The Consequences of Being Born Small – An Adaptive Perspective

Gluckman, Peter D.; Hanson, Mark A.

doi:10.1159/000091500

Cited by 91 publications

(66 citation statements)

References 106 publications

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“…When there is a mismatch between the preparation for scarcity during fetal life with the relative abundance of calories later, the result is a predisposition for caloric hoarding, childhood fat deposition, and so on. [13][14][15][16] (Maternal smoking, strongly associated with fetal deprivation in the form of intrauterine growth retardation, also contributes to the mismatch. Teen offspring of women who smoked during pregnancy are more likely to be overweight or obese than offspring of women who had never smoked or had quit smoking.…”

Section: Obesogenic Environmentmentioning

confidence: 99%

Obesity and Diabetes in Vulnerable Populations: Reflection on Proximal and Distal Causes

Candib¹

2007

The Annals of Family Medicine

140

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Around the world obesity and diabetes are climbing to epidemic proportion, even in countries previously characterized by scarcity. Likewise, people from low-income and minority communities, as well as immigrants from the developing world, increasingly visit physicians in North America with obesity, metabolic syndrome, or diabetes. Explanations limited to lifestyle factors such as diet and exercise are inadequate to explain the universality of what can be called a syndemic, a complex and widespread phenomenon in population health produced by multiple reinforcing conditions. Underlying the problem are complex factors-genetic, physiological, psychological, familial, social, economic, and political-coalescing to overdetermine these conditions. These interacting factors include events occurring during fetal life, maternal physiology and life context, the thrifty genotype, the nutritional transition, health impact of urbanization and immigration, social attributions and cultural perceptions of increased weight, and changes in food costs and availability resulting from globalization. Better appreciation of the complexity of causation underlying the worldwide epidemic of obesity and diabetes can refocus the work of clinicians and researchers to work at multiple levels to address prevention and treatment for these conditions among vulnerable populations.

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Section: Obesogenic Environmentmentioning

confidence: 99%

Obesity and Diabetes in Vulnerable Populations: Reflection on Proximal and Distal Causes

Candib¹

2007

The Annals of Family Medicine

140

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“…One theory has proposed to explain these findings through the predictive adaptive response (Gluckman & Hanson 2006), which states that the fetus is constantly interpreting the environment created by the maternal milieu and placental function and predicts the environment into which it is likely to be born. However, this prediction can be detrimental when inadequate or excessive nutrients are present following birth.…”

Section: Introductionmentioning

confidence: 99%

Maternal taurine supplementation in rats partially prevents the adverse effects of early-life protein deprivation on β-cell function and insulin sensitivity

Tang¹,

Marchand²,

Lam³

et al. 2013

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Dietary protein restriction during pregnancy and lactation in rats impairs b-cell function and mass in neonates and leads to glucose intolerance in adult offspring. Maternal taurine (Tau) supplementation during pregnancy in rats restores b-cell function and mass in neonates, but its long-term effects are unclear. The prevention of postnatal catch-up growth has been suggested to improve glucose tolerance in adult offspring of low-protein (LP)-fed mothers. The objective of this study was to examine the relative contribution of b-cell dysfunction and insulin resistance to impaired glucose tolerance in 130-day-old rat offspring of LP-fed mothers and the effects of maternal Tau supplementation on b-cell function and insulin resistance in these offspring. Pregnant rats were fed i) control, ii) LP, and iii) LPCTau diets during gestation and lactation. Offspring were given a control diet following weaning. A fourth group consisting of offspring of LP-fed mothers, maintained on a LP diet following weaning, was also studied (LP-all life). Insulin sensitivity in the offspring of LP-fed mothers was reduced in females but not in males. In both genders, LP exposure decreased b-cell function. Tau supplementation improved insulin sensitivity in females and b-cell function in males. The LP-all life diet improved b-cell function in males. We conclude that i) maternal Tau supplementation has persistent effects on improving glucose metabolism (b-cell function and insulin sensitivity) in adult rat offspring of LP-fed mothers and ii) increasing the amount of protein in the diet of offspring adapted to a LP diet after weaning may impair glucose metabolism (b-cell function) in a gender-specific manner.

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“…Importantly, in this regard, in our laboratory, we have a model of maternal protein restriction in Wistar Kyoto (WKY) rats where the IUGR offspring remain smaller throughout life when compared with nongrowth restricted offspring; these offspring also remain normotensive (7). The Thrifty Phenotype hypothesis (4,10,11) predicts that coronary heart disease, type 2 diabetes, stroke, and hypertension manifest because undernutrition during fetal life and infancy initiates altered structure, but disease only manifests when offspring demonstrate catch-up growth in adulthood. We propose that because our IUGR offspring show postnatal growth appropriate to body composition they will be programmed for improved glucose regulation in adulthood as long as catch-up growth does not occur.…”

mentioning

confidence: 99%

IUGR in the Absence of Postnatal “Catch-Up” Growth Leads to Improved Whole Body Insulin Sensitivity in Rat Offspring

et al. 2011

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A suboptimal in utero environment leads to fetal adaptations to ensure short-term survival but in the long-term may lead to disease when the postnatal growth does not reflect that in utero. This study examined the effect of IUGR on whole body insulin sensitivity and metabolic activity in adult rats. Female Wistar-Kyoto rats were fed either a normal protein diet (NPD 20% casein) or a low protein diet (LPD; 8.7% casein) during pregnancy and 2 wk of lactation. In offspring at 32 wk of age, indirect calorimetry and dual energy x-ray absorptiometry (DEXA) were performed to assess metabolic activity and body composition. Insulin sensitivity was assessed using a euglycemic-hyperinsulinemic clamp. At 3 d of age, male and female LPD offspring were 23 and 27% smaller than controls, respectively. They remained significantly smaller throughout the experimental period (ϳ10% smaller at 32 wk). Importantly, there was increased insulin sensitivity in LPD offspring (47% increase in males and 38% increase in females); pancreatic insulin content was normal. Body composition, O 2 consumption, respiratory exchange ratio (RER), and locomotor activity were not different to controls. These findings suggest that in the absence of "catch-up" growth IUGR programs for improved insulin sensitivity. O ver recent years, there has been an escalation in the incidence of metabolic syndrome and type 2 diabetes within the community, and this has been linked to a mismatch in prenatal and postnatal growth (1-3). In this regard, many epidemiological and experimental studies support the hypothesis that a suboptimal in utero environment leads to fetal adaptations to ensure short-term survival but, in turn, lead to long-term disease risk when the postnatal environment does not reflect that in utero (2-4). In addition, IUGR leads to a reduction in prenatal growth and altered ontogeny of major organs, which may also contribute to long-term disease risk (5-8). For example, IUGR, because of maternal protein restriction in rats has been shown to lead to a reduced number of cardiomyocytes in the heart (6), reduced nephron endowment in the kidney (7), and reduced ␤-cell proliferation and islet size in the pancreas (8).Hence, it is likely that altered programming of glucose metabolism coupled with direct reductions in pancreatic islet ␤ cells contribute to the development of metabolic syndrome and type 2 diabetes in infants that were growth restricted in utero, particularly when the postnatal growth trajectory is inappropriately higher than that in utero (9). Although there is substantial evidence to support this hypothesis, whether IUGR can program for improved postnatal glucose metabolism in the absence of "catch-up" growth has been relatively unexplored, and it is imperative that this alternative be rigorously tested. Importantly, in this regard, in our laboratory, we have a model of maternal protein restriction in Wistar Kyoto (WKY) rats where the IUGR offspring remain smaller throughout life when compared with nongrowth restricted offspring; thes...

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The Consequences of Being Born Small – An Adaptive Perspective

Cited by 91 publications

References 106 publications

Obesity and Diabetes in Vulnerable Populations: Reflection on Proximal and Distal Causes

Obesity and Diabetes in Vulnerable Populations: Reflection on Proximal and Distal Causes

Maternal taurine supplementation in rats partially prevents the adverse effects of early-life protein deprivation on β-cell function and insulin sensitivity

IUGR in the Absence of Postnatal “Catch-Up” Growth Leads to Improved Whole Body Insulin Sensitivity in Rat Offspring

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