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Search Results: 1 - 10 of 220659 matches for " Peter D Gluckman "
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Migrating Ovaries: Early Life Influences on Later Gonadal Function
Peter D Gluckman ,Alan S Beedle
PLOS Medicine , 2007, DOI: 10.1371/journal.pmed.0040190
Correction: Migrating Ovaries: Early Life Influences on Later Gonadal Function
Peter D Gluckman,Alan S Beedle
PLOS Medicine , 2007, DOI: 10.1371/journal.pmed.0040226
Developmental origins of health and disease: reducing the burden of chronic disease in the next generation
Peter D Gluckman, Mark A Hanson, Murray D Mitchell
Genome Medicine , 2010, DOI: 10.1186/gm135
Abstract: The concept of developmental origins of health and disease is predicated upon the assumption that environmental factors acting early in life (usually in fetal life) have profound effects on vulnerability to disease later in life, often in adulthood. The range of experimental, clinical and epidemiological data linking conditions in early life to later health is now overwhelming [1]. Initially, the focus was on a small fraction of children -those who were born small - but it is now clear that the environment impacts on the development of every child [2]. Observations and experimental approaches have generally considered nutritional changes or, classically, alterations in glucocorticosteroid exposure, reflecting the critical maturational events linked to such events. Indeed, the placenta is in a critical position to cause or modify such challenges by altering nutritional transport functions or the pattern and nature of endocrine signals impacting the fetus. Nor does the story end at birth, because epigenetic development can be influenced by how the infant is fed, and perhaps how its gut is colonized with commensal bacteria.Yet there has been considerable resistance to these ideas. Medicine is replete with reductionist biomedical thinking and this has, in some ways, limited not only our understanding but also our ability to address the challenge of some contemporary health problems. Nowhere is this clearer than in the outcomes of genome-wide association studies where, despite substantial investment, only a relatively small proportion of risk of common non-communicable diseases (NCDs) - such as cardiovascular disease and diabetes - is explained [3]. The economic and humanitarian costs of NCDs are enormous in both the developed and the developing world, and indeed they may destabilize the economies of low-income countries where recent data show that risk markers for these diseases become evident early in the process of socioeconomic improvement, and well below the level o
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.
Developmental origins of non-communicable disease: Implications for research and public health
Robert Barouki, Peter D Gluckman, Philippe Grandjean, Mark Hanson, Jerrold J Heindel
Environmental Health , 2012, DOI: 10.1186/1476-069x-11-42
Abstract: For many years biologists considered the developmental period to be controlled by a strict, hard-wired genetic program, and thus it was uncertain how it could be influenced by the environment. It is now clear that development is plastic, and that it allows the organism to respond to the surrounding environment, especially during early development when cells are differentiating and tissues are developing. This capacity is based on molecular pathways that lead to control of gene expression and induction of specific phenotypes in the absence of DNA sequence modification [1]. These pathways, as currently understood, include DNA methylation, histone covalent modification, and noncoding RNA expression. Such epigenetic modifications can be passed from one cell generation to the next and, in some cases, when germ cells are targeted, can be transgenerationally transmitted [2]. Furthermore, these changes can be cell, tissue, and sex specific, and time dependent. In many cases they may not be apparent during a latent period which may last from months to years or decades. Thus, each individual has one genome, but will hold multiple epigenomes.The ability to respond to environmental conditions can be evolutionarily advantageous by allowing fine-tuning of gene expression, likely through epigenetic mechanisms [3]. Thus, developmentally plastic processes allow the organism to adapt to changing environments in order to maintain or improve reproductive capability in part by sustaining health through the reproductive period. However, interference with these developmentally-adaptive processes may also have adverse consequences on some functions and disease risks later in life. Furthermore, these mechanisms are also sensitive to environmental stimuli other than the nutrients and physiological factors that are normative, in evolutionary terms, to the human environment. Indeed, drugs, industrial chemicals, tobacco smoke, and other environmental exposures can affect these same mechanisms l
Progressive, Transgenerational Changes in Offspring Phenotype and Epigenotype following Nutritional Transition
Graham C. Burdge,Samuel P. Hoile,Tobias Uller,Nicola A. Thomas,Peter D. Gluckman,Mark A. Hanson,Karen A. Lillycrop
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0028282
Abstract: Induction of altered phenotypes during development in response to environmental input involves epigenetic changes. Phenotypic traits can be passed between generations by a variety of mechanisms, including direct transmission of epigenetic states or by induction of epigenetic marks de novo in each generation. To distinguish between these possibilities we measured epigenetic marks over four generations in rats exposed to a sustained environmental challenge. Dietary energy was increased by 25% at conception in F0 female rats and maintained at this level to generation F3. F0 dams showed higher pregnancy weight gain, but lower weight gain and food intake during lactation than F1 and F2 dams. On gestational day 8, fasting plasma glucose concentration was higher and β-hydroxybutyrate lower in F0 and F1 dams than F2 dams. This was accompanied by decreased phosphoenolpyruvate carboxykinase (PEPCK) and increased PPARα and carnitine palmitoyl transferase-1 mRNA expression. PEPCK mRNA expression was inversely related to the methylation of specific CpG dinucleotides in its promoter. DNA methyltransferase (Dnmt) 3a2, but not Dnmt1 or Dnmt3b, expression increased and methylation of its promoter decreased from F1 to F3 generations. These data suggest that the regulation of energy metabolism during pregnancy and lactation within a generation is influenced by the maternal phenotype in the preceding generation and the environment during the current pregnancy. The transgenerational effects on phenotype were associated with altered DNA methylation of specific genes in a manner consistent with induction de novo of epigenetic marks in each generation.
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
Tissue-Specific 5′ Heterogeneity of PPARα Transcripts and Their Differential Regulation by Leptin
Emma S. Garratt, Mark H. Vickers, Peter D. Gluckman, Mark A. Hanson, Graham C. Burdge, Karen A. Lillycrop
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0067483
Abstract: The genes encoding nuclear receptors comprise multiple 5′untranslated exons, which give rise to several transcripts encoding the same protein, allowing tissue-specific regulation of expression. Both human and mouse peroxisome proliferator activated receptor (PPAR) α genes have multiple promoters, although their function is unknown. Here we have characterised the rat PPARα promoter region and have identified three alternative PPARα transcripts, which have different transcription start sites owing to the utilisation of distinct first exons. Moreover these alternative PPARα transcripts were differentially expressed between adipose tissue and liver. We show that while the major adipose (P1) and liver (P2) transcripts were both induced by dexamethasone, they were differentially regulated by the PPARα agonist, clofibric acid, and leptin. Leptin had no effect on the adipose-specific P1 transcript, but induced liver-specific P2 promoter activity via a STAT3/Sp1 mechanism. Moreover in Wistar rats, leptin treatment between postnatal day 3–13 led to an increase in P2 but not P1 transcription in adipose tissue which was sustained into adulthood. This suggests that the expression of the alternative PPARα transcripts are in part programmed by early life exposure to leptin leading to persistent change in adipose tissue fatty acid metabolism through specific activation of a quiescent PPARα promoter. Such complexity in the regulation of PPARα may allow the expression of PPARα to be finely regulated in response to environmental factors.
Population Differences in Brain Morphology and Microstructure among Chinese, Malay, and Indian Neonates
Jordan Bai, Muhammad Farid Abdul-Rahman, Anne Rifkin-Graboi, Yap-Seng Chong, Kenneth Kwek, Seang-Mei Saw, Keith M. Godfrey, Peter D. Gluckman, Marielle V. Fortier, Michael J. Meaney, Anqi Qiu
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0047816
Abstract: We studied a sample of 75 Chinese, 73 Malay, and 29 Indian healthy neonates taking part in a cohort study to examine potential differences in neonatal brain morphology and white matter microstructure as a function of ethnicity using both structural T2-weighted magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI). We first examined the differences in global size and morphology of the brain among the three groups. We then constructed the T2-weighted MRI and DTI atlases and employed voxel-based analysis to investigate ethnic differences in morphological shape of the brain from the T2-weighted MRI, and white matter microstructure measured by fractional anisotropy derived from DTI. Compared with Malay neonates, the brains of Indian neonates’ tended to be more elongated in anterior and posterior axis relative to the superior-inferior axis of the brain even though the total brain volume was similar among the three groups. Although most anatomical regions of the brain were similar among Chinese, Malay, and Indian neonates, there were anatomical variations in the spinal-cerebellar and cortical-striatal-thalamic neural circuits among the three populations. The population-related brain regions highlighted in our study are key anatomical substrates associated with sensorimotor functions.
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