Prenatal Programming of Childhood Overweight and Obesity

Huang, Jenny; Lee, Tiffany A.; Lu, Michael C.

doi:10.1007/s10995-006-0141-8

Cited by 144 publications

(105 citation statements)

References 64 publications

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“…It has been shown that protein malnutrition during gestation and/or lactation provokes alterations in metabolism when animals or humans reach adulthood. Those observations have supported Barker's or the 'Thrifty phenotype' hypothesis, which postulates that undernutrition during pregnancy imposes metabolic changes in the fetus that will be shifted to a permanent economic metabolism, including in adult life (Hales & Barker 2001); however, if the baby is exposed to a nutritional abundance after birth, the metabolic syndrome is generated, as reported for several experimental models (Vickers et al 2005, Velkoska et al 2008, Bol et al 2009) and epidemiological data from humans who underwent famine early in life (Ravelli et al 1976, Huang et al 2007). This phenomenon is also known as metabolic programming or metabolic imprinting.…”

Section: Introductionmentioning

confidence: 58%

Poor pubertal protein nutrition disturbs glucose-induced insulin secretion process in pancreatic islets and programs rats in adulthood to increase fat accumulation

Oliveira¹,

Lisboa²,

Moura³

et al. 2012

Journal of Endocrinology

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Similar to gestation/lactation, puberty is also a critical phase in which neuronal connections are still being produced and during which metabolic changes may occur if nutrition is disturbed. In the present study we aimed to determine whether peripubertal protein restriction induces metabolic programming. Thirty-day-old male rats were fed either a low protein (LP group) diet (4% w/w protein) or a normal protein (NP group) diet (23%) until 60 days of age, when they received the NP diet until they were 120 days old. Body weight (BW), food intake, fat tissue accumulation, glucose tolerance, and insulin secretion were evaluated. The nerve electrical activity was recorded to evaluate autonomous nervous system (ANS) function. Adolescent LP rats presented hypophagia and lower BW gain during the LP diet treatment (P!0.001). However, the food intake and BW gain by the LP rats were increased (P!0.001) after the NP diet was resumed. The LP rats presented mild hyperglycemia, hyperinsulinemia, severe hyperleptinemia upon fasting, peripheral insulin resistance and increased fat tissue accumulation and vagus nerve activity (P!0.05). Glucoseinduced insulin secretion was greater in the LP islets than in the NP islets; however, the cholinergic response was decreased (P!0.05). Compared with the islets from the NP rats, the LP islets showed changes in the activity of muscarinic receptors (P!0.05); in addition, the inhibition of glucose-induced insulin secretion by epinephrine was attenuated (P!0.001). Protein restriction during adolescence caused high-fat tissue accumulation in adult rats. Islet dysfunction could be related to an ANS imbalance.

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Section: Introductionmentioning

confidence: 58%

Poor pubertal protein nutrition disturbs glucose-induced insulin secretion process in pancreatic islets and programs rats in adulthood to increase fat accumulation

Oliveira¹,

Lisboa²,

Moura³

et al. 2012

Journal of Endocrinology

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“…81 However, those authors included only 8 studies of the 14 that we evaluated, primarily those with simultaneous collection of exposure and outcome data and with clinical height and weight measurement, did not calculate a pooled effect size, and did not consider publication bias. This present study overcomes these limitations and allows for an estimation of the public health impact on overweight risk resulting from maternal prenatal smoking.…”

Section: Discussionmentioning

confidence: 99%

Maternal smoking during pregnancy and child overweight: systematic review and meta-analysis

2007

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Objective: Perform a systematic review of studies reporting on the association between maternal prenatal cigarette smoking and child overweight. Design: Meta-analysis of observational studies. Data sources: Medline search and review of reference lists among studies published through June 2006. Review methods: Included studies reported an association between maternal smoking during pregnancy and risk of overweight among children at least 2 years of age. We did not include in the meta-analysis studies that provided only a continuous measure of adiposity, although those studies are discussed separately. Results: Based on results of 84 563 children reported in 14 observational studies, children whose mothers smoked during pregnancy were at elevated risk for overweight (pooled adjusted odds ratio (OR) 1.50, 95% CI: 1.36, 1.65) at ages 3-33 years, compared with children whose mothers did not smoke during pregnancy. The pooled estimate from unadjusted odds ratios (OR 1.52, 95% CI: 1.36, 1.69) was similar to the adjusted estimate, suggesting that sociodemographic and behavioral differences between smokers and nonsmokers did not explain the observed association. Although we observed evidence for publication bias, simulating a symmetric set of studies yielded a similar estimate (OR 1.40, 95% CI: 1.26, 1.55). Conclusions:Prenatal smoking exposure appears to increase rates of overweight in childhood. In parts of the world undergoing the epidemiologic transition, the continuing increase in smoking among young women could contribute to spiraling increases in rates of obesity-related health outcomes in the 21st century.

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“…Fetal overnutrition, evidenced by large infant birth weight for gestational age, is a strong predictor of obesity in childhood and later life (59)(60)(61). A caveat is that, while large infant birth weight for gestational age is generally an indicator of excess fat mass, it may also reflect other growth parameters such that a subset of large infant birth weight for gestational age infants may have increased lean mass (62,63).…”

Section: Prenatal and Postnatal Influencesmentioning

confidence: 99%

Biological, environmental, and social influences on childhood obesity

2015

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The prevalence of childhood obesity has increased globally over the past three decades, with evidence of recent leveling off in developed countries. Reduction in the, currently high, prevalence of obesity will require a full understanding of the biological and social pathways to obesity in order to develop appropriately targeted prevention strategies in early life. Determinants of childhood obesity include individual level factors, including biological, social, and behavioral risks, acting within the influence of the child's family environment, which is, in turn, imbedded in the context of the community environment. These influences act across childhood, with suggestions of early critical periods of biological and behavioral plasticity. There is evidence of sex and gender differences in the responses of boys and girls to their environments. The evidence that determinants of childhood obesity act at many levels and at different stages of childhood is of policy relevance to those planning early health promotion and primary prevention programs as it suggests the need to address the individual, the family, the physical environment, the social environment, and social policy. The purpose of this narrative review is to summarize current, and emerging, literature in a multilevel, life course framework. INTRODUCTIONThe prevalence of childhood obesity has increased globally over the past three decades, with more rapid increases recently occurring in low-income countries (1). In the United States, more than 30% of children are now overweight or obese (1), with evidence that the prevalence has leveled off (2). Children and adolescents are exhibiting obesity-related conditions such as type 2 diabetes, elevated blood pressure, low-density lipoprotein cholesterol, and higher fasting insulin levels (3-6). In addition, childhood obesity predicts adulthood obesity and its known health consequences (7,8). Treatment of obesity is notoriously difficult, with weight loss rarely sustained in adults (9). Therapeutic interventions in childhood are somewhat more successful, particularly if the intervention occurs prior to onset of puberty (10). However, real and sustained progress in combating the obesity epidemic will require a full understanding of the biological and social pathways to obesity in order to develop appropriately targeted prevention strategies in early life.Pathways to childhood obesity are complex. It is therefore helpful to discuss determinants of obesity within a conceptual framework. A multilevel conceptual model, Bronfenbrenner's Bioecological Systems Theory (11), has previously been applied to the conceptualization of childhood obesity by Davison and Birch (12). This framework depicts individual-level factors, including biological, social, and behavioral risks, as acting within the influence of the child's family environment, which is, in turn imbedded in the context of the community environment. It is also helpful to consider critical periods for obesity risk and, as will be further illustrated in a later section,...

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Prenatal Programming of Childhood Overweight and Obesity

Abstract: Our review supports prenatal programming of childhood overweight and obesity. MCH research, practice, and policy need to consider the prenatal period a window of opportunity for obesity prevention.

Cited by 144 publications

References 64 publications

Poor pubertal protein nutrition disturbs glucose-induced insulin secretion process in pancreatic islets and programs rats in adulthood to increase fat accumulation

Poor pubertal protein nutrition disturbs glucose-induced insulin secretion process in pancreatic islets and programs rats in adulthood to increase fat accumulation

Maternal smoking during pregnancy and child overweight: systematic review and meta-analysis

Biological, environmental, and social influences on childhood obesity

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