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Search Results: 1 - 10 of 402901 matches for " Deborah M Sloboda "
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Prenatal nutritional influences on obesity risk in offspring
Mark H Vickers, Deborah M Sloboda
Nutrition and Dietary Supplements , 2010, DOI: http://dx.doi.org/10.2147/NDS.S8555
Abstract: enatal nutritional influences on obesity risk in offspring Review (4830) Total Article Views Authors: Mark H Vickers, Deborah M Sloboda Published Date December 2010 Volume 2010:2 Pages 137 - 149 DOI: http://dx.doi.org/10.2147/NDS.S8555 Mark H Vickers, Deborah M Sloboda Liggins Institute and the National Research Centre for Growth and Development, University of Auckland. Auckland, New Zealand Abstract: The incidence of obesity and overweight has almost doubled in Western societies over the last 2 decades, a trend mirrored in developing nations transitioning to first-world economies. Obesity is strongly associated with the comorbidities of type 2 diabetes, hypertension, and heart disease and represents an enormous burden to health care systems. Of even more concern is the increase of around 40% in the prevalence of childhood obesity and type 2 diabetes over the last 20 years. Metabolic disease results from complex interactions of many factors, including genetic, physiologic, behavioral, and environmental influences. The recent rate at which these diseases have increased suggests that environmental, eg, epigenetic, and behavioral influences, rather than genetic causes, are fuelling the present epidemic. In this context, the developmental origins of health and disease hypothesis has highlighted the link between periconceptual, fetal, and early infant phases of life and the subsequent development of adult obesity and related metabolic disorders. Both maternal undernutrition (global and targeted) and maternal obesity elicit an obese offspring phenotype. This review will examine the role of altered maternal nutrition on obesity risk in offspring, the interactions with the postnatal nutritional environment, the possible strategies for intervention, and the role of epigenetics in the disease process.
Effects of Taurine Supplementation on Hepatic Markers of Inflammation and Lipid Metabolism in Mothers and Offspring in the Setting of Maternal Obesity
Minglan Li, Clare M. Reynolds, Deborah M. Sloboda, Clint Gray, Mark H. Vickers
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0076961
Abstract: Maternal obesity is associated with obesity and metabolic disorders in offspring. However, intervention strategies to reverse or ameliorate the effects of maternal obesity on offspring health are limited. Following maternal undernutrition, taurine supplementation can improve outcomes in offspring, possibly via effects on glucose homeostasis and insulin secretion. The effects of taurine in mediating inflammatory processes as a protective mechanism has not been investigated. Further, the efficacy of taurine supplementation in the setting of maternal obesity is not known. Using a model of maternal obesity, we examined the effects of maternal taurine supplementation on outcomes related to inflammation and lipid metabolism in mothers and neonates. Time-mated Wistar rats were randomised to either: 1) control : control diet during pregnancy and lactation (CON); 2) CON supplemented with 1.5% taurine in drinking water (CT); 3) maternal obesogenic diet (high fat, high fructose) during pregnancy and lactation (MO); or 4) MO supplemented with taurine (MOT). Maternal and neonatal weights, plasma cytokines and hepatic gene expression were analysed. A MO diet resulted in maternal hyperinsulinemia and hyperleptinemia and increased plasma glucose, glutamate and TNF-α concentrations. Taurine normalised maternal plasma TNF-α and glutamate concentrations in MOT animals. Both MO and MOT mothers displayed evidence of fatty liver accompanied by alterations in key markers of hepatic lipid metabolism. MO neonates displayed a pro-inflammatory hepatic profile which was partially rescued in MOT offspring. Conversely, a pro-inflammatory phenotype was observed in MOT mothers suggesting a possible maternal trade-off to protect the neonate. Despite protective effects of taurine in MOT offspring, neonatal mortality was increased in CT neonates, indicating possible adverse effects of taurine in the setting of normal pregnancy. These data suggest that maternal taurine supplementation may ameliorate the adverse effects observed in offspring following a maternal obesogenic diet but these effects are dependent upon prior maternal nutritional background.
Timing of Maternal Exposure to a High Fat Diet and Development of Obesity and Hyperinsulinemia in Male Rat Offspring: Same Metabolic Phenotype, Different Developmental Pathways?
Graham J. Howie,Deborah M. Sloboda,Clare M. Reynolds,Mark H. Vickers
Journal of Nutrition and Metabolism , 2013, DOI: 10.1155/2013/517384
Abstract: Objective. Offspring born to mothers either fed an obesogenic diet throughout their life or restricted to pregnancy and lactation demonstrate obesity, hyperinsulinemia, and hyperleptinemia, irrespective of their postweaning diet. We examined whether timing of a maternal obesogenic diet results in differential regulation of pancreatic adipoinsular and inflammatory signaling pathways in offspring. Methods. Female Wistar rats were randomized into 3 groups: (1) control (CONT): fed a control diet preconceptionally and during pregnancy and lactation; (2) maternal high fat (MHF): fed an HF diet throughout their life and during pregnancy and lactation; (3) pregnancy and lactation HF (PLHF): fed a control diet throughout life until mating, then HF diet during pregnancy and lactation. Male offspring were fed the control diet postweaning. Plasma and pancreatic tissue were collected, and mRNA concentrations of key factors regulating adipoinsular axis signaling were determined. Results. MHF and PLHF offspring exhibited increased adiposity and were hyperinsulinemic and hyperleptinemic compared to CONT. Despite a similar anthropometric phenotype, MHF and PLHF offspring exhibited distinctly different expression for key pancreatic genes, dependent upon maternal preconceptional nutritional background. Conclusions. These data suggest that despite using differential signaling pathways, obesity in offspring may be an adaptive outcome of early life exposure to HF during critical developmental windows. 1. Introduction Early life events contribute substantially to the likelihood of an individual becoming obese, although underlying mechanisms are not well understood. Obesity in women of reproductive age (15 to 44 years) is increasing rapidly, and up to 50% of women in this age range in the USA are now either overweight or obese [1]. This has translated to an exponential increase in the prevalence of obesity during pregnancy with up to 20% of women entering pregnancy with a BMI which would define them as obese [2]. Obesity in pregnancy increases the risks for complications of pregnancy including miscarriage, hypertension, and gestational diabetes [3–5]. Furthermore, it is now well established that maternal obesity leads to an increased risk of obesity and metabolic and cardiovascular disorders in offspring [6–9]. In view of the rising prevalence of obesity in pregnancy and its association with adverse maternal and offspring outcomes, there is a great deal of interest in understanding the mechanistic pathways that link maternal obesity and excess maternal nutrition to increased
Impaired Perinatal Growth and Longevity: A Life History Perspective
Deborah M. Sloboda,Alan S. Beedle,Cinda L. Cupido,Peter D. Gluckman,Mark H. Vickers
Current Gerontology and Geriatrics Research , 2009, DOI: 10.1155/2009/608740
Abstract: Life history theory proposes that early-life cues induce highly integrated responses in traits associated with energy partitioning, maturation, reproduction, and aging such that the individual phenotype is adaptively more appropriate to the anticipated environment. Thus, maternal and/or neonatally derived nutritional or endocrine cues suggesting a threatening environment may favour early growth and reproduction over investment in tissue reserve and repair capacity. These may directly affect longevity, as well as prioritise insulin resistance and capacity for fat storage, thereby increasing susceptibility to metabolic dysfunction and obesity. These shifts in developmental trajectory are associated with long-term expression changes in specific genes, some of which may be underpinned by epigenetic processes. This normative process of developmental plasticity may prove to be maladaptive in human environments in transition towards low extrinsic mortality and energy-dense nutrition, leading to the development of an inappropriate phenotype with decreased potential for longevity and/or increased susceptibility to metabolic disease.
Pre- and Postnatal Nutritional Histories Influence Reproductive Maturation and Ovarian Function in the Rat
Deborah M. Sloboda, Graham J. Howie, Anthony Pleasants, Peter D. Gluckman, Mark H. Vickers
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0006744
Abstract: Background While prepubertal nutritional influences appear to play a role in sexual maturation, there is a need to clarify the potential contributions of maternal and childhood influences in setting the tempo of reproductive maturation. In the present study we employed an established model of nutritional programming to evaluate the relative influences of prenatal and postnatal nutrition on growth and ovarian function in female offspring. Methods Pregnant Wistar rats were fed either a calorie-restricted diet, a high fat diet, or a control diet during pregnancy and/or lactation. Offspring then were fed either a control or a high fat diet from the time of weaning to adulthood. Pubertal age was monitored and blood samples collected in adulthood for endocrine analyses. Results We report that in the female rat, pubertal timing and subsequent ovarian function is influenced by the animal's nutritional status in utero, with both maternal caloric restriction and maternal high fat nutrition resulting in early pubertal onset. Depending on the offspring's nutritional history during the prenatal and lactational periods, subsequent nutrition and body weight gain did not further influence offspring reproductive tempo, which was dominated by the effect of prenatal nutrition. Whereas maternal calorie restriction leads to early pubertal onset, it also leads to a reduction in adult progesterone levels later in life. In contrast, we found that maternal high fat feeding which also induces early maturation in offspring was associated with elevated progesterone concentrations. Conclusions These observations are suggestive of two distinct developmental pathways leading to the acceleration of pubertal timing but with different consequences for ovarian function. We suggest different adaptive explanations for these pathways and for their relationship to altered metabolic homeostasis.
Offspring of Mothers Fed a High Fat Diet Display Hepatic Cell Cycle Inhibition and Associated Changes in Gene Expression and DNA Methylation
Kevin J. Dudley, Deborah M. Sloboda, Kristin L. Connor, Jacques Beltrand, Mark H. Vickers
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0021662
Abstract: The association between an adverse early life environment and increased susceptibility to later-life metabolic disorders such as obesity, type 2 diabetes and cardiovascular disease is described by the developmental origins of health and disease hypothesis. Employing a rat model of maternal high fat (MHF) nutrition, we recently reported that offspring born to MHF mothers are small at birth and develop a postnatal phenotype that closely resembles that of the human metabolic syndrome. Livers of offspring born to MHF mothers also display a fatty phenotype reflecting hepatic steatosis and characteristics of non-alcoholic fatty liver disease. In the present study we hypothesised that a MHF diet leads to altered regulation of liver development in offspring; a derangement that may be detectable during early postnatal life. Livers were collected at postnatal days 2 (P2) and 27 (P27) from male offspring of control and MHF mothers (n = 8 per group). Cell cycle dynamics, measured by flow cytometry, revealed significant G0/G1 arrest in the livers of P2 offspring born to MHF mothers, associated with an increased expression of the hepatic cell cycle inhibitor Cdkn1a. In P2 livers, Cdkn1a was hypomethylated at specific CpG dinucleotides and first exon in offspring of MHF mothers and was shown to correlate with a demonstrable increase in mRNA expression levels. These modifications at P2 preceded observable reductions in liver weight and liver:brain weight ratio at P27, but there were no persistent changes in cell cycle dynamics or DNA methylation in MHF offspring at this time. Since Cdkn1a up-regulation has been associated with hepatocyte growth in pathologic states, our data may be suggestive of early hepatic dysfunction in neonates born to high fat fed mothers. It is likely that these offspring are predisposed to long-term hepatic dysfunction.
Maternal Undernutrition Significantly Impacts Ovarian Follicle Number and Increases Ovarian Oxidative Stress in Adult Rat Offspring
Angelica B. Bernal,Mark H. Vickers,Mark B. Hampton,Rebecca A. Poynton,Deborah M. Sloboda
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0015558
Abstract: We have shown recently that maternal undernutrition (UN) advanced female pubertal onset in a manner that is dependent upon the timing of UN. The long-term consequence of this accelerated puberty on ovarian function is unknown. Recent findings suggest that oxidative stress may be one mechanism whereby early life events impact on later physiological functioning. Therefore, using an established rodent model of maternal UN at critical windows of development, we examined maternal UN-induced changes in offspring ovarian function and determined whether these changes were underpinned by ovarian oxidative stress.
Developmental Origins of Health and Disease
Simon C. Langley-Evans,Barbara Alexander,Harry J. McArdle,Deborah M. Sloboda
Journal of Nutrition and Metabolism , 2012, DOI: 10.1155/2012/838640
Developmental Origins of Health and Disease
Simon C. Langley-Evans,Barbara Alexander,Harry J. McArdle,Deborah M. Sloboda
Journal of Nutrition and Metabolism , 2012, DOI: 10.1155/2012/838640
Gene expression profiling in the Cynomolgus macaque Macaca fascicularis shows variation within the normal birth range
Bright Emerald, Keefe Chng, Shinya Masuda, Deborah M Sloboda, Mark H Vickers, Ravi Kambadur, Peter D Gluckman
BMC Genomics , 2011, DOI: 10.1186/1471-2164-12-509
Abstract: To explore this further, we utilised a non-human primate model Macaca fascicularis (Cynomolgus macaque) which shares with humans the same progressive history of the metabolic syndrome. Using microarray we compared tissues from neonates in the average birth weight (50-75th centile) to those of lower birth weight (5-25th centile) and studied the effect of different growth trajectories within the normal range on gene expression levels in the umbilical cord, neonatal liver and skeletal muscle.We identified 1973 genes which were differentially expressed in the three tissue types between average and low birth weight animals (P < 0.05). Gene ontology analysis identified that these genes were involved in metabolic processes including cellular lipid metabolism, cellular biosynthesis, cellular macromolecule synthesis, cellular nitrogen metabolism, cellular carbohydrate metabolism, cellular catabolism, nucleotide and nucleic acid metabolism, regulation of molecular functions, biological adhesion and development.These differences in gene expression levels between animals in the upper and lower percentiles of the normal birth weight range may point towards early life metabolic adaptations that in later life result in differences in disease risk.Clinical, experimental and epidemiological studies have highlighted a link between the early-life environment and the health and well-being of offspring in later life. An adverse maternal environment has been linked to an increased risk of developing metabolic and cardiovascular disorders including type 2 diabetes, obesity, hyperlipidemia, insulin resistance and hypertension [1-7]. An important feature of these studies is that these relationships exist within the normative birth range and do not depend on extremes of birth weight. This has led to the proposal that later life disease risk is the result of maladaptive consequences of plastic mechanisms which would normally be adaptive [8,9].It is proposed that developmental plasticity deter
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