Perinatal nutrition programs the hypothalamic melanocortin system in offspring

J. S. Wattez, Fabien Delahaye, M. A. Lukaszewski, P. Y. Risold, D. Eberlé, D. Vieau, C. Breton

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Epidemiological studies initially suggested that maternal undernutrition leading to low birth weight may predispose for long-lasting energy balance disorders. High birth weight due to maternal obesity or diabetes, inappropriate early postnatal nutrition, and rapid catch-up growth, may also sensitize to increased risk of obesity. As stated by the Developmental Origin of Health and Disease concept, the perinatal perturbation of fetus/neonate nutrient supply might be a crucial determinant of individual programming of body weight set-point. The hypothalamic melanocortin system composed of the melanocortin receptor 4, its agonist α-melanin-stimulating hormone (α-MSH), and its antagonist agouti-related protein (AgRP) is considered as the main central anorexigenic pathway controlling energy homeostasis. Studies in numerous animal models demonstrated that this system is a prime target of developmental programming by maternal nutritional manipulation. In rodents, the perinatal period of life corresponds largely to the period of brain maturation (i. e., melanocortin neuronal differentiation and development of their neural projections). In contrast, these phenomena essentially take place before birth in bigger mammals. Despite these different developmental time windows, altricial and precocial species share several common offspring programming mechanisms. Offspring from malnourished dams present a hypothalamic melanocortin system with a series of alterations: impaired neurogenesis and neuronal functionality, disorganization of feeding pathways, modified glucose sensing, and leptin/insulin resistance. Overall, these alterations may account for the long-lasting dysregulation of energy balance and obesity. Following maternal malnutrition, hormonal and epigenetic mechanisms might be responsible for melanocortin system programming in offspring.

Original languageEnglish (US)
Pages (from-to)980-990
Number of pages11
JournalHormone and Metabolic Research
Volume45
Issue number13
DOIs
StatePublished - Dec 2013

Fingerprint

Melanocortins
Nutrition
Mothers
Obesity
Energy balance
Malnutrition
Agouti-Related Protein
Receptor, Melanocortin, Type 4
Hormone Antagonists
Computer systems programming
Mammals
Melanins
Neurogenesis
Low Birth Weight Infant
Medical problems
Leptin
Birth Weight
Epigenomics
Dams
Nutrients

Keywords

  • appetite programming
  • arcuate nucleus
  • epigenetic mechanisms
  • gene expression
  • gestation
  • lactation

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical
  • Endocrinology, Diabetes and Metabolism

Cite this

Wattez, J. S., Delahaye, F., Lukaszewski, M. A., Risold, P. Y., Eberlé, D., Vieau, D., & Breton, C. (2013). Perinatal nutrition programs the hypothalamic melanocortin system in offspring. Hormone and Metabolic Research, 45(13), 980-990. https://doi.org/10.1055/s-0033-1357182

Perinatal nutrition programs the hypothalamic melanocortin system in offspring. / Wattez, J. S.; Delahaye, Fabien; Lukaszewski, M. A.; Risold, P. Y.; Eberlé, D.; Vieau, D.; Breton, C.

In: Hormone and Metabolic Research, Vol. 45, No. 13, 12.2013, p. 980-990.

Research output: Contribution to journalArticle

Wattez, JS, Delahaye, F, Lukaszewski, MA, Risold, PY, Eberlé, D, Vieau, D & Breton, C 2013, 'Perinatal nutrition programs the hypothalamic melanocortin system in offspring', Hormone and Metabolic Research, vol. 45, no. 13, pp. 980-990. https://doi.org/10.1055/s-0033-1357182
Wattez, J. S. ; Delahaye, Fabien ; Lukaszewski, M. A. ; Risold, P. Y. ; Eberlé, D. ; Vieau, D. ; Breton, C. / Perinatal nutrition programs the hypothalamic melanocortin system in offspring. In: Hormone and Metabolic Research. 2013 ; Vol. 45, No. 13. pp. 980-990.
@article{42c51335df7e47b7bdaa3b28985b7503,
title = "Perinatal nutrition programs the hypothalamic melanocortin system in offspring",
abstract = "Epidemiological studies initially suggested that maternal undernutrition leading to low birth weight may predispose for long-lasting energy balance disorders. High birth weight due to maternal obesity or diabetes, inappropriate early postnatal nutrition, and rapid catch-up growth, may also sensitize to increased risk of obesity. As stated by the Developmental Origin of Health and Disease concept, the perinatal perturbation of fetus/neonate nutrient supply might be a crucial determinant of individual programming of body weight set-point. The hypothalamic melanocortin system composed of the melanocortin receptor 4, its agonist α-melanin-stimulating hormone (α-MSH), and its antagonist agouti-related protein (AgRP) is considered as the main central anorexigenic pathway controlling energy homeostasis. Studies in numerous animal models demonstrated that this system is a prime target of developmental programming by maternal nutritional manipulation. In rodents, the perinatal period of life corresponds largely to the period of brain maturation (i. e., melanocortin neuronal differentiation and development of their neural projections). In contrast, these phenomena essentially take place before birth in bigger mammals. Despite these different developmental time windows, altricial and precocial species share several common offspring programming mechanisms. Offspring from malnourished dams present a hypothalamic melanocortin system with a series of alterations: impaired neurogenesis and neuronal functionality, disorganization of feeding pathways, modified glucose sensing, and leptin/insulin resistance. Overall, these alterations may account for the long-lasting dysregulation of energy balance and obesity. Following maternal malnutrition, hormonal and epigenetic mechanisms might be responsible for melanocortin system programming in offspring.",
keywords = "appetite programming, arcuate nucleus, epigenetic mechanisms, gene expression, gestation, lactation",
author = "Wattez, {J. S.} and Fabien Delahaye and Lukaszewski, {M. A.} and Risold, {P. Y.} and D. Eberl{\'e} and D. Vieau and C. Breton",
year = "2013",
month = "12",
doi = "10.1055/s-0033-1357182",
language = "English (US)",
volume = "45",
pages = "980--990",
journal = "Hormone and Metabolic Research",
issn = "0018-5043",
publisher = "Georg Thieme Verlag",
number = "13",

}

TY - JOUR

T1 - Perinatal nutrition programs the hypothalamic melanocortin system in offspring

AU - Wattez, J. S.

AU - Delahaye, Fabien

AU - Lukaszewski, M. A.

AU - Risold, P. Y.

AU - Eberlé, D.

AU - Vieau, D.

AU - Breton, C.

PY - 2013/12

Y1 - 2013/12

N2 - Epidemiological studies initially suggested that maternal undernutrition leading to low birth weight may predispose for long-lasting energy balance disorders. High birth weight due to maternal obesity or diabetes, inappropriate early postnatal nutrition, and rapid catch-up growth, may also sensitize to increased risk of obesity. As stated by the Developmental Origin of Health and Disease concept, the perinatal perturbation of fetus/neonate nutrient supply might be a crucial determinant of individual programming of body weight set-point. The hypothalamic melanocortin system composed of the melanocortin receptor 4, its agonist α-melanin-stimulating hormone (α-MSH), and its antagonist agouti-related protein (AgRP) is considered as the main central anorexigenic pathway controlling energy homeostasis. Studies in numerous animal models demonstrated that this system is a prime target of developmental programming by maternal nutritional manipulation. In rodents, the perinatal period of life corresponds largely to the period of brain maturation (i. e., melanocortin neuronal differentiation and development of their neural projections). In contrast, these phenomena essentially take place before birth in bigger mammals. Despite these different developmental time windows, altricial and precocial species share several common offspring programming mechanisms. Offspring from malnourished dams present a hypothalamic melanocortin system with a series of alterations: impaired neurogenesis and neuronal functionality, disorganization of feeding pathways, modified glucose sensing, and leptin/insulin resistance. Overall, these alterations may account for the long-lasting dysregulation of energy balance and obesity. Following maternal malnutrition, hormonal and epigenetic mechanisms might be responsible for melanocortin system programming in offspring.

AB - Epidemiological studies initially suggested that maternal undernutrition leading to low birth weight may predispose for long-lasting energy balance disorders. High birth weight due to maternal obesity or diabetes, inappropriate early postnatal nutrition, and rapid catch-up growth, may also sensitize to increased risk of obesity. As stated by the Developmental Origin of Health and Disease concept, the perinatal perturbation of fetus/neonate nutrient supply might be a crucial determinant of individual programming of body weight set-point. The hypothalamic melanocortin system composed of the melanocortin receptor 4, its agonist α-melanin-stimulating hormone (α-MSH), and its antagonist agouti-related protein (AgRP) is considered as the main central anorexigenic pathway controlling energy homeostasis. Studies in numerous animal models demonstrated that this system is a prime target of developmental programming by maternal nutritional manipulation. In rodents, the perinatal period of life corresponds largely to the period of brain maturation (i. e., melanocortin neuronal differentiation and development of their neural projections). In contrast, these phenomena essentially take place before birth in bigger mammals. Despite these different developmental time windows, altricial and precocial species share several common offspring programming mechanisms. Offspring from malnourished dams present a hypothalamic melanocortin system with a series of alterations: impaired neurogenesis and neuronal functionality, disorganization of feeding pathways, modified glucose sensing, and leptin/insulin resistance. Overall, these alterations may account for the long-lasting dysregulation of energy balance and obesity. Following maternal malnutrition, hormonal and epigenetic mechanisms might be responsible for melanocortin system programming in offspring.

KW - appetite programming

KW - arcuate nucleus

KW - epigenetic mechanisms

KW - gene expression

KW - gestation

KW - lactation

UR - http://www.scopus.com/inward/record.url?scp=84890553065&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84890553065&partnerID=8YFLogxK

U2 - 10.1055/s-0033-1357182

DO - 10.1055/s-0033-1357182

M3 - Article

VL - 45

SP - 980

EP - 990

JO - Hormone and Metabolic Research

JF - Hormone and Metabolic Research

SN - 0018-5043

IS - 13

ER -