The DOI matches its Crossref record; 70 of the 70 references it cites were found in a registry or an index.
Maternal High-Fat Diet and Fetal Programming: Increased Proliferation of Hypothalamic Peptide-Producing Neurons That Increase Risk for Overeating and Obesity
Open accessAbstract
Recent studies in adult and weanling rats show that dietary fat, in close association with circulating lipids, can stimulate expression of hypothalamic peptides involved in controlling food intake and body weight. In the present study, we examined the possibility that a fat-rich diet during pregnancy alters the development of these peptide systems in utero , producing neuronal changes in the offspring that persist postnatally in the absence of the diet and have long-term consequences. The offspring of dams on a high-fat diet (HFD) versus balanced diet (BD), from embryonic day 6 to postnatal day 15 (P15), showed increased expression of orexigenic peptides, galanin, enkephalin, and dynorphin, in the paraventricular nucleus and orexin and melanin-concentrating hormone in the perifornical lateral hypothalamus. The increased density of these peptide-expressing neurons, evident in newborn offspring as well as P15 offspring cross-fostered at birth to dams on the BD, led us to examine events that might be occurring in utero . During gestation, the HFD stimulated the proliferation of neuroepithelial and neuronal precursor cells of the embryonic hypothalamic third ventricle. It also stimulated the proliferation and differentiation of neurons and their migration toward hypothalamic areas where ultimately a greater proportion of the new neurons expressed the orexigenic peptides. This increase in neurogenesis, closely associated with a marked increase in lipids in the blood, may have a role in producing the long-term behavioral and physiological changes observed in offspring after weaning, including an increase in food intake, preference for fat, hyperlipidemia, and higher body weight.
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Cites
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A high-fat, ketogenic diet induces a unique metabolic state in mice
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Cited by
The role of maternal obesity in the risk of neuropsychiatric disorders
Rivera, H. M., Christiansen, K. J., & Sullivan, E. L. (2015) · Frontiers in Neuroscience · doi:10.3389/fnins.2015.00194 · Cited by 307
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Obesity in Type 1 Diabetes: Pathophysiology, Clinical Impact, and Mechanisms
Corbin, K. D., Driscoll, K. A., Pratley, R. E., Smith, S. R., Maahs, D. M., Mayer-Davis, E. J., & Advancing Care for Type 1 Diabetes and Obesity Network (ACT1ON) (2018) · Endocrine Reviews · doi:10.1210/er.2017-00191 · Cited by 262
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Metadata
- Authors
- Chang, G.-Q., Gaysinskaya, V., Karatayev, O., & Leibowitz, S. F.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-11-12
- Volume
- 28
- Issue
- 46
- Pages
- 12107-12119
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2014366175
- Cited by
- 372
- References
- 70
- FWCI
- 9.58
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Chang, G.-Q., Gaysinskaya, V., Karatayev, O., & Leibowitz, S. F. (2008). Maternal High-Fat Diet and Fetal Programming: Increased Proliferation of Hypothalamic Peptide-Producing Neurons That Increase Risk for Overeating and Obesity. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.2642-08.2008
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