P863 - MATERNAL STEVIA INTAKE - A PROGRAMMER OF OFFSPRING’S METABOLIC DYSFUNCTION?

P863

MATERNAL STEVIA INTAKE - A PROGRAMMER OF OFFSPRING’S METABOLIC DYSFUNCTION?

I. Bracchi^1,2,*, M. Barbosa³, M. I. Vieira⁴, S. Brandão³, A. C. Esteves³, C. Martins⁵, I. Rocha^6,7, D. Pestana⁸, R. Negrão¹, E. Keating¹

¹RISE-Health, Departament of Biomedicine-Unit of Biochemistry, Faculty of Medicine, University of Porto, ²ESS, Polytechnic of Porto, ³ Departament of Biomedicine-Unit of Biochemistry, Faculty of Medicine, University of Porto, ⁴Department Biomedicine, Unit of Biochemistry, Faculty of Medicine, University of Porto, ⁵Faculty of Nutrition and Food Sciences, University of Porto, ⁶Faculty of Health Sciences, Fernando Pessoa University, Porto, ⁷Nutrition & Metabolism, NOVA Medical School|FCM, NOVA University Lisbon, ⁸CHRC|Nutrition and Metabolism, NOVA Medical School|FCM, NOVA University Lisbon, Lisbon, Portugal

Rationale: Recently the World Health Organization recommended restricting non-sugar sweeteners (NSS) consumption and emphasized the need to evaluate their safety during early developmental stages. We aim to investigate the role of maternal Rebaudioside A (RebA) consumption—the main sweetener component of Stevia—as a fetal programmer of metabolic dysfunction.

Methods: Female Sprague Dawley rats received RebA (n=8) in the drinking water (4 mg steviol equivalents/kg body weight/day, the European Food Safety Authority’s acceptable daily intake) from 4 weeks before mating until weaning, or water (control, C, n=8). Offspring (G1) were weaned into standard diet until 10 months of age. G1 morphometry, food and water intake were assessed. Oral glucose tolerance (OGTT) and insulin sensitivity tests (IST) were performed at 2, 6 and 10 months. Blood levels of leptin, ghrelin and adiponectin were quantified by ELISA. T-test or 2-way ANOVA were used for comparisons between groups as appropriate.

Results: RebA G1 females presented greater weight gain from 30 weeks of age when compared to controls (p=0.0165). No differences were found in food and water intake, nor in leptin or ghrelin levels. At 10 months of age, RebA reduced insulin sensitivity in G1 females (p=0.0200) and it impaired glycemia normalization 2h-post OGTT in males (p=0.0197). Additionally, RebA reduced adiponectin levels in G1 offspring and it changed the evolution of adiponectin levels between 2 and 10 months of age (for females: p<0.0001 and p=0.0279 for RebA and Age x RebA interaction, respectively; for males: p=0.0089 and p=0.0097 for RebA and Age x RebA interaction, respectively).

Conclusion: These findings evidence that early RebA exposure programs the offspring for increased weight gain and for insulin resistance (in females), and for a degree of dysglycemia (in males). Importantly, adiponectin appears as an early player in fetal programming of metabolic dysfunction by RebA.

Disclosure of Interest: None declared