# Food and the brain: Neural and endocrine control of feeding, metabolism, and reproduction

**Authors:** Naira da Silva Mansano, Calvin Vinh Lieu, Alfonso Abizaid

PMC · DOI: 10.1111/jne.70104 · Journal of Neuroendocrinology · 2025-10-28

## TL;DR

The paper explores how metabolic hormones control feeding, energy balance, and reproduction, with a focus on their role in puberty onset and obesity treatment.

## Contribution

The paper highlights novel insights into how metabolic hormones like leptin and ghrelin regulate puberty and feeding behavior, offering potential targets for obesity treatment.

## Key findings

- Leptin and insulin promote puberty onset by activating hypothalamic pathways related to ovulation.
- Ghrelin drives hunger and feeding behavior by acting on hypothalamic and extrahypothalamic brain regions.
- These hormones offer potential therapeutic targets for obesity treatment by modulating food intake and energy expenditure.

## Abstract

Feeding and reproductive function are regulated by intricate systems that monitor food availability and energy stores, and on the basis of energy status, promote or put a brake on reproduction. This is particularly evident in the systems that regulate feeding and reproductive state in female mammals. Here we describe some of the systems that regulate feeding and reproductive state focusing on how metabolic hormones impact the onset of puberty as discussed in the panel session presented at the recent Panamerican Neuroendocrine Society meeting in Santos, Brazil. Indeed, hormones like leptin and insulin, which are released when levels of energy resources are increasing, may be critical signals that activate hypothalamic pathways related to ovulation in females to cause the onset of puberty. In adults, increasing levels of these hormones signal to the hypothalamus to reduce food intake and increase energy expenditure. In contrast, hormones like ghrelin impact hypothalamic and extrahypothalamic brain regions to drive hunger and the motivation to eat ultimately increasing feeding behavior and decreasing energy expenditure. Based on these actions, we describe some potential targets for the treatment of obesity and the mechanisms by which these targets work to improve human health.

## Linked entities

- **Diseases:** obesity (MONDO:0011122)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}
- **Diseases:** obesity (MESH:D009765)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12799328/full.md

## References

116 references — full list in the complete paper: https://tomesphere.com/paper/PMC12799328/full.md

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Source: https://tomesphere.com/paper/PMC12799328