The role of oxygen in prenatal growth: studies in the chick embryo

Giussani, Dino A.; Salinas, Carlos; Villena, Mercedes; Blanco, Carlos E.

doi:10.1113/jphysiol.2007.141572

Cited by 102 publications

(114 citation statements)

References 26 publications

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“…Some experimental studies of growth under manipulated O 2 are consistent with the WBE expectations; exposure to chronic hypoxia results in a decrease in adult size in some insects (Klok and Harrison 2009;Harrison et al 2010) as well as reduced growth rates in fish (Wang et al 2009), American alligators Alligator mississippiensis (Owerkowicz et al 2009), and embryonic mammals and birds (de Grauw et al 1986;Giussani et al 2007). For many species, processes like growth respond to hypoxia in a threshold manner and only under extreme conditions (Chabot and Dutil 1999;McNatt and Rice 2004).…”

Section: Testing Growth Models I: Changing Environmentssupporting

confidence: 53%

Testing Metabolic Theories

Kearney

White

2012

The American Naturalist

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JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org. abstract: Metabolism is the process by which individual organisms acquire energy and materials from their environment and use them for maintenance, differentiation, growth, and reproduction. There has been a recent push to build an individual-based metabolic underpinning into ecological theory-that is, a metabolic theory of ecology. However, the two main theories of individual metabolism that have been applied in ecology-Kooijman's dynamic energy budget (DEB) theory and the West, Brown, and Enquist (WBE) theoryhave fundamentally different assumptions. Surprisingly, the core assumptions of these two theories have not been rigorously compared from an empirical perspective. Before we can build an understanding of ecology on the basis of individual metabolism, we must resolve the differences between these theories and thus set the appropriate foundation. Here we compare the DEB and WBE theories in detail as applied to ontogenetic growth and metabolic scaling, from which we identify circumstances where their predictions diverge most strongly. Promising experimental areas include manipulative studies of tissue regeneration, body shape, body condition, temperature, and oxygen. Much empirical work designed specifically with DEB and WBE theory in mind is required before any consensus can be reached on the appropriate theoretical basis for a metabolic theory of ecology.

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Section: Testing Growth Models I: Changing Environmentssupporting

confidence: 53%

Testing Metabolic Theories

Kearney

White

2012

The American Naturalist

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“…Animal models of maternal hypoxia recapitulate these findings, demonstrating that IUGR can result from maternal hypoxia (95,96) . Giussani et al initially, using a chick embryo model (97) and subsequently a rat model (98) demonstrated that this IUGR was due to the hypoxia per se, and not maternal malnutrition, as severe hypoxia can result in reduced maternal food intake. Maternal hypoxia has also been shown to programme cardiac dysfunction in these rat and chick embryo models (99,100) , including promotion of fetal cardiac overload, leading to ventricular and aortic wall thickening (101) and endothelial dysfunction (102) .…”

Section: Maternal Hypoxiamentioning

confidence: 99%

The impact of early nutrition on the ageing trajectory

Tarry-Adkins

Ozanne

2014

Proc. Nutr. Soc.

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Epidemiological studies, including those in identical twins, and in individuals in utero during periods of famine have provided robust evidence of strong correlations between low birthweight and subsequent risk of disease in later life, including type 2 diabetes (T2D), CVD, and metabolic syndrome. These and studies in animal models have suggested that the early environment, especially early nutrition, plays an important role in mediating these associations. The concept of early life programming is therefore widely accepted; however the molecular mechanisms by which early environmental insults can have long-term effects on a cell and consequently the metabolism of an organism in later life, are relatively unclear. So far, these mechanisms include permanent structural changes to the organ caused by suboptimal levels of an important factor during a critical developmental period, changes in gene expression caused by epigenetic modifications (including DNA methylation, histone modification and microRNA) and permanent changes in cellular ageing. Many of the conditions associated with early-life nutrition are also those which have an age-associated aetiology. Recently, a common molecular mechanism in animal models of developmental programming and epidemiological studies has been development of oxidative stress and macromolecule damage, specifically DNA damage and telomere shortening. These are phenotypes common to accelerated cellular ageing. Thus, this review will encompass epidemiological and animal models of developmental programming with specific emphasis on cellular ageing and how these could lead to potential therapeutic interventions and strategies which could combat the burden of common age-associated disease, such as T2D and CVD.

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“…Of note, multigenerational highaltitude populations demonstrate protection against the effects of high-altitude hypoxia on fetal growth (14)(15)(16)(17)(18). Experimental studies in animal models support the likelihood that prenatal hypoxia can program cardiac, vascular, and metabolic dysfunction in the adult offspring (19)(20)(21), and that high-altitude ancestry protects against the effect of chronic hypoxic development on fetal growth (22).…”

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confidence: 99%

Graduated effects of high-altitude hypoxia and highland ancestry on birth size

et al. 2013

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Background: We present a cohort of ca. 25,000 birth records from Bolivia of men and women who are currently adults. We used this cohort to test the hypothesis that high altitude reduces birth weight and that highland ancestry confers graduated protection against this effect. Methods: Birth records were obtained from obstetric clinics and hospitals in La Paz (3,600 m) and Santa Cruz (420 m). Only singleton, healthy term (>37 wk) pregnancies of nonsmoking mothers were included. Andean, Mestizo, or European ancestry was determined by validated analysis of parental surnames. results: High altitude reduced body weight (3,396 ± 3 vs. 3,090 ± 6 g) and length (50.8 ± 0 vs. 48.7 ± 0 cm) at birth (P < 0.001). Highland ancestry partially protected against the effects of high altitude on birth weight (Andean = 3,148 ± 15 g; Mestizo = 3,081 ± 6 g; and European = 2,957 ± 32 g; trend P < 0.001) but not on birth length. The effects of high-altitude pregnancy on birth size were similar for male and female babies. conclusion: High altitude reduces birth weight and highland native ancestry confers graduated protection. Given previous studies linking reduced birth weight with increased risk of cardiovascular disease, further study is warranted to test whether adults from high-altitude pregnancy are at increased risk of developing cardiovascular disease.i n addition to the interaction between our genetic makeup and traditional lifestyle risk factors, such as smoking and obesity, it is now accepted that the quality of the environment in prenatal life programs cardiovascular health and the risk of developing heart disease (1). Overwhelming evidence derived from human studies dating back more than two decades and encompassing six continents now links development under suboptimal intrauterine conditions with low birth weight and increased rates of coronary heart disease and the metabolic syndrome (2-8). Epidemiologic studies relating the type of suboptimal intrauterine condition with physiological dysfunction in later life have largely focused on human populations undergoing alterations in maternal nutrition or on human pregnancy affected by maternal psychological stress or by exposure to stress hormones (9-11). This focus on the nutrient supply to the fetus or on maternofetal stress in humans is supported by a large number of investigations in experimental animal models demonstrating that cardiovascular dysfunction in adulthood can be programmed in pregnancy by inappropriate nutrition or by exposure to glucocorticoid excess (1,12,13).In addition to the alterations in maternal nutrition and maternal stress, fetal hypoxia is one of the most common suboptimal conditions in complicated pregnancy. More than 140 million people live at altitudes >2,500 m where lowered oxygen availability has been shown to reduce fetal growth and birth weight, thus comprising the largest single human group at risk for fetal growth restriction. Of note, multigenerational highaltitude populations demonstrate protection against the effects of high-altitude hypoxi...

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The role of oxygen in prenatal growth: studies in the chick embryo

Cited by 102 publications

References 26 publications

Testing Metabolic Theories

Testing Metabolic Theories

The impact of early nutrition on the ageing trajectory

Graduated effects of high-altitude hypoxia and highland ancestry on birth size

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