The hypothalamic POMC mRNA expression is upregulated in prenatally undernourished male rat offspring under high-fat diet

Lukaszewski, Marie-Amélie; Butruille, Laura; Moitrot, Emmanuelle; Montel, Valérie; Dickes-Coopman, Anne; Lésage, Jean; Laborie, Christine; Vieau, Didier; Breton, Christophe

doi:10.1016/j.peptides.2013.03.013

Cited by 9 publications

(13 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast to AgRP, we found that NPY, POMC and CRH were not affected by 35 days of HF diet in the present study. These results are inconsistent with studies in mammals which showed that NPY, POMC and CRH levels were affected by a HF diet (Guan et al, 1998;Chavez et al, 1998;Lin et al, 2000;Lukaszewski et al, 2013), implying a genetic bluntness in the response to dietary fat in avian species.…”

Section: Involvement Of Agrp In the Hf-induced Decrease In Food Intakecontrasting

confidence: 58%

“…Additionally, the release of these neuropeptides is closely associated with dietary fat level. Mice fed a higher fat diet had lower NPY and AgRP mRNA levels (Lin et al, 2000;Wang et al, 2002) and higher POMC mRNA levels (Lukaszewski et al, 2013). Therefore, we hypothesized that the response of hypothalamic neuropeptides to energy status could be changed by the dietary fat level.…”

Section: Introductionmentioning

confidence: 97%

See 1 more Smart Citation

Dietary fat alters the response of hypothalamic neuropeptide Y to subsequent energy intake in broiler chickens

Wang

Liu

et al. 2016

Journal of Experimental Biology

View full text Add to dashboard Cite

Dietary fat affects appetite and appetite-related peptides in birds and mammals; however, the effect of dietary fat on appetite is still unclear in chickens faced with different energy statuses. Two experiments were conducted to investigate the effects of dietary fat on food intake and hypothalamic neuropeptides in chickens subjected to two feeding states or two diets. In Experiment 1, chickens were fed a high-fat (HF) or low-fat (LF) diet for 35 days, and then subjected to fed (HF-fed, LF-fed) or fasted (HF-fasted, LF-fasted) conditions for 24 h. In Experiment 2, chickens that were fed a HF or LF diet for 35 days were fasted for 24 h and then re-fed with HF (HF-RHF, LF-RHF) or LF (HF-RLF, LF-RLF) diet for 3 h. The results showed that chickens fed a HF diet for 35 days had increased body fat deposition despite decreasing food intake even when the diet was altered during the re-feeding period (P<0.05). LF diet (35 days) promoted agouti-related peptide (AgRP) expression compared with HF diet (P<0.05) under both fed and fasted conditions. LF-RHF chickens had lower neuropeptide Y (NPY) expression compared with LF-RLF chickens; conversely, HF-RHF chickens had higher NPY expression than HF-RLF chickens (P<0.05). These results demonstrate: (1) that HF diet decreases food intake even when the subsequent diet is altered; (2) the orexigenic effect of hypothalamic AgRP; and (3) that dietary fat alters the response of hypothalamic NPY to subsequent energy intake. These findings provide a novel view of the metabolic perturbations associated with long-term dietary fat over-ingestion in chickens.

show abstract

Section: Involvement Of Agrp In the Hf-induced Decrease In Food Intakecontrasting

confidence: 58%

Section: Introductionmentioning

confidence: 97%

Dietary fat alters the response of hypothalamic neuropeptide Y to subsequent energy intake in broiler chickens

Wang

Liu

et al. 2016

Journal of Experimental Biology

View full text Add to dashboard Cite

show abstract

“…The obese phenotype is associated with reduced satiety responses to leptin and impaired ARC signaling responses to leptin, as well as with increased responses to appetite stimulatory factors, such as ghrelin, and an increased ratio of appetite to satiety gene expression . Altered POMC mRNA expression seen in different studies suggests that this polypeptide is a key target for developmental programming in this IUGR model . These alterations were similarly seen in other animal models, such as baboons, lambs, and piglets .…”

Section: Neurobehavioral Aspects Of Nutritional Securitymentioning

confidence: 57%

Neurobehavioral determinants of nutritional security in fetal growth–restricted individuals

Portella¹,

Silveira

2014

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

Fetal growth restriction results from a failure to achieve a higher growth potential and has been associated with many maternal conditions, such as chronic diseases (infections, hypertension, and some cases of diabetes and obesity), exposures (tobacco smoke, drugs), and malnutrition. This early adversity induces a series of adaptive physiological responses aimed at improving survival, but imposing increased risk for developing chronic nontransmittable diseases (obesity, type II diabetes, cardiovascular disease) in the long term. Recently, mounting evidence has shown that fetal growth impairment is related to altered feeding behavior and preferences through the life course. When living in countries undergoing nutritional transition, in which individuals experience the coexistence of underweight and overweight problems (the "double burden of malnutrition"), fetal growth-restricted children can be simultaneously growth restricted and overweight-a double burden of malnutrition at the individual level. Considering food preferences as an important aspect of nutrition security, we will summarize the putative neurobiological mechanisms at the core of the relationship between fetal growth and nutrition security over the life course and the evidence linking early life adversity to later food preferences.

show abstract

“…These adaptations are likely through epigenetic modifications. One system, the glucocorticoid signaling pathway has been demonstrated to be programmed in response to prenatal environments (Bolten et al, 2013; Conradt et al, 2013; Khulan and Drake, 2012; Lukaszewski et al, 2013; Reynolds, 2013) and these programming changes have been observed into adulthood (Goldstein et al, 2014; Khalife et al, 2013), including the transmission of the altered programming across generations (Luo et al, 2014). Further, there is support for the suggestion that altered glucocorticoid receptor (GR) programming could impact adult health (Brunton and Russell, 2011; Harris and Seckl, 2011; Merlot et al, 2008; Sarkar et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Prenatal arsenic exposure alters the programming of the glucocorticoid signaling system during embryonic development

Caldwell

Labrecque

Solomon

et al. 2015

Neurotoxicology and Teratology

View full text Add to dashboard Cite

The glucocorticoid system, which plays a critical role in a host of cellular functions including mood disorders and learning and memory, has been reported to be disrupted by arsenic. In previous work we have developed and characterized a prenatal moderate arsenic exposure (50 ppb) model and identified several deficits in learning and memory and mood disorders, as well as alterations within the glucocorticoid receptor signaling system in the adolescent mouse. In these present studies we assessed the effects of arsenic on the glucocorticoid receptor (GR) pathway in both the placenta and the fetal brain in response at two critical periods, embryonic days 14 and 18. The focus of these studies was on the 11β-hydroxysteroid dehydrogenase enzymes (11β-HSD1 and 11β-HSD2) which play a key role in glucorticoid synthesis, as well as the expression and set point of the GR negative feedback regulation. Negative feedback regulation is established early in development. At E14 we found arsenic exposure significantly decreased expression of both protein and message in brain of GR and the 11β-HSD1, while 11β-HSD2 enzyme protein levels were increased but mRNA levels were decreased in the brain. These changes in brain protein continued into the E18 time point, but mRNA levels were no longer significantly altered. Placental HSD11B2 mRNA was not altered by arsenic treatment but protein levels were elevated at E14. GR placental protein levels were decreased at E18 in the arsenic exposed condition. This suggests that arsenic exposure may alter GR expression levels as a consequence of a prolonged developmental imbalance between 11β-HSD1 and 11β-HSD2 protein expression despite decreased 11HSDB2 mRNA. The suppression of GR and the failure to turn down 11β-HSD2 protein expression during fetal development may lead to an altered set point for GR signaling throughout adulthood. To our knowledge, these studies are the first to demonstrate that gestational exposure to moderate levels of arsenic results in altered fetal programming of the glucocorticoid system.

show abstract

The hypothalamic POMC mRNA expression is upregulated in prenatally undernourished male rat offspring under high-fat diet

Cited by 9 publications

References 57 publications

Dietary fat alters the response of hypothalamic neuropeptide Y to subsequent energy intake in broiler chickens

Dietary fat alters the response of hypothalamic neuropeptide Y to subsequent energy intake in broiler chickens

Neurobehavioral determinants of nutritional security in fetal growth–restricted individuals

Prenatal arsenic exposure alters the programming of the glucocorticoid signaling system during embryonic development

Contact Info

Product

Resources

About