease. Hepatology. 2013; 57, 2525–2531.CrossRefGoogle ScholarPubMed
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