Hostname: page-component-8448b6f56d-sxzjt Total loading time: 0 Render date: 2024-04-18T10:59:56.763Z Has data issue: false hasContentIssue false
  • English
  • Français

The effect of maternal intake of sucrose or high-fructose corn syrup (HFCS)-55 during gestation and lactation on lipogenic gene expression in rat offspring at 3 and 12 weeks of age

Published online by Cambridge University Press:  18 June 2018

H. Kaur ,
C. R. Toop ,
B. S. Muhlhausler  and
S. Gentili
H. Kaur
Affiliation:
School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, Australia
C. R. Toop
Affiliation:
School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, Australia
B. S. Muhlhausler
Affiliation:
School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, Australia Food and Nutrition Research Group, Department of Food and Wine Sciences, School of Agriculture, Food and Wine, The University of Adelaide, Adelaide, Australia. Healthy Mothers, Babies and Children’s Theme, South Australian Health and Medical Research Institute, Adelaide, Australia
S. Gentili*
Affiliation:
School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, Australia
*
Address for correspondence: S. Gentili, School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, Australia. E-mail: sheridan.gentili@unisa.edu.au
Get access Rights & Permissions [Opens in a new window]

Abstract

Perinatal exposure to sucrose or high-fructose corn syrup-55 (HFCS-55) in rats has previously been associated with altered hepatic fat content and composition post-weaning, although the effects on hepatic metabolism are unknown. The current study aimed to determine the sex-specific effects of maternal consumption of sucrose or HFCS-55 on the expression of hepatic lipogenic genes in the offspring. Liver samples were collected from offspring of albino Wistar rats provided with ad libitum access to either water (control), 10% sucrose or 10% HFCS-55 solution during pregnancy and lactation at 3 weeks (control n=16, sucrose n=22, HFCS-55 n=16) and 12 weeks (control n=16, sucrose n=10, HFCS-55 n=16) of age. Hepatic expression of the transcription factors such as carbohydrate response element-binding protein, sterol regulatory element-binding protein-1c and downstream genes was determined by quantitative real-time PCR. Sucrose-exposed offspring had higher hepatic SREBP-1c messenger RNA expression compared with control and HFCS-55 groups at both 3 weeks (P=0.01) and 12 weeks (P=0.03) of age. There were no differences in the expression of other hepatic lipogenic genes between groups at either 3 or 12 weeks. Thus, perinatal exposure to sucrose may be more detrimental to offspring hepatic metabolism compared with HFCS-55, independent of sex, and it will be important to evaluate the longer-term effects of perinatal sucrose exposure in future studies.

Keywords

HFCS-55liveroffspringpregnancysucrose
Type
Brief Report
Information
Journal of Developmental Origins of Health and Disease , Volume 9 , Issue 5 , October 2018 , pp. 481 - 486
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2018 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Danaei, G, Finucane, MM, Lu, Y, et al. National, regional, and global trends in fasting plasma glucose and diabetes prevalence since 1980: systematic analysis of health examination surveys and epidemiological studies with 370 country-years and 2.7 million participants. Lancet. 2011; 378, 31–40.Google Scholar
2. World Health Organization. Guideline: Sugars Intake for Adults and Children. 2015. World Health Organization: Geneva.Google Scholar
3. Ma, Y, He, FJ, Yin, Y, Hashem, KM, MacGregor, GA. Gradual reduction of sugar in soft drinks without substitution as a strategy to reduce overweight, obesity, and type 2 diabetes: a modelling study. Lancet Diabetes Endocrinol. 2016; 4, 105–114.Google Scholar
4. Walker, RW, Dumke, KA, Goran, MI. Fructose content in popular beverages made with and without high-fructose corn syrup. Nutrition. 2014; 30, 928–935.Google Scholar
5. Stanhope, KL, Schwarz, JM, Keim, NL, et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. J Clin Invest. 2009; 119, 1322–1334.Google Scholar
6. Bizeau, ME, Pagliassotti, MJ. Hepatic adaptations to sucrose and fructose. Metabolism. 2005; 54, 1189–1201.Google Scholar
7. Mukai, Y, Kumazawa, M, Sato, S. Fructose intake during pregnancy up-regulates the expression of maternal and fetal hepatic sterol regulatory element-binding protein-1c in rats. Endocrine. 2013; 44, 79–86.Google Scholar
8. 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.Google Scholar
9. Miyazaki, M, Dobrzyn, A, Man, WC, et al. Stearoyl-CoA desaturase 1 gene expression is necessary for fructose-mediated induction of lipogenic gene expression by sterol regulatory element-binding protein-1c-dependent and-independent mechanisms. J Biol Chem. 2004; 279, 25164–25171.Google Scholar
10. 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.Google Scholar
11. Kelley, GL, Allan, G, Azhar, S. High dietary fructose induces a hepatic stress response resulting in cholesterol and lipid dysregulation. Endocrinology. 2004; 145, 548–555.Google Scholar
12. Stanhope, KL, Schwarz, J-M, Havel, PJ. Adverse metabolic effects of dietary fructose: results from recent epidemiological, clinical, and mechanistic studies. Curr Opin Lipidol. 2013; 24, 198–206.Google Scholar
13. Bray, GA. Energy and fructose from beverages sweetened with sugar or high-fructose corn syrup pose a health risk for some people. Adv Nutr. 2013; 4, 220–225.Google Scholar
14. Alzamendi, A, Castrogiovanni, D, Gaillard, RC, Spinedi, E, Giovambattista, As. Increased male offspring’s risk of metabolic-neuroendocrine dysfunction and overweight after fructose-rich diet intake by the lactating mother. Endocrinology. 2010; 151, 4214–4223.Google Scholar
15. Toop, C, Muhlhausler, B, O’Dea, K, Gentili, S. Consumption of sucrose, but not high fructose corn syrup, leads to increased adiposity and dyslipidaemia in the pregnant and lactating rat. J Dev Orig Health Dis. 2015; 6, 38–46.Google Scholar
16. Toop, CR, Muhlhausler, BS, O’Dea, K, Gentili, S. Impact of perinatal exposure to sucrose or high fructose corn syrup (HFCS-55) on adiposity and hepatic lipid composition in rat offspring. J Physiol. 2017; 595, 4379–4398.Google Scholar
17. Folch, J, Lees, M, Sloane Stanley, G. A simple method for the isolation and purification of total lipids from animal tissues. J Biol Chem. 1957; 226, 497–509.Google Scholar
18. Priego, T, Sánchez, J, Picó, C, Palou, A. Sex‐differential expression of metabolism‐related genes in response to a high‐fat diet. Obesity. 2008; 16, 819–826.Google Scholar
19. Sanchez, J, Palou, A, Pico, C. Response to carbohydrate and fat refeeding in the expression of genes involved in nutrient partitioning and metabolism: striking effects on fibroblast growth factor-21 induction. Endocrinology. 2009; 150, 5341–5350.Google Scholar
20. Liu, F, Xie, M, Chen, D, Li, J, Ding, W. Effect of (dipic-Cl) on lipid metabolism disorders in the liver of STZ-Induced diabetic rats. J Diabetes Res. 2013; 2013, 956737.Google Scholar
21. Gugusheff, J, Sim, P, Kheng, A, et al. The effect of maternal and post-weaning low and high glycaemic index diets on glucose tolerance, fat deposition and hepatic function in rat offspring. J Dev Orig Health Dis. 2016; 7, 320–329.Google Scholar
22. Lustig, RH. Fructose: it’s “alcohol without the buzz”. Adv Nutr. 2013; 4, 226–235.Google Scholar
23. Matsuzaka, T, Shimano, H. Insulin‐dependent and ‐independent regulation of sterol regulatory element‐binding protein‐1c. J Diabetes Investig. 2013; 4, 411–412.Google Scholar
24. Porstmann, T, Santos, CR, Griffiths, B, et al. SREBP activity is regulated by mTORC1 and contributes to Akt-dependent cell growth. Cell Metab. 2008; 8, 224–236.Google Scholar
25. Dibble, CC, Manning, BD. Signal integration by mTORC1 coordinates nutrient input with biosynthetic output. Nat Cell Biol. 2013; 15, 555–564.Google Scholar
26. Kasturi, R, Joshi, VC. Hormonal regulation of stearoyl coenzyme A desaturase activity and lipogenesis during adipose conversion of 3T3-L1 cells. J Biol Chem. 1982; 257, 12224–12230.Google Scholar
27. Levy, JR, Clore, JN, Stevens, W. Dietary n-3 polyunsaturated fatty acids decrease hepatic triglycerides in Fischer 344 rats. Hepatology. 2004; 39, 608–616.Google Scholar