Tania Romano
La Trobe University
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Publication
Featured researches published by Tania Romano.
American Journal of Physiology-endocrinology and Metabolism | 2015
Jessica F. Briffa; Andrew J. McAinch; Tania Romano; Mary E. Wlodek; Deanne H. Hryciw
Emerging research has highlighted the importance of leptin in fetal growth and development independent of its essential role in the maintenance of hunger and satiety through the modulation of neuropeptide Y and proopiomelanocortin neurons. Alterations in maternal-placental-fetal leptin exchange may modify the development of the fetus and contribute to the increased risk of developing disease in adulthood. In addition, leptin also plays an important role in reproductive functions, with plasma leptin concentrations rising in pregnant women, peaking during the third trimester. Elevated plasma leptin concentrations occur at the completion of organogenesis, and research in animal models has demonstrated that leptin is involved in the development and maturation of a number of organs, including the heart, brain, kidneys, and pancreas. Elevated maternal plasma leptin is associated with maternal obesity, and reduced fetal plasma leptin is correlated with intrauterine growth restriction. Alterations in plasma leptin during development may be associated with an increased risk of developing a number of adulthood diseases, including cardiovascular, metabolic, and renal diseases via altered fetal development and organogenesis. Importantly, research has shown that leptin antagonism after birth significantly reduces maturation of numerous organs. Conversely, restoration of the leptin deficiency after birth in growth-restricted animals restores the offsprings body weight and improves organogenesis. Therefore, leptin appears to play a major role in organogenesis, which may adversely affect the risk of developing a number of diseases in adulthood. Therefore, greater understanding of the role of leptin during development may assist in the prevention and treatment of a number of disease states that occur in adulthood.
Bone | 2009
Tania Romano; John D. Wark; Julie A. Owens; Mary E. Wlodek
Low birth weight increases the risk of developing adult onset cardiovascular and metabolic diseases. Recently being born small has also been identified as a risk factor for adverse bone growth, development and adult fracture risk. Evidence also suggests that accelerated growth in offspring of normal birth weight, following periods of slowed growth, can also independently program adult diseases. The aim of this study was to determine the relative roles of prenatal and postnatal growth restriction on adult bone characteristics and strength. Bilateral uterine vessel ligation (Restricted) or sham surgery (Control) was performed on gestational day 18 in WKY rats to induce fetal growth restriction. Control, Reduced (reduced Control litter size to match Restricted) and Restricted pups were cross-fostered onto different Control (normal lactation) or Restricted (impaired lactation) mothers 1 day after birth. Femur length, dimensions, strength, mineral content and density were quantified using DXA and pQCT analysis. Markers of bone turnover were measured in offspring at 6 months. Restricted pups were born lighter than Controls with males, not females, remaining smaller than Control-on-Control at 6 months (P<0.05). Pups born of normal weight from a reduced litter suckling on a Restricted mother (Reduced-on-Restricted) grew slowly during lactation then quicker after weaning compared to Controls (P<0.05). Cortical bone mineral content, dimensions and strength were lower in Restricted-on-Restricted and Reduced-on-Restricted offspring compared to Controls with lower density in Reduced-on-Restricted females (P<0.05). The stress strain index of bone bending strength remained lower in the Restricted male offspring when body weight adjustments were made. Cross-fostering Restricted females, but not males, onto mothers with normal lactation (Restricted-on-Control) restored growth and bone parameters to Controls (P<0.05). Being born small, or postnatal growth restriction for normal birth weight offspring followed by accelerated growth, programs bone content and strength deficits. Deficits were corrected by improving postnatal nutrition for females born small, highlighting sex specific programming outcomes and impact of postnatal nutrition. These findings suggest a link between growth restriction and adult bone health with additional studies needed to further explore this link in humans.
Bone | 2010
Tania Romano; John D. Wark; Mary E. Wlodek
Low birth weight and poor childhood growth program a variety of adult diseases including bone disorders such as osteoporosis. We have previously reported that offspring born small, as a result of uteroplacental insufficiency, have shorter femurs, lower bone mineral content and a bone strength deficit as adults. The aim of this study was to determine the effects of calcium supplementation from adolescence on growth restricted male and female offspring which have a programmed bone deficit. Bilateral uterine vessel ligation (Restricted) or sham surgery (Control) was performed on gestational day 18 in WKY rats to induce uteroplacental insufficiency and growth restriction. At 2 months pups were allocated to one of four diet groups: diet 1-constant normal calcium diet, diet 2-variable normal calcium diet, diet 3-constant high calcium diet, diet 4-variable high calcium diet. Diet groups 1 and 3 were fed their respective diets constantly for the duration of the study. In groups 2 and 4, rats were fed one diet for 5 days, followed by a switch to a low calcium diet for the next 5 days. At 6 months Dual Energy Xray Absorptiometry (DXA) and Peripheral Quantitative Computed Tomography (pQCT) were performed on the right femur. Bone turnover markers were measured at 4 months. Male and female Restricted offspring were born 14% lighter compared to Controls (p<0.05). At 6 months both male and female Restricted offspring remained smaller and had shorter femurs compared to Controls (p<0.05). Restricted males and females had reduced trabecular and cortical content compared to Controls, regardless of diet (p<0.05). Trabecular bone density was lower in Restricted females only (p<0.05). A constant high calcium diet increased cortical BMD in Restricted male and both female groups (p<0.05). Measures of bone geometry indicated that Restricted offspring have narrower bones with preservation of absolute cortical thickness (p<0.05). Importantly, the stress strain index of bone bending strength was lower in male and female Restricted offspring, regardless of diet by up to 9.0% and 7.8%, respectively. DXA results were similar to pQCT results. Being born small, due to uteroplacental insufficiency, programs reduced adult femur length, dimensions and stress strain index. Supplementation with a high calcium diet from adolescence can increase adult cortical bone density in low birth weight males and females, and normal weight females. This increase in bone density was not sufficient to rescue the bone dimension and strength deficits which were programmed in utero, suggesting that the early life environment is critical for bone programming.
Journal of Developmental Origins of Health and Disease | 2014
S. van der Linde; Tania Romano; Glenn D. Wadley; A. J. Jeffries; Mary E. Wlodek; Deanne H. Hryciw
Uteroplacental insufficiency resulting in intrauterine growth restriction has been associated with the development of cardiovascular disease, coronary heart disease and increased blood pressure, particularly in males. The molecular mechanisms that result in the programming of these phenotypes are not clear. This study investigated the expression of cardiac JAK/STAT signalling genes in growth restricted offspring born small due to uteroplacental insufficiency. Bilateral uterine vessel ligation was performed on day 18 of pregnancy to induce growth restriction (Restricted) or sham surgery (Control). Cardiac tissue at embryonic day (E) 20, postnatal day (PN) 1, PN7 and PN35 in male and female Wistar (WKY) rats (n=7-10 per group per age) was isolated and mRNA extracted. In the heart, there was an effect of age for males for all genes examined there was a decrease in expression after PN1. With females, JAK2 expression was significantly reduced after E20, while PI3K in females was increased at E30 and PN35. Further, mRNA expression was significantly altered in JAK/STAT signalling targets in Restricteds in a sex-specific manner. Compared with Controls, in males, JAK2 and STAT3 were significantly reduced in the Restricted, while in females SOCS3 was significantly increased and PI3K significantly decreased in the Restricted offspring. Finally, there were specific differences in the levels of gene expression within the JAK/STAT pathway when comparing males to females. Thus, growth restriction alters specific targets in the JAK/STAT signalling pathway, with altered JAK2 and STAT3 potentially contributing to the increased risk of cardiovascular disease in the growth restricted males.
Reproduction, Fertility and Development | 2015
Tania Romano; John D. Wark; Mary E. Wlodek
Recent evidence links low birthweight and poor adult bone health. We characterised bone size, mineral content, density and strength (stress strain index of bone bending strength (SSI)) in rats from weaning to 12 months. Bilateral uterine vessel ligation (Restricted) or sham surgery (Control) was performed on gestational Day 18 in rats inducing uteroplacental insufficiency. Postmortem of male and female offspring was performed at postnatal Day 35 and at 2, 4, 6 and 12 months. Femur mineral content, density and strength were measured using quantitative computed tomography (pQCT). Restricted pups were born 10%-15% lighter and remained smaller with shorter femurs than Controls (P<0.05). Male and female Restricted rats had lower trabecular bone content compared with Controls (P<0.05), without trabecular density changes. Cortical content was reduced in Restricted males (Day 35 and 6 and 12 months) and at all ages in Restricted females (P<0.05). Cortical density was lower at Day 35 in Restricted males (P<0.05). SSI was lower at Day 35 and at 6 and 12 months in Restricted males, and at all ages in Restricted females (P<0.05). Skeletal deficits were detected in Restricted offspring with gender-specific differences during juvenile and adolescent periods. Bone deficits observed at 6 months in males were greater than at 12 months, indicating that aging can exacerbate programmed bone phenotypes.
Reproduction, Fertility and Development | 2014
Tania Romano; John D. Wark; Mary E. Wlodek
Fluctuations in maternal bone mass during pregnancy and lactation facilitate calcium transfer to offspring. Uteroplacental insufficiency causes fetal growth restriction and programs poor adult bone health. We aimed to characterise maternal skeletal phenotype during normal pregnancy and pregnancy complicated by uteroplacental insufficiency. Uteroplacental restriction (Restricted) or sham surgery (Control) was performed on gestational Day 18 (term=22 days) in pregnant Wistar-Kyoto rats. Maternal right femurs were collected on embryonic Day 20, postnatal Day 1 and Weeks 5, 7 and 9 postnatal. Dual-energy X-ray absorptiometry was used to quantify global bone mineral content, density and body composition. Peripheral quantitative computed tomography was utilised to determine trabecular and cortical content, density, circumferences and strength. Control rats exhibited expected reductions in trabecular and cortical content, density and bone strength from embryonic Day 20 to postnatal Day 1 (P<0.05). These skeletal alterations were absent in Restricted rats. By postnatal Day 7, bone parameters in Control and Restricted rats were not different from non-pregnant rats, indicating restoration of maternal bone. The lack of bone loss in mothers suffering uteroplacental insufficiency suggests that calcium transfer to pups would be impaired. This reduction in calcium availability is a likely contributor to the programming of poor adult bone health in growth-restricted offspring.
Acta Physiologica | 2018
James S. M. Cuffe; Jessica F. Briffa; Shannyn Rosser; Andrew L. Siebel; Tania Romano; Deanne H. Hryciw; Mary E. Wlodek; Karen M. Moritz
Uteroplacental insufficiency in rats reduces nephron endowment, leptin concentrations and programmes cardiorenal disease in offspring. Cross‐fostering growth‐restricted (Restricted) offspring onto a mother with normal lactation restores leptin concentrations and nephron endowment. This study aimed to determine whether the reduced nephron endowment in Restricted offspring is due to delayed glomerular formation and dysregulation of renal genes regulating branching morphogenesis, apoptosis or leptin signalling. Furthermore, we aimed to investigate whether cross‐fostering Restricted offspring onto Control mothers could improve glomerular maturation and restore renal gene abundance.
The Journal of Physiology | 2017
Jessica F. Briffa; Rachael O'Dowd; Karen M. Moritz; Tania Romano; Lisa R. Jedwab; Andrew J. McAinch; Deanne H. Hryciw; Mary E. Wlodek
Uteroplacental insufficiency compromises maternal mammary development, milk production and pup organ development; this is ameliorated by cross‐fostering, which improves pup growth and organ development and prevents adult diseases in growth‐restricted (Restricted) offspring by enhancing postnatal nutrition. Leptin is transported to the fetus from the mother by the placenta; we report reduced plasma leptin concentrations in Restricted fetuses associated with sex‐specific alterations in placental leptin transporter expression. Pup plasma leptin concentrations were also reduced during suckling, which may suggest reduced milk leptin transport or leptin reabsorption. Mothers suckled by Restricted pups had impaired mammary development and changes in milk fatty acid composition with no alterations in milk leptin; cross‐fostering restored pup plasma leptin concentrations, which may be correlated to improved milk composition and intake. Increased plasma leptin and altered milk fatty acid composition in Restricted pups suckling mothers with normal lactation may improve postnatal growth and prevent adult diseases.
Reproduction, Fertility and Development | 2015
Tania Romano; Deanne H. Hryciw; Kerryn T. Westcott; Mary E. Wlodek
Being born small programs adult diseases later in life, with the early postnatal growth rate in growth-restricted offspring playing a role in the reduction of the risk of disease in adulthood. In addition, early postnatal growth is critical for puberty onset (PO). Using cross-fostering, we determined the effects of growth restriction and prenatal and postnatal environments on PO and sex steroids. Bilateral uterine vessel ligation (Restricted) or sham surgery (Control), performed on Gestational Day 18 in Wistar-Kyoto rats induced fetal growth restriction. Control, Reduced (Control litter size reduced to five pups) and Restricted pups were cross-fostered onto different Control (normal lactation) or Restricted (impaired lactation) mothers on Day 1. The day of vaginal opening (females) and balanopreputial separation (males) characterised PO. Blood was sampled for sex steroid and leptin analysis. Restricted pups were born lighter than Controls (P<0.05). PO was delayed by 3.4-4 days in Restricted-on-Restricted males and females (P<0.05). Plasma leptin concentrations at PO were lower in both sexes in all groups compared with Restricted-on-Control and Control-on-Control (P<0.05). PO occurred earlier in Restricted-on-Control (~2 days) with normal leptin concentrations and accelerated growth compared with Restricted-on-Restricted (P<0.05). Testosterone concentrations were lower in male Restricted-on-Restricted than Control-on-Control at 6 months (P<0.05). Restricted-on-Restricted females had lower progesterone at PO compared with Control-on-Control (P<0.05). Female Restricted-on-Restricted had lower oestradiol, with Restricted-on-Control having higher testosterone concentrations at 6 months than Control-on-Control (P<0.05). Growth restriction reduced postnatal growth and leptin concentrations, delaying PO in both sexes and programming altered sex steroids. This highlights the importance of the interaction between prenatal and postnatal growth in the programming of adult reproductive status.
Bone | 2015
Kristina Anevska; Linda A. Gallo; Melanie Tran; Andrew J. Jefferies; John D. Wark; Mary E. Wlodek; Tania Romano
Low birth weight, due to uteroplacental insufficiency, results in programmed bone deficits in the first generation (F1). These deficits may be passed onto subsequent generations. We characterized the effects of being born small on maternal bone health during pregnancy; and aimed to characterize the contribution of the maternal environment and germ line effects to bone health in F2 offspring from mothers born small. Bilateral uterine vessel ligation (or sham) surgery was performed on female F0 WKY rats on gestational day 18 (term 22days) to induce uteroplacental insufficiency and fetal growth restriction. Control and Restricted F1 female offspring were allocated to a non-pregnant or pregnant group. To generate F2 offspring, F1 females were allocated to either non-embryo or embryo transfer groups. Embryo transfer was performed on gestational day 1, where second generation (F2) embryos were gestated (donor-in-recipient) in either a Control (Control-in-Control, Restricted-in-Control) or Restricted (Control-in-Restricted, Restricted-in-Restricted) mother. Restricted F1 females were born 10-15% lighter than Controls. Restricted non-pregnant females had shorter femurs, reduced trabecular and cortical bone mineral contents, trabecular density and bone geometry measures determined by peripheral quantitative computed tomography (pQCT) compared to non-pregnant Controls. Pregnancy restored the bone deficits that were present in F1 Restricted females. F2 non-embryo transfer male and female offspring were born of normal weight, while F2 embryo transfer males and females gestated in a Control mother (Control-in-Control, Restricted-in-Control) were heavier at birth compared to offspring gestated in a Restricted mother (Restricted-in-Restricted, Control-in-Restricted). Male F2 Restricted embryo groups (Restricted-in-Control and Restricted-in-Restricted) had accelerated postnatal growth. There was no transmission of bone deficits present at 35days or 6months in F2 offspring. Embryo transfer procedure had confounding effects preventing the separation of maternal environment and germ line contribution to outcomes. Deficits present in F1 non-pregnant Restricted females were absent during late gestation, indicating that pregnant F1 Restricted females experienced gains in bone. These beneficial maternal pregnancy adaptations may have prevented transmission of bone deficits to F2 offspring.