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Updated: Mar 23, 2026
Functional Interrogation of Adult Hypothalamic Neurogenesis with Focal Radiological Inhibition
Published on: November 14, 2013
Prenatal fat exposure and hypothalamic PPAR β/δ: Possible relationship to increased neurogenesis of orexigenic
G-Q Chang1, O Karatayev1, O Lukatskaya1
1Laboratory of Behavioral Neurobiology, The Rockefeller University, New York, NY, USA.
Insights
Prenatal exposure to a high-fat diet increases the number of neurons expressing specific appetite-regulating peptides in offspring brains. This is linked to the fatty acid-sensitive transcription factor peroxisome proliferator-activated receptor beta/delta (PPAR β/δ).
Area of Science:
- Neuroscience
- Developmental Biology
- Metabolic Research
Background:
- Gestational exposure to high-fat diets alters maternal fatty acids.
- This can increase neurons stimulating consummatory behavior in offspring's hypothalamus and amygdala.
Purpose of the Study:
- Investigate the effect of prenatal high-fat diet on peroxisome proliferator-activated receptor beta/delta (PPAR β/δ) in postnatal offspring.
- Determine the relationship between PPAR β/δ and orexigenic neuropeptides (orexin, melanin-concentrating hormone, enkephalin).
Main Methods:
- Examined postnatal offspring (day 15) brains after gestational high-fat diet exposure.
- Used immunohistochemistry to assess PPAR β/δ, cell proliferation (BrdU), neuronal marker (NeuN), and neuropeptide co-localization.
Main Results:
- High-fat diet increased PPAR β/δ neuron density in the PVN, PFLH, and CeA.
- Demonstrated increased proliferation and density of new PPAR β/δ neurons.
- Showed PPAR β/δ co-localization with orexin, melanin-concentrating hormone, and enkephalin, indicating increased genesis of peptide-producing neurons.
Conclusions:
- Prenatal high-fat diet promotes the development of specific neurons in the hypothalamus and amygdala.
- PPAR β/δ is anatomically linked to increased proliferation of neuropeptide-producing neurons in offspring exposed to dietary fat.
- Findings highlight a mechanism linking maternal diet to offspring appetite regulation pathways.
Abstract:
Gestational exposure to a fat-rich diet, while elevating maternal circulating fatty acids, increases in the offspring's hypothalamus and amygdala the proliferation and density of neurons that express neuropeptides known to stimulate consummatory behavior. To understand the relationship between these phenomena, this study examined in the brain of postnatal offspring (day 15) the effect of prenatal fat exposure on the transcription factor, peroxisome proliferator-activated receptor (PPAR) β/δ, which is sensitive to fatty acids, and the relationship of PPAR β/δ to the orexigenic neuropeptides, orexin, melanin-concentrating hormone, and enkephalin. Prenatal exposure to a fat-rich diet compared to low-fat chow increased the density of cells immunoreactive for PPAR β/δ in the hypothalamic paraventricular nucleus (PVN), perifornical lateral hypothalamus (PFLH), and central nucleus of the amygdala (CeA), but not the hypothalamic arcuate nucleus or basolateral amygdaloid nucleus. It also increased co-labeling of PPAR β/δ with the cell proliferation marker, BrdU, or neuronal marker, NeuN, and the triple labeling of PPAR β/δ with BrdU plus NeuN, indicating an increase in proliferation and density of new PPAR β/δ neurons. Prenatal fat exposure stimulated the double-labeling of PPAR β/δ with orexin or melanin-concentrating hormone in the PFLH and enkephalin in the PVN and CeA and also triple-labeling of PPAR β/δ with BrdU and these neuropeptides, indicating that dietary fat increases the genesis of PPAR β/δ neurons that produce these peptides. These findings demonstrate a close anatomical relationship between PPAR β/δ and the increased proliferation and density of peptide-expressing neurons in the hypothalamus and amygdala of fat-exposed offspring.
