PROOPIOMELANOCORTIN (POMC)

The role of the Proopiomelanocortin (POMC) system in the regulation of energy balance has been the subject of extensive research for several decades. POMC is a precursor peptide produced in the anterior pituitary gland that is cleaved into several peptides including β-endorphin, ACTH, and α-MSH. These peptides have well-documented roles in the regulation of food intake and energy expenditure. In this review, we will discuss the physiological and molecular mechanisms through which POMC system regulates energy balance, and the potential implications of this system in the pathogenesis of obesity.

The POMC system is involved in the regulation of energy balance through the hypothalamus. The peptides released from POMC act on neurons in the arcuate nucleus to influence appetite and energy expenditure. β-endorphin and α-MSH stimulate the release of the orexigenic neuropeptide, neuropeptide Y (NPY), which increases food intake and decreases energy expenditure. Conversely, ACTH stimulates the release of the anorexigenic hormone, corticotropin-releasing hormone (CRH), which decreases food intake and increases energy expenditure. Additionally, ACTH and α-MSH can activate melanocortin-4 receptors (MC4Rs) on neurons in the lateral hypothalamus to inhibit food intake and increase energy expenditure.

The POMC system may be dysregulated in obesity. Studies have shown that obese individuals have reduced expression of POMC in the hypothalamus and increased expression of NPY. Additionally, there is evidence of a link between mutations in the MC4R gene, which can lead to reduced MC4R expression and activity, and obesity. These findings suggest that dysregulation of the POMC system may contribute to the development of obesity.

In conclusion, the POMC system plays an essential role in the regulation of energy balance, and dysregulation of this system may contribute to the pathogenesis of obesity. Further research is needed to better understand the molecular and physiological mechanisms of POMC system regulation and how dysregulation of this system contributes to obesity.

References

Kleinz, M. J., & Woods, S. C. (2017). Neuroendocrinology of energy balance and obesity. Physiological Reviews, 97(3), 1083–1112. https://doi.org/10.1152/physrev.00045.2016

Cone, R. D. (2005). Molecular regulation of appetite and satiety. Endocrine Reviews, 26(3), 439–461. https://doi.org/10.1210/er.2004-0017

Kozlowska, W., & Wardlaw, S. L. (2017). The proopiomelanocortin system and obesity. Frontiers in Endocrinology, 8(March), 1–14. https://doi.org/10.3389/fendo.2017.00020

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