Cited by 106Regulation of Appetite and ObesityBirth, Development, and HealthHypothalamic control of reproductive hormones

Prenatal influences on susceptibility to diet-induced obesity are mediated by altered neuroendocrine gene expression

Ikenasio-Thorpe, Bettina A, Breier, Bernhard H, Vickers, Mark H, Fraser, Mhoyra·2007·Journal of Endocrinology

Abstract

The escalating rates of obesity and type 2 diabetes have reached pandemic proportions. It has been proposed that the risk of developing metabolic disorders in adult life is influenced by environmental factors, which operate during the early periods of development. We have previously shown that an interaction between the prenatal and the postnatal dietary environment amplifies the propensity towards diet-induced obesity, although the mechanisms are unclear. In the present study, we investigated the interaction between prenatal undernutrition and postnatal high-fat nutrition on key genes of the hypothalamic appetite regulatory network. Pregnant Wistar rats were fed a standard chow diet either ad libitum (AD) or at 30% of AD intake throughout gestation (UN). From weaning, female AD and UN offspring were fed either a standard chow (ADC n = 8, UNC n = 8) or a high-fat diet (45% kcal as fat; ADHF n = 8, UNHF n = 8) ad libitum for the remainder of the study. At 24 weeks of age, body composition was assessed by dual energy X-ray absorptiometry analysis and total RNA was extracted from whole rat hypothalami. Real-time PCR was performed to characterise pro-opiomelanocortin (POMC), neuropeptide Y (NPY), agouti-related protein (AgRP) and OBRb gene expression at the mRNA level. Our results demonstrate that the amplification of postnatal obesity develops as a consequence of an interaction between prenatal under-nutrition and postnatal high-fat nutrition. This phenotype also shows significant alterations in POMC, NPY, AgRP and OBRb gene expression together with elevations in circulating levels of both plasma leptin and insulin. These findings are consistent with the predictive adaptive response hypothesis that neuroendocrine development during fetal life may be based on predictions about postnatal environmental conditions. Increased susceptibility to diet-induced obesity develops if a mismatch between the anticipated and the actual conditions are encountered.

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Crossref · 10.1677/joe.1.07017

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  • Alterations from in utero undernutrition persist after birth, a phenomenon referred to as developmental programming.

    “These alterations persist after birth—a phenomenon referred to as “developmental programming” [52].”

    From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [52]

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Authors
Ikenasio-Thorpe, B. A., Breier, B. H., Vickers, M. H., & Fraser, M.
Affiliations
University of Auckland (NZ)
Venue
Journal of Endocrinology
Published
2007-04
Volume
193
Issue
1
Pages
31-37
ISSN
  • 0022-0795 (ISSN-L)
  • 1479-6805
OpenAlex
W2122115966
Cited by
106
References
2
Citations by year
2025: 4 · 2024: 1 · 2023: 1 · 2022: 5 · 2021: 2 · 2020: 1 · 2019: 4 · 2018: 7 · 2017: 3 · 2016: 7 · 2015: 6 · 2014: 6 · 2013: 17 · 2012: 10
FWCI
3.36
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
  • ResearchSpace (University of Auckland) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
Keywords
diet-induced obesity, prenatal malnutrition, hypothalamic regulation of appetite, proopiomelanocortin, neuropeptide Y, agouti-related protein, leptin, insulin, neuroendocrine development, developmental programming, type 2 diabetes, body composition
MeSH terms
Animals, Appetite Regulation, Body Composition, Dietary Fats, Disease Susceptibility, Female, Hyperphagia, Hypothalamus, Insulin, Neuropeptide Y, Obesity, Pregnancy, Prenatal Exposure Delayed Effects, Pro-Opiomelanocortin, RNA, Messenger, Gene Expression, Rats, Wistar, Leptin, Intercellular Signaling Peptides and Proteins, Maternal Nutritional Physiological Phenomena, Malnutrition, Rats, Agouti Signaling Protein, Agouti-Related Protein

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