Perinatal Food Deprivation Induces Marked Alterations of the Hypothalamo-Pituitary-Adrenal Axis in 8-Month-Old Male Rats both under Basal Conditions and after a Dehydration Period

Sebaai, Naima; Lésage, Jean; Breton, Christophe; Vieau, Didier; Deloof, Sylvie

doi:10.1159/000078098

Cited by 46 publications

(20 citation statements)

References 50 publications

(69 reference statements)

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“…Similar variations were observed in the different areas investigated. hypercorticosteronemia accompanied by disturbed glucocorticoid feedback, leading to 8-mo-old male rats that were unable to cope with severe stress (14,46). Our data demonstrated hypercorticosteronemia in FR30 rats as early as 4 mo of age and a blunted increase of corticosterone after fasting.…”

Section: Discussionmentioning

confidence: 63%

Maternal prenatal undernutrition alters the response of POMC neurons to energy status variation in adult male rat offspring

Breton¹,

Lukaszewski²,

Risold³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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demiological studies suggest that maternal undernutrition predisposes the offspring to development of energy balance metabolic pathologies in adulthood. Using a model of a prenatal maternal 70% foodrestricted diet (FR30) in rats, we evaluated peripheral parameters involved in nutritional regulation, as well as the hypothalamic appetite-regulatory system, in nonfasted and 48-h-fasted adult offspring. Despite comparable glycemia in both groups, mild glucose intolerance, with a defect in glucose-induced insulin secretion, was observed in FR30 animals. They also exhibited hyperleptinemia, despite similar visible fat deposits. Using semiquantitative RT-PCR, we observed no basal difference of hypothalamic proopiomelanocortin (POMC) and neuropeptide Y (NPY) gene expression, but a decrease of the OB-Rb and an increase of insulin receptor mRNA levels, in FR30 animals. These animals also exhibited basal hypercorticosteronemia and a blunted increase of corticosterone in fasted compared with control animals. After fasting, FR30 animals showed no marked reduction of POMC mRNA levels or intensity of ␤-endorphin-immunoreactive fiber projections. By contrast, NPY gene expression and immunoreactive fiber intensity increased. FR30 rats also displayed subtle alterations of food intake: body weight-related food intake was higher and light-dark phase rhythm and refeeding time course were modified after fasting. At rest, in the morning, hyperinsulinemia and a striking increase in the number of c-Fos-containing cells in the arcuate nucleus were observed. About 30% of the c-Fos-expressing cells were POMC neurons. Our data suggest that maternal undernutrition differently programs the long-term appetite-regulatory system of offspring, especially the response of POMC neurons to energy status and food intake rhythm. maternal undernutrition; appetite programming; hypothalamus; arcuate nucleus; feeding rhythm IN ADDITION TO LIFESTYLE and dietary factors, increasing evidence suggests that the origin of some metabolic disorders that manifest in adult life may be traced to development. Indeed, epidemiological studies have shown that adverse environmental factors leading to intrauterine growth retardation (IUGR) and low birth weight may predispose individuals to later onset of energy balance metabolic pathology development (9,17,18,20,29). This has led to the concept of the developmental origin of adult diseases, also called "fetal programming," or the Barker hypothesis (4). As illustrated by the Dutch Famine Study, offspring of women exposed to famine during early pregnancy displayed an increased risk of adiposity and glucose intolerance, as well as hypertension, later in life (41).To obtain insights into the underlying mechanisms, numerous animal models, including maternal undernutrition, have been developed to promote intrauterine fetal programming (47,56). These studies confirmed that impaired fetal development has long-term metabolic consequences, sensitizing the offspring to hyperphagia and obesity, particularly when they are fed a hyperca...

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Section: Discussionmentioning

confidence: 63%

Maternal prenatal undernutrition alters the response of POMC neurons to energy status variation in adult male rat offspring

Breton¹,

Lukaszewski²,

Risold³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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“…Nevertheless, the effects of fetal programming may manifest differently in an age-dependent manner. Differential and age-dependent effects of early life experiences on HPA axis function have been reported [39,40,41]. For this purpose, we examined the effects of maternal DIO in both young adult (3-month-old) and aged adult (12-month-old) offspring.…”

Section: Discussionmentioning

confidence: 99%

Prenatal Exposure to Maternal Obesity Alters Anxiety and Stress Coping Behaviors in Aged Mice

et al. 2015

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Background: There is growing evidence that maternal obesity and prenatal exposure to a high-fat diet program fetal development to regulate the physiology and behavior of the offspring in adulthood. Yet the extent to which the maternal dietary environment contributes to adult disease vulnerability remains unclear. In the current study we tested whether prenatal exposure to maternal obesity increases the offspring's vulnerability to stress-related psychiatric disorders. Methods: We used a mouse model of maternal diet-induced obesity to investigate whether maternal obesity affects the response to adult chronic stress exposure in young adult (3-month-old) and aged adult (12-month-old) offspring. Results: Long-lasting, delayed impairments to anxiety-like behaviors and stress coping strategies resulted on account of prenatal exposure to maternal obesity. Although maternal obesity did not change the offspring's behavioral response to chronic stress per se, we demonstrate that the behavioral outcomes induced by prenatal exposure to maternal obesity parallel the deleterious effects of adult chronic stress exposure in aged male mice. We found that the glucocorticoid receptor (GR, Nr3c1) is upregulated in various hypothalamic nuclei on account of maternal obesity. In addition, gene expression of a known regulator of the GR, FKBP51, is increased specifically within the paraventricular nucleus. Conclusions: These findings indicate that maternal obesity parallels the deleterious effects of adult chronic stress exposure, and furthermore identifies GR/FKBP51 signaling as a novel candidate pathway regulated by maternal obesity.

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“…The results of the present study suggest that prenatal famine exposure does not affect functioning of the HPA axis at the adrenal level, but it may affect functioning at a higher level. Experiments in which rats were pre-or perinatally undernourished showed physiological and functional changes at the levels of the hippocampus and hypothalamus (5,28). Higher levels of the HPA axis can be tested by means of psychological stressors (29).…”

Section: Discussionmentioning

confidence: 99%

Hypothalamic–pituitary–adrenal axis activity in adults who were prenatally exposed to the Dutch famine

Rooij¹,

Painter²,

Phillips³

et al. 2006

eur j endocrinol

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Objective: The hypothalamic-pituitary-adrenal (HPA) axis has been proposed to be susceptible to fetal programming, the process by which an adverse fetal environment elicits permanent physiological and metabolic alterations predisposing to disease in later life. It is hypothesized that fetal exposure to poor circumstances alters the set point of the HPA axis, leading to increased HPA axis activity and subsequent increased cortisol concentrations. In this study, we tested the hypothesis that prenatal exposure to famine during different periods of gestation is associated with increased activity of the HPA axis. Design and methods: We assessed plasma cortisol concentrations after a dexamethasone suppression and an ACTH 1-24 -stimulation test in a group of 98 men and women randomly sampled from the Dutch famine birth cohort. Cohort members were born as term singletons around the 1944-1945 Dutch famine. Results: Cortisol profiles after dexamethasone suppression and ACTH 1-24 stimulation were similar for participants exposed to famine during late, mid-or early gestation (PZ0.78). Cortisol concentrations after dexamethasone suppression test did not differ between those exposed and those unexposed to famine in utero (mean difference K2% (95% confidence interval (CI) K27 to 23)). Neither peak cortisol concentration (20 nmol/l (95% CI K27 to 66)), cortisol increment (K5 nmol/l (95% CI K56 to 47)) or cortisol area under the curve post-ACTH 1-24 injection (4% (95% CI K4 to 12)) differed between exposed and unexposed participants. Conclusions: Prenatal famine exposure does not seem to affect HPA axis activity at adult age, at least not at the adrenal level. This does not exclude altered HPA axis activity at the levels of the hippocampus and hypothalamus.European Journal of Endocrinology 155 153-160

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Perinatal Food Deprivation Induces Marked Alterations of the Hypothalamo-Pituitary-Adrenal Axis in 8-Month-Old Male Rats both under Basal Conditions and after a Dehydration Period

Cited by 46 publications

References 50 publications

Maternal prenatal undernutrition alters the response of POMC neurons to energy status variation in adult male rat offspring

Maternal prenatal undernutrition alters the response of POMC neurons to energy status variation in adult male rat offspring

Prenatal Exposure to Maternal Obesity Alters Anxiety and Stress Coping Behaviors in Aged Mice

Hypothalamic–pituitary–adrenal axis activity in adults who were prenatally exposed to the Dutch famine

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