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  • (2023) Seyed Tajaddini, Aynaz
    Thesis
    Much evidence indicates that maternal obesity programs a range of complications in offspring, highlighting the need to identify beneficial interventions. The present thesis examined if the programmed effects of maternal obesity on offspring are exacerbated by exposure to a high-fat, high-sugar ‘Cafeteria’ (Caf) diet and investigated the effects of a healthy diet intervention in adulthood. The first study examined whether a diet switch intervention could reverse the adverse effects of an unhealthy postweaning diet in male and female rat offspring born to dams fed standard chow or a high-fat, high-sugar, Caf diet. Weanling offspring from Caf dams were smaller and lighter, yet had more retroperitoneal (RP) fat, particularly in males. Maternal obesity enhanced the impact of postweaning Caf exposure on adult (14-week-old) body weight, RP fat, liver mass and plasma leptin in males but not females. Maternal Caf diet significantly increased relative expression of ACACA and Fasn in male and female weanling liver, whereas PPARα was increased in males from Caf dams. Hepatic CPT-1 expression was reduced in adult males from Caf fed dams. The results underline the sex-specific detrimental effects of maternal obesity on offspring; maternal obesity exacerbated the obesogenic phenotype produced by postweaning Caf diet in male, but not female offspring. A subset of rats from this first cohort were maintained on their postweaning diets until 22 weeks of age, when postweaning Caf groups were switched to chow for a further 5 weeks. Switching from Caf to chow in adulthood suppressed energy intake below groups maintained on chow. Consequently, body weight and adiposity fell in switched groups, but remained significantly higher than chow-fed controls. The diet switch improved a deficit in place recognition memory observed in Caf-fed groups, with no significant change over time in chow-fed groups. Importantly, the effects of the switch did not differ between offspring born to chow or Caf-fed dams. Thus, in these older adult offspring a healthy dietary intervention led to benefits regardless of prior exposure to maternal obesity. To complement these data, our second study investigated if the programming effects of maternal obesity were aggravated by offspring exposure to a Caf diet when introduced in adulthood. Male and female offspring from lean and obese dams were weaned onto chow until 9 weeks of age; siblings were then either continued on chow or switched to Caf diet for 5 weeks. Offspring from Caf dams were smaller than those from chow dams at birth, and exhibited greater adiposity, plasma glucose and leptin levels at weaning in both sexes. Offspring of Caf dams exhibited elevated liver triglyceride content at weaning but no significant changes in the liver antioxidant enzymes GPx, SOD, and CAT. The switch to Caf diet elevated body weight and fat mass, with more pronounced effects in females than males. As in our first study, adult males (14 week old) from Caf-fed dams exhibited increased body weight, adiposity, and plasma insulin and leptin levels relative to offspring from chow dams. In female offspring, only RP fat mass and plasma insulin were increased by maternal obesity. Moreover, there were behavioural effect of maternal obesity (reduced anxiety-like behaviour) on offspring. Thus, the effects of maternal Caf diet exposure were absent until a cafeteria diet challenge in adulthood, indicating that Caf diet-induced maternal obesity programs a latent vulnerability to obesogenic diet exposure in offspring, particularly in males. Further studies are needed to investigate the beneficial effects of reprogramming strategies such as healthy diet intervention in offspring, which are likely to be influenced by the duration, timing and mode of intervention.