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胃饥饿素/LEAP - 2失衡在神经性厌食症中的作用

The role of dysregulated ghrelin/LEAP-2 balance in anorexia nervosa.

作者信息

Tezenas du Montcel Chloé, Duriez Philibert, Cao Jingxian, Lebrun Nicolas, Ramoz Nicolas, Viltart Odile, Gorwood Philip, Tolle Virginie

机构信息

Université Paris Cité, UMR-S 1266 INSERM, Institut de Psychiatrie et Neuroscience de Paris (IPNP), 75014 Paris, France.

Clinique des Maladies Mentales et de l'Encéphale, GHU Paris Psychiatrie et Neurosciences, Hôpital Sainte-Anne, 75014 Paris, France.

出版信息

iScience. 2023 Sep 22;26(11):107996. doi: 10.1016/j.isci.2023.107996. eCollection 2023 Nov 17.

DOI:10.1016/j.isci.2023.107996
PMID:37867951
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10587521/
Abstract

LEAP-2 is a ghrelin antagonist with an anorexigenic drive. This study investigates the evolution of plasma ghrelin and LEAP-2 concentrations in 29 patients with anorexia nervosa (AN) before and after refeeding and compares it to physiological adaptations during fasting in healthy controls or to mouse model of chronic food restriction and refeeding. Acute and chronic food restriction decrease LEAP-2 and increase ghrelin concentrations in both humans and mice, while patients with AN displayed higher ghrelin and LEAP-2 concentrations before than after refeeding (p = 0.043). After 6 months follow-up, patients with unstable weight gain (n = 17) had significantly decreased LEAP-2 concentrations after refeeding (p = 0.044), in contrast to patients with stable weight gain (n = 12). We provide evidence that the ghrelin/LEAP-2 system is not regulated according to the nutritional status in AN, in contrast to what is physiologically expected when coping with food restriction.

摘要

LEAP-2是一种具有厌食作用的胃饥饿素拮抗剂。本研究调查了29例神经性厌食症(AN)患者在重新进食前后血浆胃饥饿素和LEAP-2浓度的变化,并将其与健康对照者禁食期间的生理适应性变化或慢性食物限制及重新进食的小鼠模型进行比较。急性和慢性食物限制会降低人类和小鼠体内的LEAP-2并增加胃饥饿素浓度,而AN患者在重新进食前的胃饥饿素和LEAP-2浓度高于重新进食后(p = 0.043)。经过6个月的随访,体重增加不稳定的患者(n = 17)在重新进食后LEAP-2浓度显著降低(p = 0.044),而体重增加稳定的患者(n = 12)则不然。我们提供的证据表明,与应对食物限制时的生理预期相反,AN患者体内的胃饥饿素/LEAP-2系统不受营养状况的调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e89/10587521/e6cc8cc84e91/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e89/10587521/e8f352fa52af/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e89/10587521/5ec0dd55f762/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e89/10587521/2a9785128041/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e89/10587521/c708c6085733/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e89/10587521/e6cc8cc84e91/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e89/10587521/e8f352fa52af/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e89/10587521/5ec0dd55f762/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e89/10587521/2a9785128041/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e89/10587521/c708c6085733/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e89/10587521/e6cc8cc84e91/gr4.jpg

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