Dopaminergic neurons in the paraventricular hypothalamus extend the food consumption phase

Feeding behavior is controlled by various neural networks in the brain that are involved in different feeding phases: Food procurement, consumption, and termination. However, the specific neural circuits controlling the food consumption phase remain poorly understood. Here, we investigated the roles of dopaminergic neurons in the paraventricular nucleus of the hypothalamus (PVH) in the feeding behavior in mice. Our results indicated that the PVH dopaminergic neurons were critical for extending the food consumption phase and involved in the development of obesity through epigenetic mechanisms. These neurons synchronized with proopiomelanocortin neurons during consumption, were stimulated by proopiomelanocortin activation, and projected to the lateral habenula (LHb), where dopamine receptor D2 was involved in the increase in food consumption. In addition, upregulated tyrosine hydroxylase (TH) expression in PVH was associated with obesity and indispensable for obesity induction in mice lacking <i>Dnmt3a</i>. Taken together, our results highlight the roles of PVH dopaminergic neurons in promoting food consumption and obesity induction.

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Publication Details

Journal
Proceedings of the National Academy of Sciences
Published
2025-03-28
DOI
https://doi.org/10.1073/pnas.2411069122
Citations
3
Primary Topic
Regulation of Appetite and Obesity
Type
article
Field-Weighted Citation Impact
2.74

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article

Dopaminergic neurons in the paraventricular hypothalamus extend the food consumption phase

Hiroshi Ichinose, Itaru Imayoshi, Noriyuki Koibuchi, Daisuke Kohno et al.
3 citations
Proceedings of the National Academy of Sciences
Regulation of Appetite and Obesity
2.74
article

Dopaminergic neurons in the paraventricular hypothalamus extend the food consumption phase

Hiroshi Ichinose, Itaru Imayoshi, Noriyuki Koibuchi, Daisuke Kohno, Chiho Sumi‐Ichinose, Izuki Amano, Chiharu Yoshikawa, Haruka Tsuneoka, Winda Ariyani, Tadahiro Kitamura
article en
3 citations

Abstract

Feeding behavior is controlled by various neural networks in the brain that are involved in different feeding phases: Food procurement, consumption, and termination. However, the specific neural circuits controlling the food consumption phase remain poorly understood. Here, we investigated the roles of dopaminergic neurons in the paraventricular nucleus of the hypothalamus (PVH) in the feeding behavior in mice. Our results indicated that the PVH dopaminergic neurons were critical for extending the food consumption phase and involved in the development of obesity through epigenetic mechanisms. These neurons synchronized with proopiomelanocortin neurons during consumption, were stimulated by proopiomelanocortin activation, and projected to the lateral habenula (LHb), where dopamine receptor D2 was involved in the increase in food consumption. In addition, upregulated tyrosine hydroxylase (TH) expression in PVH was associated with obesity and indispensable for obesity induction in mice lacking <i>Dnmt3a</i>. Taken together, our results highlight the roles of PVH dopaminergic neurons in promoting food consumption and obesity induction.

Proceedings of the National Academy of SciencesVol. 122(13)
Fujita Health University (JP), Gunma University (JP), Kyoto University (JP), Shanghai Institute for Science of Science (CN), Life Science Institute (JP), Living Systems (United States) (US), Institute of Science Tokyo (JP)
Naito Foundation, Takeda Science Foundation, Japan Agency for Medical Research and Development, Japan Foundation for Pediatric Research, Lastentautien Tutkimussäätiö, Manpei Suzuki Diabetes Foundation, Japan Science Society, Mishima Kaiun Memorial Foundation, Lotte Foundation, Japan Society for the Promotion of Science, Japan Science and Technology Agency, Institute for Molecular and Cellular Regulation, Gunma University, Core Research for Evolutional Science and Technology, Moonshot Research and Development Program
Zero hunger
Openalex Percentile: Top 11%
Regulation of Appetite and Obesity
2.74
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