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Dive into the research topics where Stephanie A. Segovia is active.

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Featured researches published by Stephanie A. Segovia.


BioMed Research International | 2014

Maternal Obesity, Inflammation, and Developmental Programming

Stephanie A. Segovia; Mark H. Vickers; Clint Gray; Clare M. Reynolds

The prevalence of obesity, especially in women of child-bearing age, is a global health concern. In addition to increasing the immediate risk of gestational complications, there is accumulating evidence that maternal obesity also has long-term consequences for the offspring. The concept of developmental programming describes the process in which an environmental stimulus, including altered nutrition, during critical periods of development can program alterations in organogenesis, tissue development, and metabolism, predisposing offspring to obesity and metabolic and cardiovascular disorders in later life. Although the mechanisms underpinning programming of metabolic disorders remain poorly defined, it has become increasingly clear that low-grade inflammation is associated with obesity and its comorbidities. This review will discuss maternal metainflammation as a mediator of programming in insulin sensitive tissues in offspring. Use of nutritional anti-inflammatories in pregnancy including omega 3 fatty acids, resveratrol, curcumin, and taurine may provide beneficial intervention strategies to ameliorate maternal obesity-induced programming.


Nutrients | 2015

Early Life Nutrition and Energy Balance Disorders in Offspring in Later Life

Clare M. Reynolds; Clint Gray; Minglan Li; Stephanie A. Segovia; Mark H. Vickers

The global pandemic of obesity and type 2 diabetes is often causally linked to changes in diet and lifestyle; namely increased intake of calorically dense foods and concomitant reductions in physical activity. Epidemiological studies in humans and controlled animal intervention studies have now shown that nutritional programming in early periods of life is a phenomenon that affects metabolic and physiological functions throughout life. This link is conceptualised as the developmental programming hypothesis whereby environmental influences during critical periods of developmental plasticity can elicit lifelong effects on the health and well-being of the offspring. The mechanisms by which early environmental insults can have long-term effects on offspring remain poorly defined. However there is evidence from intervention studies which indicate altered wiring of the hypothalamic circuits that regulate energy balance and epigenetic effects including altered DNA methylation of key adipokines including leptin. Studies that elucidate the mechanisms behind these associations will have a positive impact on the health of future populations and adopting a life course perspective will allow identification of phenotype and markers of risk earlier, with the possibility of nutritional and other lifestyle interventions that have obvious implications for prevention of non-communicable diseases.


Physiological Reports | 2015

Maternal high fat and/or salt consumption induces sex‐specific inflammatory and nutrient transport in the rat placenta

Clare M. Reynolds; Mark H. Vickers; Claudia J. Harrison; Stephanie A. Segovia; Clint Gray

Maternal high fat and salt consumption are associated with developmental programming of disease in adult offspring. Inadequacies in placental nutrient transport may explain these ‘programmed effects’. Diet‐induced inflammation may have detrimental effects on placental function leading to alteration of key nutrient transporters. We examined the effects of maternal high fat and/or salt diets on markers of placental nutrient transport and inflammation. Sprague–Dawley rats were assigned to (1) control (CD; 1% Salt 10% kcal from fat); (2) high salt (SD; 4% salt, 10% kcal from fat); (3) high fat (HF; 1% Salt 45% kcal from fat) or (4) high fat high salt (HFSD; 4% salt, 45% kcal from fat) 21 days prior to and throughout gestation. At embryonic day 18, dams were killed by isoflurane anesthesia followed by decapitation; placenta/fetuses were weighed, sexed, and collected for molecular analysis. Maternal SD, HF, and HFSD consumption decreased weight of placenta derived from male offspring; however, weight of placenta derived from female offspring was only reduced with maternal HF diet. This was associated with increased expression of LPL, SNAT2, GLUT1, and GLUT4 in placenta derived from male offspring suggesting increased fetal exposure to free fatty acids and glucose. Maternal SD, HF, and HFSD diet consumption increased expression of proinflammatory mediators IL‐1β, TNFα, and CD68 in male placenta. Our results suggest that a proinflammatory placental profile results in detrimental alterations in nutrient transport which may contribute to the developmental origins of cardio‐metabolic disturbances in offspring throughout life.


BioMed Research International | 2015

Developmental Programming of Nonalcoholic Fatty Liver Disease: The Effect of Early Life Nutrition on Susceptibility and Disease Severity in Later Life

Minglan Li; Clare M. Reynolds; Stephanie A. Segovia; Clint Gray; Mark H. Vickers

Nonalcoholic fatty liver disease (NAFLD) is fast becoming the most common liver disease globally and parallels rising obesity rates. The developmental origins of health and disease hypothesis have linked alterations in the early life environment to an increased risk of metabolic disorders in later life. Altered early life nutrition, in addition to increasing risk for the development of obesity, type 2 diabetes, and cardiovascular disease in offspring, is now associated with an increased risk for the development of NAFLD. This review summarizes emerging research on the developmental programming of NAFLD by both maternal obesity and undernutrition with a particular focus on the possible mechanisms underlying the development of hepatic dysfunction and potential strategies for intervention.


Physiological Reports | 2014

High fat and/or high salt intake during pregnancy alters maternal meta‐inflammation and offspring growth and metabolic profiles

Clare M. Reynolds; Mark H. Vickers; Claudia J. Harrison; Stephanie A. Segovia; Clint Gray

A high intake of fat or salt during pregnancy perturbs placental function, alters fetal development, and predisposes offspring to metabolic disease in adult life. Despite its relevance to modern dietary habits, the developmental programming effects of excessive maternal fat and salt, fed in combination, have not been examined. We investigated the effects of moderately high maternal fat and/or salt intake on maternal metainflammation and its consequences on fetal and weanling growth and metabolic profile. Female Sprague–Dawley rats were fed a standard control diet (CD), 4% salt diet (SD), 45% fat diet (HF) or 4% salt/45% fat combined diet (HFSD) 3 weeks prior to and throughout pregnancy and lactation. Plasma and tissue samples were collected at day 18 of pregnancy from mother and fetus, and at postnatal day 24 in weanlings. Markers of adipose tissue inflammation, macrophage infiltration, lipogenesis, nutrient transport, and storage were altered in pregnant dams receiving high‐fat and/or ‐salt diets. This was accompanied by increased fat mass in high‐fat groups and differential hepatic lipid and glucose homeostasis. Offspring of high fat‐fed mothers had reduced fetal weight, displayed catch‐up growth, increased fat mass, and altered metabolic profiles at weaning. Maternal diets high in fat and/or salt affect maternal metabolic parameters, fetal growth and development, metabolic status, and adipoinsular axis in the weanling. Results presented here highlight the importance of diet in expectant mothers or women considering pregnancy. Furthermore, the potential for maternal nutritional intervention strategies may be employed to modify the metabolic disease risk in adult offspring during later life.


Journal of Nutritional Biochemistry | 2015

Maternal supplementation with conjugated linoleic acid in the setting of diet-induced obesity normalises the inflammatory phenotype in mothers and reverses metabolic dysfunction and impaired insulin sensitivity in offspring

Stephanie A. Segovia; Mark H. Vickers; Xiaoyuan D. Zhang; Clint Gray; Clare M. Reynolds

Maternal consumption of a high-fat diet significantly impacts the fetal environment and predisposes offspring to obesity and metabolic dysfunction during adulthood. We examined the effects of a high-fat diet during pregnancy and lactation on metabolic and inflammatory profiles and whether maternal supplementation with the anti-inflammatory lipid conjugated linoleic acid (CLA) could have beneficial effects on mothers and offspring. Sprague-Dawley rats were fed a control (CD; 10% kcal from fat), CLA (CLA; 10% kcal from fat, 1% total fat as CLA), high-fat (HF; 45% kcal from fat) or high fat with CLA (HFCLA; 45% kcal from fat, 1% total fat as CLA) diet ad libitum 10days prior to and throughout gestation and lactation. Dams and offspring were culled at either late gestation (fetal day 20, F20) or early postweaning (postnatal day 24, P24). CLA, HF and HFCLA dams were heavier than CD throughout gestation. Plasma concentrations of proinflammatory cytokines interleukin-1β and tumour necrosis factor-α were elevated in HF dams, with restoration in HFCLA dams. Male and female fetuses from HF dams were smaller at F20 but displayed catch-up growth and impaired insulin sensitivity at P24, which was reversed in HFCLA offspring. HFCLA dams at P24 were protected from impaired insulin sensitivity as compared to HF dams. Maternal CLA supplementation normalised inflammation associated with consumption of a high-fat diet and reversed associated programming of metabolic dysfunction in offspring. This demonstrates that there are critical windows of developmental plasticity in which the effects of an adverse early-life environment can be reversed by maternal dietary interventions.


Scientific Reports | 2015

Maternal salt and fat intake causes hypertension and sustained endothelial dysfunction in fetal, weanling and adult male resistance vessels

Clint Gray; Claudia J. Harrison; Stephanie A. Segovia; Clare M. Reynolds; Mark H. Vickers

Maternal salt and fat intake can independently programme adult cardiovascular status, increasing risk of cardiovascular disease in offspring. Despite its relevance to modern western-style dietary habits, the interaction between increased maternal salt and fat intake has not been examined. Female virgin Sprague-Dawley rats were fed, a standard control diet (CD) (10% kcal fat, 1% NaCl), High-fat diet (HF) (45% kcal fat, 1% NaCl), High-salt diet (SD) (10% kcal fat, 4% NaCl), High-fat high-salt diet (HFSD) (45% kcal fat, 4% NaCl) prior to pregnancy, during pregnancy and throughout lactation. Fetal, weanling and adult vessels were mounted on a pressure myograph at fetal day 18, weaning day 21 and day 135 of adulthood. Increased blood pressure in SD, HFD and HFSD male offspring at day 80 and 135 of age was consistent with perturbed vascular function in fetal, weanling and adult vessels. Maternal salt intake reduced EDHF and calcium-mediated vasodilation, maternal fat reduced NO pathways and maternal fat and salt intake, a combination of the two pathways. Adult offspring cardiovascular disease risk may, in part, relate to vascular adaptations caused by maternal salt and/or fat intake during pregnancy, leading to persistent vascular dysfunction and sustained higher resting blood pressure throughout life.


Biology of Reproduction | 2015

Conjugated Linoleic Acid Supplementation During Pregnancy and Lactation Reduces Maternal High-Fat-Diet-Induced Programming of Early-Onset Puberty and Hyperlipidemia in Female Rat Offspring

Clare M. Reynolds; Stephanie A. Segovia; Xiaohuan D. Zhang; Clint Gray; Mark H. Vickers

ABSTRACT A maternal high-fat (HF) diet during pregnancy and lactation can result in adverse metabolic and reproductive outcomes in female offspring independent of postnatal diet. Interventions during critical windows of developmental plasticity may prevent developmental programming in offspring. The effects of maternal supplementation with the anti-inflammatory lipid conjugated linoleic acid (CLA) on early-onset puberty, metabolic dysfunction, and estrous cycle dysfunction was assessed. Sprague-Dawley rats were randomly assigned to a purified control diet (CD; 10% kcal from fat), CD with CLA (CLA; 10% kcal from fat, 1% CLA), HF (45% kcal from fat) or HF with CLA (HFCLA; 45% kcal from fat, 1% CLA). Diets were fed ad libitum for 10 days prior to time mating and throughout gestation and lactation. Offspring plasma/tissues were taken at Day 24 (prepubertal) or Day 150 (adult). Puberty was assessed from Day 26 and estrous cycle from Day 128. Female offspring from HF mothers had lower birth weights but by Postnatal Day 24 had exhibited catch-up growth concomitant with increased fat mass, hyperleptinemia, and dyslipidemia. Maternal CLA supplementation reversed these effects. Early-onset puberty was only observed in HF offspring; this was reversed in HFCLA offspring. In adulthood, despite no evidence of glucose intolerance or altered insulin sensitivity, HF offspring displayed increased fat mass, dyslipidemia, disrupted estrous cyclicity. and hyperleptinemia; this was reversed by maternal CLA supplementation. Data presented in this study demonstrate the importance of diet in women of reproductive age and during pregnancy on reproductive and metabolic parameters in their offspring and that supplementation with CLA during critical windows of development may represent a therapeutic strategy in the prevention of early-life programming of metabolic and reproductive dysfunction.


American Journal of Physiology-regulatory Integrative and Comparative Physiology | 2016

Maternal conjugated linoleic acid supplementation reverses high-fat diet induced skeletal muscle atrophy and inflammation in adult male rat offspring

Chantal A. Pileggi; Stephanie A. Segovia; James F. Markworth; Clint Gray; Xiaoyuan D. Zhang; Amber M. Milan; Cameron J. Mitchell; Matthew Philip Greig Barnett; Nicole C. Roy; Mark H. Vickers; Clare M. Reynolds; David Cameron-Smith

A high-saturated-fat diet (HFD) during pregnancy and lactation leads to metabolic disorders in offspring concomitant with increased adiposity and a proinflammatory phenotype in later life. During the fetal period, the impact of maternal diet on skeletal muscle development is poorly described, despite this tissue exerting a major influence on life-long metabolic health. This study investigated the effect of a maternal HFD on skeletal muscle anabolic, catabolic, and inflammatory signaling in adult rat offspring. Furthermore, the actions of maternal-supplemented conjugated linoleic acid (CLA) on these measures of muscle phenotype were investigated. A purified control diet (CD; 10% kcal fat), a CD supplemented with CLA (CLA; 10% kcal fat, 1% total fat as CLA), a high-fat (HFD; 45% kcal fat from lard), or a HFD supplemented with CLA (HFCLA; 45% kcal fat from lard, 1% total fat as CLA) was fed ad libitum to female Sprague-Dawley rats for 10 days before mating and throughout gestation and lactation. Male offspring received a standard chow diet from weaning, and the gastrocnemius was collected for analysis at day 150. Offspring from HF and HFCLA mothers displayed lower muscular protein content accompanied by elevated monocyte chemotactic protein-1, IL-6, and IL-1β concentrations. Phosphorylation of NF-κBp65 (Ser(536)) and expression of the catabolic E3 ligase muscle ring finger 1 (MuRF1) were increased in HF offspring, an effect reversed by maternal CLA supplementation. The present study demonstrates the importance of early life interventions to ameliorate the negative effects of poor maternal diet on offspring skeletal muscle development.


American Journal of Physiology-regulatory Integrative and Comparative Physiology | 2016

Oxidized fish oil in rat pregnancy causes high newborn mortality and increases maternal insulin resistance

Benjamin B. Albert; Mark H. Vickers; Clint Gray; Clare M. Reynolds; Stephanie A. Segovia; José G. B. Derraik; Paul Lewandowski; Manohar L. Garg; David Cameron-Smith; Paul Hofman; Wayne S. Cutfield

Fish oil is commonly taken by pregnant women, and supplements sold at retail are often oxidized. Using a rat model, we aimed to assess the effects of supplementation with oxidized fish oil during pregnancy in mothers and offspring, focusing on newborn viability and maternal insulin sensitivity. Female rats were allocated to a control or high-fat diet and then mated. These rats were subsequently randomized to receive a daily gavage treatment of 1 ml of unoxidized fish oil, a highly oxidized fish oil, or control (water) throughout pregnancy. At birth, the gavage treatment was stopped, but the same maternal diets were fed ad libitum throughout lactation. Supplementation with oxidized fish oil during pregnancy had a marked adverse effect on newborn survival at day 2, leading to much greater odds of mortality than in the control (odds ratio 8.26) and unoxidized fish oil (odds ratio 13.70) groups. In addition, maternal intake of oxidized fish oil during pregnancy led to increased insulin resistance at the time of weaning (3 wks after exposure) compared with control dams (HOMA-IR 2.64 vs. 1.42; P = 0.044). These data show that the consumption of oxidized fish oil is harmful in rat pregnancy, with deleterious effects in both mothers and offspring.

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Clint Gray

University of Auckland

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