Prenatal influences on susceptibility to diet-induced obesity are mediated by altered neuroendocrine gene expression
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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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]
Cites
Region-Specific Leptin Resistance within the Hypothalamus of Diet-Induced Obese Mice
Münzberg, H., Flier, J. S., & Bjørbæk, C. (2004) · Endocrinology · doi:10.1210/en.2004-0726 · Cited by 737 · see citing works
Seufert, J., Kieffer, T. J., Leech, C. A., Holz, G. G., Moritz, W., Ricordi, C., & Habener, J. F. (1999) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.84.2.5460 · Cited by 278 · see citing works
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The Pathophysiology of Gestational Diabetes Mellitus
Plows, J. F., Stanley, J. L., Baker, P. N., Reynolds, C. M., & Vickers, M. H. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19113342 · Cited by 1,874 · see citing works
“These alterations persist after birth—a phenomenon referred to as “developmental programming” [52].”
BackgroundSelf-citationTen Putative Contributors to the Obesity Epidemic
McAllister, E. J., Dhurandhar, N. V., Keith, S. W., Aronne, L. J., Barger, J., Baskin, M., Benca, R. M., Biggio, J., Boggiano, M. M., Eisenmann, J. C., et al. (2009) · Critical Reviews in Food Science and Nutrition · doi:10.1080/10408390903372599 · Cited by 710 · see citing works
Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective
Gluckman, P. D., & Hanson, M. A. (2008) · International Journal of Obesity · doi:10.1038/ijo.2008.240 · Cited by 333 · see citing works
Long-term metabolic risk among children born premature or small for gestational age.
Mericq, V., Martinez-Aguayo, A., Uauy, R., Iñiguez, G., Van der Steen, M., & Hokken-Koelega, A. (2017) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2016.127 · Cited by 257 · see citing works
- Authors
- Ikenasio-Thorpe, B. A., Breier, B. H., Vickers, M. H., & Fraser, M.
- Affiliations
- University of Auckland (NZ)
- Venue
- Journal of Endocrinology
- Publisher
- Bioscientifica
- 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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