The coronavirus disease 2019 (COVID-19) pandemic resulted in physical isolation measures in many parts of the world. In Australia, nationwide restrictions included staying at home, unless seeking medical care, providing care, purchasing food, undertaking exercise, or attending work in an essential service. All undergraduate university classes transitioned to online, mostly home-based learning. We, therefore, examined the effect of isolation measures during the early phase of the COVID-19 pandemic in Australia (March/April) on diet (24-h recall) and physical activity (Active Australia Survey) patterns in third-year biomedical students. Findings were compared with students enrolled in the same course in the previous two years. In females, but not males, energy intake was ~20% greater during the pandemic, and snacking frequency and energy density of consumed snacks also increased compared with 2018 and 2019. Physical activity was impacted for both sexes during the pandemic with ~30% fewer students achieving “sufficient” levels of activity, defined by at least 150 min over at least five sessions, compared with the previous two years. In a follow-up study six to eight weeks later (14–18% response rate), during gradual easing of nationwide restrictions albeit continued gym closures and online learning, higher energy intake in females and reduced physical activity levels in both sexes persisted. These data demonstrate the health impacts of isolation measures, with the potential to affect long-term diet and activity behaviours.

It is well established that erythropoiesis occurs first in the yolk sac, then in the liver, subsequently moving to the bone marrow and, in rodents, the spleen during development. The origin of the erythropoietic precursors and some factors suggested to be important for the changing location of erythropoiesis are discussed in this review. Until recently, the major site of erythropoietin (Epo) production in the fetus was thought to be the liver, but studies have shown now that the Epo gene is expressed strongly in the fetal kidney, even in the temporary mesonephros. The metanephric Epo mRNA is upregulated by anemia, downregulated by glucocorticoids, and contributes substantially to circulating hormone levels in hemorrhaged ovine fetuses. Other sites of Epo and Epo receptor production, likely to have important actions during development, are the placenta and the brain.

This review highlights the important roles the mesonephros may play in development. In the ovine fetus it is an excretory and endocrine organ and may contribute to the formation of normal gonads and adrenals. The metanephros of the ovine fetus has the important function of providing large quantities of dilute urine for the maintenance of amniotic and allantoic fluid volumes, essential for normal placentation and development.

partly attributed to different placenta-regulated growth strategies of the male and female fetus. Pregnancy is known to be a major risk factor for unmasking a number of conditions and can be considered a 'second hit' for women who were born small. As such, female offspring often develop impairments of physiology for the first time during pregnancy that present as pregnancy complications. Numerous maternal stressors can further increase the risk of developing a maternal complication during pregnancy. Importantly, these maternal complications can have long-term consequences for both the mother after pregnancy and the developing fetus. Conditions such as preeclampsia, gestational diabetes and hypertension as well as thyroid, liver and kidney diseases are all conditions that can complicate pregnancy and have long-term consequences for maternal and offspring health. Babies born to mothers who develop these conditions are often at a greater risk of developing disease in adulthood. This has implications as a mechanism for transmission of disease across generations. In this review, we discuss the evidence surrounding long-term intergenerational implications of being born small and/or experiencing stress during pregnancy on programming outcomes. Abstract figure legend Sex-specific fetal programming and the transgenerational transmission of diseases. Perturbations of the fetal environment during critical periods of development can have many consequences in postnatal life. This is primarily regulated by the placenta, which is known to respond to stressful stimuli in a sex-specific manner. Individuals exposed to suboptimal conditions in utero are programmed for various diseases including cardiovascular and metabolic diseases. Females programmed during fetal life have increased risk of developing pregnancy complications. The germ cells of exposed individuals may also be compromised. Together, they contribute to an adverse fetal environment and places the next generation of offspring at risk of adverse health. Importantly, stress is known to exacerbate these programmed outcomes during fetal and postnatal life.

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Treatment of nine pregnant Merino ewes (64.0 +/- 0.4 days of gestation) with dexamethasone (D; 0.76 mg/h for 48 h) resulted in significant alterations in fetal fluids compared with eight saline-infused control animals (S; 63.0 +/- 0.9 days). There was a substantial increase in allantoic fluid volume (177 +/- 18 ml, D vs. 31 +/- 6, S) but no change in amniotic fluid volume (248 +/- 12 ml, D; 305 +/- 24, S). For allantoic fluid there was a significant decrease in osmolality (213 +/- 4 mosmol/kg water, D; 230 +/- 5, S) and alterations in composition. Amniotic fluid osmolality was unchanged (292 +/- 2 mosmol/kg water, D; 293 +/- 1, S), but amniotic fluid composition was affected. In four fetuses in which bladder and amniotic cannulas were inserted at gestational age 68-75 days, fetal urine flow rate increased from a mean of 4.1 +/- 1.1 to 13.8 +/- 2.6 ml/h after 24 h and 11.8 +/- 3.0 ml/h at 48 h for a similar maternal D infusion, whereas no such increase occurred in four control fetuses. All the fetal urine voided during a 3.5- to 4-h infusion of 51Cr-labeled EDTA into the fetal bladder was directed to the allantois. The results suggest that the increase in allantoic fluid volume resulted from increased fetal urine output into the allantoic compartment, although the composition of the excess allantoic fluid differed substantially from that of fetal urine. There was a greater incidence of abnormal cotyledons in the D-infused ewes.(ABSTRACT TRUNCATED AT 250 WORDS)

Previously, we have shown that fetal uninephrectomy (uni-x) causes hypertension in female sheep by 2 years of age. Whilst the hypertension was not exacerbated by 5 years of age, these uni-x sheep had greater reductions in renal blood flow (RBF). To further explore these early indications of a decline in renal function, we investigated the renal response to a saline load (25 ml/kg/40 min) in 5-year old female uni-x and sham sheep. Basal mean arterial pressure was ∼15 mmHg greater (PGroup<0.001), and sodium excretion (∼50%), glomerular filtration rate (∼30%, GFR) and RBF (∼40%) were all significantly lower (PGroup<0.01) in uni-x compared to sham animals. In response to saline loading, sodium excretion increased significantly in both groups (PTime<0.001), however this response was blunted in uni-x sheep (PGroupxTime<0.01). This was accompanied with an attenuated increase in GFR and fractional sodium excretion (both PGroupxTime<0.05), and reduced activation of the renin-angiotensin system (both P<0.05), as compared to the sham group. The reduction in sodium excretion was associated with up-regulations in the renal gene expression of NHE3 and Na+/K+ ATPase α and β subunits in the kidney cortex of the uni-x compared to the sham animals (P<0.05). Notably, neither group completely excreted the saline load within the recovery period, but the uni-x retained a higher percentage of the total volume (uni-x: 48±7%; sham: 22±9%, P<0.05). In conclusion, a reduced ability to efficiently regulate extracellular fluid homeostasis is evident in female sheep at 5 years of age, which was exacerbated in animals born with a congenital nephron deficit. Whilst there was no overt exacerbation of hypertension and renal insufficiency with age in the uni-x sheep, these animals may be more vulnerable to secondary renal insults.

Prenatal alcohol exposure (PAE) results in well-characterized neurological, behavioral, and cognitive deficits in offspring. However, the effects on other health outcomes have not been comprehensively described. We used a systematic review methodology to survey published clinical and preclinical studies investigating a broad range of health outcomes in offspring with PAE. This study specifically reports on outcomes related to metabolism and body composition. The literature was systematically searched across 4 electronic databases (PubMed, CINAHL, Embase, and Web of Science), resulting in 3,230 articles following duplicate removal. Titles and abstracts were reviewed against specific inclusion/exclusion criteria, with 242 articles meeting the criteria for full-text assessment of eligibility. Articles with ineligible study type were removed (127) and articles added from reference lists (15) and an updated search closer to submission (9) for a total of 139 studies. Although 5 health domains were identified, here we focus on metabolism and body composition. Details of alcohol exposure, offspring demographics, and sample sizes were tabulated and quality of reporting assessed. Findings were summarized for body composition (percentage fat mass), physiological and molecular outcomes related to glucose metabolism, and outcomes related to lipid metabolism. There were 32 included studies (2 case-control, 1 prospective longitudinal cohort, and 29 preclinical). Studies had a range of alcohol exposures, both dosage and timing, although all clinical studies had heavy PAE and/or evidence of fetal alcohol syndrome in offspring. The preclinical studies provided evidence of glucose intolerance and/or insulin resistance; dyslipidemia and/ or hypercholesterolemia; and increased adiposity in offspring with PAE. Due to the paucity of clinical studies, we recommend further studies be conducted to obtain a complete assessment of long-term metabolic health outcomes in children and adults with PAE, particularly in those diagnosed with fetal alcohol spectrum disorder.