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The interwar period represents an era of emerging growth and maturity in Australian foreign and defence relations, with a distinct focus shift from Imperial to regional matters. However, this expression of independent policy has been largely overlooked in the existing literature. Rather, Australian policy makers of this era have been framed as disinterested in policy making, lacking direction and preferring 'to deal with the world one step removed through Whitehall'. Such interpretations have overlooked significant policy changes throughout this period, painting Australia as a timid and na ve nation, content to follow Britain's every policy and demand.

Uteroplacental insufficiency impairs kidney development and programs male‐onset cardiorenal disease, which can be transmitted to subsequent generations. Maternal lifestyle factors can independently influence fetal kidney development, highlighting that the lifestyle of growth‐restricted females can have further influence on F2 kidney development. In this study, we examined the impact of maternal growth restriction with or without additional lifestyle factors on F2 male kidney development. Uteroplacental insufficiency (Restricted) or sham (Control) surgery was performed on embryonic day 18 in Wistar–Kyoto rats. F1 females were fed a Chow or High‐fat diet from weaning (5 weeks of age). At 16 weeks, females were randomly allocated to an exercise group: no exercise (Sedentary); exercised prior to and during pregnancy (Exercise); or exercised only during pregnancy (PregEx). Females were mated at 20 weeks, with F2 male kidneys collected (embryonic day 20). Maternal growth restriction alone reduced nephron endowment by 29%, whereas additional lifestyle factors in Restricted dams reduced nephron endowment by ∼43%. Interestingly, Exercise only in High‐fat dams did not alter nephron endowment, which is likely to be attributable to significant kidney remodelling and/or enhanced resource availability. This study demonstrates that growth‐restricted dams that experience multiple maternal lifestyle factors (i.e. High‐fat diet and PregEx) impair the development of male F2 kidneys to a more severe extent than fetuses exposed to maternal growth restriction alone or a single maternal lifestyle factor in dams of normal birth weight (i.e. high‐fat feeding or exercise alone). Importantly, positive lifestyle interventions (Exercise) in a high‐fat environment compounded by adverse metabolic programming (Restriction) can be beneficial to fetal kidney development, which might prevent the transgenerational programming of cardiorenal disease. What is the central question of this study? Uteroplacental insufficiency impairs kidney development, programming male‐onset cardiorenal disease, which can be transmitted transgenerationally. What impact do lifestyle factors in growth‐restricted dams have on second‐generation kidney development? What is the main finding and its importance? Lifestyle factors in growth‐restricted dams compromise fetal nephron endowment to a greater extent than growth restriction alone. Exercise prior to and throughout pregnancy maintains normal nephron endowment in high‐fat dams. Understanding the underlying mechanism(s) might offer therapeutic interventions for infants born small to improve their own and their children's cardiorenal health, breaking the transgenerational cycle.

Linoleic acid (LA), an n-6 polyunsaturated fatty acid (PUFA), is essential for fetal growth and development. A maternal high LA (HLA) diet alters cardiovascular development in adolescent rats and hepatic function in adult rats in a sex-specific manner. We investigated the effects of an HLA diet on adolescent offspring hepatic lipids and hepatic lipid metabolism gene expression, and the ability of the postnatal diet to alter these effects. Female Wistar Kyoto rats were fed low LA (LLA; 1.44% energy from LA) or high LA (HLA; 6.21% energy from LA) diets during pregnancy and gestation/lactation. Offspring, weaned at postnatal day (PN) 25, were fed LLA or HLA and euthanised at PN40 (n = 6–8). Maternal HLA increased circulating uric acid, decreased hepatic cholesterol and increased hepatic Pparg in males, whereas only hepatic Srebf1 and Hmgcr increased in females. Postnatal (post-weaning) HLA decreased liver weight (% body weight) and increased hepatic Hmgcr in males, and decreased hepatic triglycerides in females. Maternal and postnatal HLA had an interaction effect on Lpl, Cpt1a and Pparg in females. These findings suggest that an HLA diet both during and after pregnancy should be avoided to improve offspring disease risk.

Linoleic acid (LA), an n-6 polyunsaturated fatty acid (PUFA), is obtained from the maternal diet during pregnancy, and is essential for normal fetal growth and development. A maternal high-LA (HLA) diet alters maternal and offspring fatty acids, maternal leptin and male/female ratio at embryonic (E) day 20 (E20). We investigated the effects of an HLA diet on embryonic offspring renal branching morphogenesis, leptin signalling, megalin signalling and angiogenesis gene expression. Female Wistar Kyoto rats were fed low-LA (LLA; 1.44% energy from LA) or high-LA (HLA; 6.21% energy from LA) diets during pregnancy and gestation/lactation. Offspring were sacrificed and mRNA from kidneys was analysed by real-time PCR. Maternal HLA decreased the targets involved in branching morphogenesis Ret and Gdnf in offspring, independent of sex. Furthermore, downstream targets of megalin, namely mTOR, Akt3 and Prkab2, were reduced in offspring from mothers consuming an HLA diet, independent of sex. There was a trend of an increase in the branching morphogenesis target Gfra1 in females (p = 0.0517). These findings suggest that an HLA diet during pregnancy may lead to altered renal function in offspring. Future research should investigate the effects an HLA diet has on offspring kidney function in adolescence and adulthood.

Background/Objectives: Dietary fibre promotes health, partly by mediating gut microbiota and short-chain fatty acid (SCFA) production. Pregnancy alters the relationship between dietary composition and the gut microbiota, and it is unclear if fibre intake during late pregnancy alters the abundance of SCFA bacteria and circulating SFCA concentrations. The aim of this study was to determine the impact of dietary fibre on faecal microbiome composition and circulating concentrations of SCFA acetate, butyrate, and propionate in late pregnancy. We also aimed to assess the impact of propionate treatment on placental function using cultured placental explants. Methods: 16S rRNA gene amplicon sequencing was performed on faecal DNA collected at 28 weeks of gestation from participants enrolled in the SPRING cohort study consuming a low or adequate fibre diet. Circualting SCFA were assessed. Placental explants were treated with sodium propionate. Results: Fibre intake did not impact microbial diversity or richness but did impact the abundance of specific bacterial genera. Pregnant participants with low-fibre diets had a greater abundance of Bacteroides and Sutterella, and dietary fibre intake (mg/day) negatively correlated with genera, including Sutterella, Bilophila, and Bacteroides. SCFA concentrations did not differ between groups but circulating concentrations of acetate, propionate, and butyrate did correlate with the abundance of key bacterial genera. Propionate treatment of placental explants did not alter mRNA expression of fatty acid receptors, antioxidants, or markers of apoptosis, nor did it impact pAMPK levels. Conclusions: This study demonstrates that the impact of dietary fibre on SCFA concentrations in pregnant women is modest, although this relationship may be difficult to discern given that other dietary factors differed between groups. Furthermore, this study demonstrates that propionate does not impact key pathways in placental tissue, suggesting that previous associations between this SCFA and placental dysfunction may be due to other maternal factors.