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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

  • H. Kaur (a1), C. R. Toop (a1), B. S. Muhlhausler (a1) (a2) (a3) and S. Gentili (a1)

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.

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Corresponding author

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

References

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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, 3140.
2. World Health Organization. Guideline: Sugars Intake for Adults and Children. 2015. World Health Organization: Geneva.
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, 105114.
4. Walker, RW, Dumke, KA, Goran, MI. Fructose content in popular beverages made with and without high-fructose corn syrup. Nutrition. 2014; 30, 928935.
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, 13221334.
6. Bizeau, ME, Pagliassotti, MJ. Hepatic adaptations to sucrose and fructose. Metabolism. 2005; 54, 11891201.
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, 7986.
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.
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, 2516425171.
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, 13781387.
11. Kelley, GL, Allan, G, Azhar, S. High dietary fructose induces a hepatic stress response resulting in cholesterol and lipid dysregulation. Endocrinology. 2004; 145, 548555.
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, 198206.
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, 220225.
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, 42144223.
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, 3846.
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, 43794398.
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, 497509.
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, 819826.
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, 53415350.
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.
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, 320329.
22. Lustig, RH. Fructose: it’s “alcohol without the buzz”. Adv Nutr. 2013; 4, 226235.
23. Matsuzaka, T, Shimano, H. Insulin‐dependent and ‐independent regulation of sterol regulatory element‐binding protein‐1c. J Diabetes Investig. 2013; 4, 411412.
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, 224236.
25. Dibble, CC, Manning, BD. Signal integration by mTORC1 coordinates nutrient input with biosynthetic output. Nat Cell Biol. 2013; 15, 555564.
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, 1222412230.
27. Levy, JR, Clore, JN, Stevens, W. Dietary n-3 polyunsaturated fatty acids decrease hepatic triglycerides in Fischer 344 rats. Hepatology. 2004; 39, 608616.

Keywords

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

  • H. Kaur (a1), C. R. Toop (a1), B. S. Muhlhausler (a1) (a2) (a3) and S. Gentili (a1)

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