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Deborah M. Sloboda, PhD

Associate Professor, Department of Biochemistry and Biomedical Sciences

Associate member of the Department of Obstetrics and Gynecology and the Department of Pediatrics

Canada Research Chair in Perinatal Programming

Secretary, International Society of Developmental Origins of Health and Disease

Email: sloboda@mcmaster.ca

Lab website: http://www.slobodalab.com

Facebook: SlobodaLab

Twitter:@Sloboda_Lab

Chronic disease results from a complex interaction of many factors, including genetic, behavioural, and environmental influences. It is now well established that a relationship exists between the periconceptional, fetal and early infant phases of life and the subsequent development of chronic diseases including obesity and Type 2 diabetes. This relationship, the “developmental origins of health and disease” (DOHaD), suggests that the embryo/fetus/neonate makes adaptations in response to early life cues, resulting in adjustments in homeostatic systems that are maladaptive in postnatal life, leading to an increased risk of chronic disease in adulthood and/or the inheritance of risk factors across generations. A multitude of “modifying” cues inducing developmental adaptations have been identified that result in a common adult phenotype characterized by obesity, insulin resistance, behavioural, reproductive and stress-related disorders. Among these, early life nutrition has been the most studied and is the focus of our lab. Our primary interest is determining the relationship between perinatal nutritional adversity and maternal-fetal-placental development and offspring phenotype. The perinatal environment provides a potential therapeutic target for intervention and prevention, and focusing on this developmental window of vulnerability may translate into improved interventional strategies to stem the growing epidemic of obesity.

Main Research Themes

  • The maternal microbiome, fetal and placental development and offspring obesity
    In these studies we investigate how shifts in the pregnant gut microbiome mediate maternal adaptation to pregnancy and how these microbial shifts impact placental, fetal and offspring development. These studies are part of our long-term goal of determining the underlying early life precipitating factors that confer an increased risk of obesity and metabolic disease in offspring of obese mothers.
  • Maternal nutritional impacts on offspring reproduction
    In these studies we are interested in understanding the relationship between early life nutrition and impacts on ovarian function and whether changes in germ cell development underpin transgenerational transmittance of chronic disease risk.

NSERC: ER stress links early life nutritional stress and metabolic outcome.

  1. Ribeiro, TA, Prates, KV, Pavanello, A, Malta, A, Tófolo, LP, Martins, IP et al.. Acephate exposure during a perinatal life program to type 2 diabetes. Toxicology. 2016;372 :12-21. doi: 10.1016/j.tox.2016.10.010. PubMed PMID:27765684 .
  2. Gütling, H, Bionaz, M, Sloboda, DM, Ehrlich, L, Braun, F, Gramzow, AK et al.. The importance of selecting the right internal control gene to study the effects of antenatal glucocorticoid administration in human placenta. Placenta. 2016;44 :19-22. doi: 10.1016/j.placenta.2016.05.011. PubMed PMID:27452434 .
  3. Braun, T, Weichert, A, Gil, HC, Sloboda, DM, Tutschek, B, Harder, T et al.. Fetal and neonatal outcomes after term and preterm delivery following betamethasone administration in twin pregnancies. Int J Gynaecol Obstet. 2016;134 (3):329-35. doi: 10.1016/j.ijgo.2016.02.016. PubMed PMID:27365289 .
  4. Kozyrskyj, AL, Sloboda, DM. Perinatal programming of gut microbiota and immunity. J Dev Orig Health Dis. 2016;7 (1):2-4. . PubMed PMID:27073823 .
  5. Pedrana, G, Viotti, H, Lombide, P, Sanguinetti, G, Pino, C, Cavestany, D et al.. In utero betamethasone affects 3β-hydroxysteroid dehydrogenase and inhibin-α immunoexpression during testis development. J Dev Orig Health Dis. 2016;7 (4):342-9. doi: 10.1017/S2040174416000118. PubMed PMID:27019950 .
  6. Sanches, JR, França, LM, Chagas, VT, Gaspar, RS, Dos Santos, KA, Gonçalves, LM et al.. Polyphenol-Rich Extract of Syzygium cumini Leaf Dually Improves Peripheral Insulin Sensitivity and Pancreatic Islet Function in Monosodium L-Glutamate-Induced Obese Rats. Front Pharmacol. 2016;7 :48. doi: 10.3389/fphar.2016.00048. PubMed PMID:27014062 PubMed Central PMC4785152.
  7. Tsoulis, MW, Chang, PE, Moore, CJ, Chan, KA, Gohir, W, Petrik, JJ et al.. Maternal High-Fat Diet-Induced Loss of Fetal Oocytes Is Associated with Compromised Follicle Growth in Adult Rat Offspring. Biol. Reprod. 2016;94 (4):94. doi: 10.1095/biolreprod.115.135004. PubMed PMID:26962114 PubMed Central PMC4861169.
  8. Ayonrinde, OT, Adams, LA, Doherty, DA, Mori, TA, Beilin, LJ, Oddy, WH et al.. Adverse metabolic phenotype of adolescent girls with non-alcoholic fatty liver disease plus polycystic ovary syndrome compared with other girls and boys. J. Gastroenterol. Hepatol. 2016;31 (5):980-7. doi: 10.1111/jgh.13241. PubMed PMID:26589977 .
  9. 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 (11):e0141962. doi: 10.1371/journal.pone.0141962. PubMed PMID:26562417 PubMed Central PMC4643022.
  10. Wallace, JG, Gohir, W, Sloboda, DM. The impact of early life gut colonization on metabolic and obesogenic outcomes: what have animal models shown us?. J Dev Orig Health Dis. 2016;7 (1):15-24. doi: 10.1017/S2040174415001518. PubMed PMID:26399435 .
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