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Enteric neurons increase maternal food intake during reproduction.

ABSTRACT: Reproduction induces increased food intake across females of many animal species^1-4, providing a physiologically relevant paradigm for the exploration of appetite regulation. Here, by examining the diversity of enteric neurons in Drosophila melanogaster, we identify a key role for gut-innervating neurons with sex- and reproductive state-specific activity in sustaining the increased food intake of mothers during reproduction. Steroid and enteroendocrine hormones functionally remodel these neurons, which leads to the release of their neuropeptide onto the muscles of the crop-a stomach-like organ-after mating. Neuropeptide release changes the dynamics of crop enlargement, resulting in increased food intake, and preventing the post-mating remodelling of enteric neurons reduces both reproductive hyperphagia and reproductive fitness. The plasticity of enteric neurons is therefore key to reproductive success. Our findings provide a mechanism to attain the positive energy balance that sustains gestation, dysregulation of which could contribute to infertility or weight gain.

SUBMITTER: Hadjieconomou D

PROVIDER: S-EPMC7610780 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Gs-coupled GPCR signalling in AgRP neurons triggers sustained increase in food intake.

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mTORC1-dependent increase in oxidative metabolism in POMC neurons regulates food intake and action of leptin.

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FoxO1 target Gpr17 activates AgRP neurons to regulate food intake.

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2013-04-09 | E-GEOD-45858 | biostudies-arrayexpress

GFRAL-expressing Neurons Suppress Food Intake via Aversive Pathways

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Heparin Increases Food Intake through AgRP Neurons.

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| S-EPMC6310124 | biostudies-literature

Immediate increase in food intake following exercise messages.

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| S-EPMC4807735 | biostudies-literature

FoxO1 target Gpr17 activates AgRP neurons to regulate food intake.

2013-04-09 | GSE45858 | GEO

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| S-EPMC3968853 | biostudies-literature

Dnmt1/3a deletion in prefrontal cortical neurons reduces palatable food intake

Project description:DNA methylation is an important regulatory mechanism in the control of neuronal function. Both during development and following exposure to salient stimuli, plasticity in the methylation of cytosine residues leads to a change in neuron excitability that subsequently sculpts animal behavior. However, while the response of DNA methyltransferase enzymes in adult neurons to stimuli such as drugs of abuse have been described, less is known about how these enzymes regulate methylation at specific loci to change an animal’s inclination to ingest natural rewards. Specifically, we do not understand how changes in methylation within important brain areas known to regulate palatable food intake can affect ingestion, and detailed investigation of the neurophysiological and genomic effects of perturbing methyltransferase function has not been pursued. By deleting DNA methyltransferase 1 and 3a in the mouse prefrontal cortex, we observed the requirement for these enzymes in the regulation of nutrient rich food consumption in the absence of any effect on the intake of low fat and low sugar chow. We also determined that the deletion profoundly affected neuron excitability within pyramidal cells resident in superficial layers II/III of the cortex but had little effect in deep layer V neurons. Finally, reduced representation bisulfite sequencing revealed both hypo and hypermethylation in response to methyltransferase deletion, an effect that was observed in binding sites for retinoic acid receptor beta (RARβ) located within regulatory regions of genes known to affect neuronal function. Together, our data suggest that alterations in the actions of RARβ could shift neuronal activity to reduce palatable food intake.

2021-05-24 | GSE175380 | GEO

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Project description:Smoking decreases appetite, and smokers often report that they smoke to control their weight. Understanding the neurobiological mechanisms underlying the anorexic effects of smoking would facilitate the development of novel treatments to help with smoking cessation and to prevent or treat obesity. By using a combination of pharmacological, molecular genetic, electrophysiological, and feeding studies, we found that activation of hypothalamic ?3?4 nicotinic acetylcholine receptors leads to activation of pro-opiomelanocortin (POMC) neurons. POMC neurons and subsequent activation of melanocortin 4 receptors were critical for nicotinic-induced decreases in food intake in mice. This study demonstrates that nicotine decreases food intake and body weight by influencing the hypothalamic melanocortin system and identifies critical molecular and synaptic mechanisms involved in nicotine-induced decreases in appetite.

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