Long-Term Energy Deficit in Mice Causes ...
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Article dans une revue scientifique: Article original
DOI :
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Title :
Long-Term Energy Deficit in Mice Causes Long-Lasting Hypothalamic Alterations after Recovery.
Author(s) :
Méquinion, Mathieu [Auteur]
Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 [JPArc]
Le Thuc, Ophélia [Auteur]
Institut de pharmacologie moléculaire et cellulaire [IPMC]
Zgheib, Sara [Auteur]
Marrow Adiposity & Bone Lab - Adiposité Médullaire et Os - ULR 4490 [MABLab (ex-pmoi)]
Alexandre, David [Auteur]
Différenciation et communication neuronale et neuroendocrine [DC2N]
Chartrel, Nicolas [Auteur]
Différenciation et communication neuronale et neuroendocrine [DC2N]
Rovère, Carole [Auteur]
Institut de pharmacologie moléculaire et cellulaire [IPMC]
Hardouin, Pierre [Auteur]
Physiopathologie des Maladies Osseuses Inflammatoires (PMOI) - ULR 4490
Viltart, Odile [Auteur]
Sciences Cognitives et Sciences Affectives (SCALab) - UMR 9193 [SCALab]
Chauveau, Christophe [Auteur]
Physiopathologie des Maladies Osseuses Inflammatoires (PMOI) - ULR 4490
Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 [JPArc]
Le Thuc, Ophélia [Auteur]
Institut de pharmacologie moléculaire et cellulaire [IPMC]
Zgheib, Sara [Auteur]
Marrow Adiposity & Bone Lab - Adiposité Médullaire et Os - ULR 4490 [MABLab (ex-pmoi)]
Alexandre, David [Auteur]
Différenciation et communication neuronale et neuroendocrine [DC2N]
Chartrel, Nicolas [Auteur]
Différenciation et communication neuronale et neuroendocrine [DC2N]
Rovère, Carole [Auteur]
Institut de pharmacologie moléculaire et cellulaire [IPMC]
Hardouin, Pierre [Auteur]

Physiopathologie des Maladies Osseuses Inflammatoires (PMOI) - ULR 4490
Viltart, Odile [Auteur]

Sciences Cognitives et Sciences Affectives (SCALab) - UMR 9193 [SCALab]
Chauveau, Christophe [Auteur]
Physiopathologie des Maladies Osseuses Inflammatoires (PMOI) - ULR 4490
Journal title :
Neuroendocrinology
Abbreviated title :
Neuroendocrinology
Volume number :
105
Pages :
372-383
Publication date :
2017-11
ISSN :
1423-0194
English keyword(s) :
Agouti-Related Protein
Animals
Body Weight
Cytokines
Disease Models, Animal
Eating
Female
Hypolipoproteinemias
Hypothalamic Hormones
Hypothalamus
Leptin
Melanins
Mice
Mice, Inbred C57BL
Neuropeptide Y
Neuropeptides
Orexins
Pituitary Hormones
RNA, Messenger
Receptors, Leptin
Receptors, Neuropeptide
Animal model
Anorexia nervosa
Anorexigenic peptides
Hypothalamus
Leptin
Long-term energy deficit
Orexigenic peptides
Refeeding
Animals
Body Weight
Cytokines
Disease Models, Animal
Eating
Female
Hypolipoproteinemias
Hypothalamic Hormones
Hypothalamus
Leptin
Melanins
Mice
Mice, Inbred C57BL
Neuropeptide Y
Neuropeptides
Orexins
Pituitary Hormones
RNA, Messenger
Receptors, Leptin
Receptors, Neuropeptide
Animal model
Anorexia nervosa
Anorexigenic peptides
Hypothalamus
Leptin
Long-term energy deficit
Orexigenic peptides
Refeeding
HAL domain(s) :
Sciences cognitives
English abstract : [en]
Although the short-term effects of fasting or energy deficit on hypothalamic neuropeptide circuitries are now better understood, the effects of long-term energy deficit and refeeding remain to be elucidated. We showed that ...
Show more >Although the short-term effects of fasting or energy deficit on hypothalamic neuropeptide circuitries are now better understood, the effects of long-term energy deficit and refeeding remain to be elucidated. We showed that after a long-term energy deficit, mice exhibited persistent hypoleptinemia following the refeeding period despite restoration of fat mass, ovarian activity, and feeding behavior. We aimed to examine the hypothalamic adaptations after 10 weeks of energy deficit and after 10 further weeks of nutritional recovery. To do so, we assessed the mRNA levels of the leptin receptor and the main orexigenic and anorexigenic peptides, and their receptors regulated by leptin. Markers of hypothalamic inflammation were assessed as leptin can also participate in this phenomenon. Long-term time-restricted feeding and separation induced significant increase in mRNA levels of hypothalamic orexigenic peptides, while both Y1 and Y5 receptor mRNAs were downregulated. No changes occurred in the mRNA levels of orexin (OX), melanin-concentrating hormone, pro-opiomelanocortin, 26RFa (26-amino acid RF-amide peptide), and their receptors despite an increase in the expression of melanocortin receptors (MC3-R and MC4-R) and OXR1 (OX receptor 1). The refeeding period induced an overexpression of leptin receptor mRNA in the hypothalamus. The other assessed mRNA levels were normalized except for Y2, Y5, MC3-R, and MC4-R, which remained upregulated. No convincing changes were observed in neuroinflammatory markers, even if interleukin-1β mRNA levels were increased in parallel with those of Iba1 (ionized calcium-binding adaptor molecule 1), a marker of microglial activation. Normalization of leptin-regulated functions and hypothalamic gene expressions in refed mice with low plasma leptin levels could be sustained by recalibration of hypothalamic sensitivity to leptin.Show less >
Show more >Although the short-term effects of fasting or energy deficit on hypothalamic neuropeptide circuitries are now better understood, the effects of long-term energy deficit and refeeding remain to be elucidated. We showed that after a long-term energy deficit, mice exhibited persistent hypoleptinemia following the refeeding period despite restoration of fat mass, ovarian activity, and feeding behavior. We aimed to examine the hypothalamic adaptations after 10 weeks of energy deficit and after 10 further weeks of nutritional recovery. To do so, we assessed the mRNA levels of the leptin receptor and the main orexigenic and anorexigenic peptides, and their receptors regulated by leptin. Markers of hypothalamic inflammation were assessed as leptin can also participate in this phenomenon. Long-term time-restricted feeding and separation induced significant increase in mRNA levels of hypothalamic orexigenic peptides, while both Y1 and Y5 receptor mRNAs were downregulated. No changes occurred in the mRNA levels of orexin (OX), melanin-concentrating hormone, pro-opiomelanocortin, 26RFa (26-amino acid RF-amide peptide), and their receptors despite an increase in the expression of melanocortin receptors (MC3-R and MC4-R) and OXR1 (OX receptor 1). The refeeding period induced an overexpression of leptin receptor mRNA in the hypothalamus. The other assessed mRNA levels were normalized except for Y2, Y5, MC3-R, and MC4-R, which remained upregulated. No convincing changes were observed in neuroinflammatory markers, even if interleukin-1β mRNA levels were increased in parallel with those of Iba1 (ionized calcium-binding adaptor molecule 1), a marker of microglial activation. Normalization of leptin-regulated functions and hypothalamic gene expressions in refed mice with low plasma leptin levels could be sustained by recalibration of hypothalamic sensitivity to leptin.Show less >
Language :
Anglais
Audience :
Internationale
Popular science :
Non
Administrative institution(s) :
Université de Lille
CNRS
CHU Lille
CNRS
CHU Lille
Submission date :
2022-05-06T14:57:28Z
2022-05-11T10:27:40Z
2022-05-11T10:27:40Z
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