AI Article Synopsis
- AgRP neurons are crucial for driving hunger, and too much food intake is a major cause of obesity and metabolic issues.
- Research using special mouse models shows that the microRNA miR-33 significantly regulates AgRP neurons, with its absence leading to increased eating, weight gain, and metabolic problems in the mice.
- The study identifies a key pathway influenced by a non-coding RNA that affects hunger by managing several energy-related processes linked to AgRP neuron activation, suggesting new treatment options for obesity and metabolism-related diseases.
Article Abstract
AgRP neurons drive hunger, and excessive nutrient intake is the primary driver of obesity and associated metabolic disorders. While many factors impacting central regulation of feeding behavior have been established, the role of microRNAs in this process is poorly understood. Utilizing unique mouse models, we demonstrate that miR-33 plays a critical role in the regulation of AgRP neurons, and that loss of miR-33 leads to increased feeding, obesity, and metabolic dysfunction in mice. These effects include the regulation of multiple miR-33 target genes involved in mitochondrial biogenesis and fatty acid metabolism. Our findings elucidate a key regulatory pathway regulated by a non-coding RNA that impacts hunger by controlling multiple bioenergetic processes associated with the activation of AgRP neurons, providing alternative therapeutic approaches to modulate feeding behavior and associated metabolic diseases.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10923783 | PMC |
| http://dx.doi.org/10.1038/s41467-024-46427-0 | DOI Listing |
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