Developmental programming of energy balance regulation: is physical activity more ‘programmable’ than food intake?

Zhu, Shaoyu; Eclarinal, Jesse; Baker, Maria S.; Li, Ge; Waterland, Robert A.

doi:10.1017/s0029665115004127

Cited by 19 publications

(24 citation statements)

References 44 publications

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“…More recently, however, there is a growing appreciation that this model of maternal influences on caloric intake in offspring is over simplistic: although alterations in maternal nutrition are closely correlated with early growth rates, they rarely persist to adulthood 10,11 . In fact, a recent meta-analysis of 35 rodent studies did not find evidence that maternal influences on susceptibility of offspring to diet-induced obesity are due to changes in caloric intake 12 .…”

Section: Introductionmentioning

confidence: 99%

Feeding circuit development and early-life influences on future feeding behaviour

Zeltser

2018

Nat Rev Neurosci

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A wide range of maternal exposures - undernutrition, obesity, diabetes, stress and infection - are associated with an increased risk of metabolic disease in offspring. Developmental influences can cause persistent structural changes in hypothalamic circuits regulating food intake in the service of energy balance. The physiological relevance of these alterations has been called into question because maternal impacts on daily caloric intake do not persist to adulthood. Recent behavioural and epidemiological studies in humans provide evidence that the relative contribution of appetitive traits related to satiety, reward and the emotional aspects of food intake regulation changes across the lifespan. This Opinion article outlines a neurodevelopmental framework to explore the possibility that crosstalk between developing circuits regulating different modalities of food intake shapes future behavioural responses to environmental challenges.

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Section: Introductionmentioning

confidence: 99%

Feeding circuit development and early-life influences on future feeding behaviour

Zeltser

2018

Nat Rev Neurosci

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“…Development of this area of the brain is formed during the early stages of development (E12) and, therefore, can be altered by adverse conditions like EDC exposure. The exposure window to EDC is critical as the central control of feeding behaviors develops both in utero and neonatally (Toda et al, 2017; Zhu et al, 2016). A previous review in this journal described the potential interplay between EDC and maternal programming on the control of energy homeostasis (Schneider et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Perinatal exposure to endocrine disrupting compounds and the control of feeding behavior—An overview

Walley

Roepke

2018

Hormones and Behavior

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Endocrine disrupting compounds (EDC) are ubiquitous environmental contaminants that can interact with steroid and nuclear receptors or alter hormone production. Many studies have reported that perinatal exposure to EDC including bisphenol A, PCB, dioxins, and DDT disrupt energy balance, body weight, adiposity, or glucose homeostasis in rodent offspring. However, little information exists on the effects of perinatal EDC exposure on the control of feeding behaviors and meal pattern (size, frequency, duration), which may contribute to their obesogenic properties. Feeding behaviors are controlled centrally through communication between the hindbrain and hypothalamus with inputs from the emotion and reward centers of the brain and modulated by peripheral hormones like ghrelin and leptin. Discrete hypothalamic nuclei (arcuate nucleus, paraventricular nucleus, lateral and dorsomedial hypothalamus, and ventromedial nucleus) project numerous reciprocal neural connections between each other and to other brain regions including the hindbrain (nucleus tractus solitarius and parabrachial nucleus). Most studies on the effects of perinatal EDC exposure examine simple crude food intake over the course of the experiment or for a short period in adult models. In addition, these studies do not examine EDC's impacts on the feeding neurocircuitry of the hypothalamus-hindbrain, the response to peripheral hormones (leptin, ghrelin, cholecystokinin, etc.) after refeeding, or other feeding behavior paradigms. The purpose of this review is to discuss those few studies that report crude food or energy intake after perinatal EDC exposure and to explore the need for deeper investigations in the hypothalamic-hindbrain neurocircuitry and discrete feeding behaviors.

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“…Similarly, early postnatal nutrition influences voluntary physical activity in adulthood [10]. However, whether effects of early life environment on metabolic and cardiovascular traits are caused, at least in part, by programming effects on physical activity has received little attention [11]. …”

Section: Introductionmentioning

confidence: 99%

A maternal high-fat, high-sucrose diet has sex-specific effects on fetal glucocorticoids with little consequence for offspring metabolism and voluntary locomotor activity in mice

et al. 2017

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Maternal overnutrition and obesity during pregnancy can have long-term effects on offspring physiology and behaviour. These developmental programming effects may be mediated by fetal exposure to glucocorticoids, which is regulated in part by placental 11β-hydroxysteroid dehydrogenase (11β-HSD) type 1 and 2. We tested whether a maternal high-fat, high-sucrose diet would alter expression of placental 11β-HSD1 and 2, thereby increasing fetal exposure to maternal glucocorticoids, with downstream effects on offspring physiology and behaviour. C57BL/6J mice were fed a high-fat, high-sucrose (HFHS) diet or a nutrient-matched low-fat, no-sucrose control diet prior to and during pregnancy and lactation. At day 17 of gestation, HFHS dams had ~20% lower circulating corticosterone levels than controls. Furthermore, there was a significant interaction between maternal diet and fetal sex for circulating corticosterone levels in the fetuses, whereby HFHS males tended to have higher corticosterone than control males, with no effect in female fetuses. However, placental 11β-HSD1 or 11β-HSD2 expression did not differ between diets or show an interaction between diet and sex. To assess potential long-term consequences of this sex-specific effect on fetal corticosterone, we studied locomotor activity and metabolic traits in adult offspring. Despite a sex-specific effect of maternal diet on fetal glucocorticoids, there was little evidence of sex-specific effects on offspring physiology or behaviour, although HFHS offspring of both sexes had higher circulating corticosterone at 9 weeks of age. Our results suggest the existence of as yet unknown mechanisms that mitigate the effects of altered glucocorticoid exposure early in development, making offspring resilient to the potentially negative effects of a HFHS maternal diet.

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Developmental programming of energy balance regulation: is physical activity more ‘programmable’ than food intake?

Cited by 19 publications

References 44 publications

Feeding circuit development and early-life influences on future feeding behaviour

Feeding circuit development and early-life influences on future feeding behaviour

Perinatal exposure to endocrine disrupting compounds and the control of feeding behavior—An overview

A maternal high-fat, high-sucrose diet has sex-specific effects on fetal glucocorticoids with little consequence for offspring metabolism and voluntary locomotor activity in mice

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