دورية أكاديمية
أعرض في EDS

Neonatal overnutrition causes early alterations in the central response to peripheral ghrelin.

التفاصيل البيبلوغرافية
العنوان: Neonatal overnutrition causes early alterations in the central response to peripheral ghrelin.
المؤلفون: Collden G; Inserm U1172, Jean-Pierre Aubert Research Center, University Lille 2, Lille 59045, France., Balland E; Inserm U1172, Jean-Pierre Aubert Research Center, University Lille 2, Lille 59045, France., Parkash J; Inserm U1172, Jean-Pierre Aubert Research Center, University Lille 2, Lille 59045, France., Caron E; Inserm U1172, Jean-Pierre Aubert Research Center, University Lille 2, Lille 59045, France., Langlet F; Inserm U1172, Jean-Pierre Aubert Research Center, University Lille 2, Lille 59045, France., Prevot V; Inserm U1172, Jean-Pierre Aubert Research Center, University Lille 2, Lille 59045, France., Bouret SG; The Saban Research Institute, Developmental Neuroscience Program, Children's Hospital Los Angeles, University of Southern California, Los Angeles, CA 90027, USA ; Inserm U1172, Jean-Pierre Aubert Research Center, University Lille 2, Lille 59045, France.
المصدر: Molecular metabolism [Mol Metab] 2014 Oct 24; Vol. 4 (1), pp. 15-24. Date of Electronic Publication: 2014 Oct 24 (Print Publication: 2015).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier GmbH Country of Publication: Germany NLM ID: 101605730 Publication Model: eCollection Cited Medium: Print ISSN: 2212-8778 (Print) Linking ISSN: 22128778 NLM ISO Abbreviation: Mol Metab Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [München] : Elsevier GmbH, 2012-
مستخلص: Objective: Excess nutrient supply and rapid weight gain during early life are risk factors for the development of obesity during adulthood. This metabolic malprogramming may be mediated by endocrine disturbances during critical periods of development. Ghrelin is a metabolic hormone secreted from the stomach that acts centrally to promote feeding behavior by binding to growth hormone secretagogue receptors in the arcuate nucleus of the hypothalamus. Here, we examined whether neonatal overnutrition causes changes in the ghrelin system.
Methods: We used a well-described mouse model of divergent litter sizes to study the effects of postnatal overfeeding on the central and peripheral ghrelin systems during postnatal development.
Results: Mice raised in small litters became overweight during lactation and remained overweight with increased adiposity as adults. Neonatally overnourished mice showed attenuated levels of total and acyl ghrelin in serum and decreased levels of Ghrelin mRNA expression in the stomach during the third week of postnatal life. Normalization of hypoghrelinemia in overnourished pups was relatively ineffective at ameliorating metabolic outcomes, suggesting that small litter pups may present ghrelin resistance. Consistent with this idea, neonatally overnourished pups displayed an impaired central response to peripheral ghrelin. The mechanisms underlying this ghrelin resistance appear to include diminished ghrelin transport into the hypothalamus.
Conclusions: Early postnatal overnutrition results in central resistance to peripheral ghrelin during important periods of hypothalamic development. Because ghrelin signaling has recently been implicated in the neonatal programming of metabolism, these alterations in the ghrelin system may contribute to the metabolic defects observed in postnatally overnourished mice.
References: JAMA. 2012 Feb 1;307(5):483-90. (PMID: 22253364)
J Neurosci. 2012 Aug 15;32(33):11486-94. (PMID: 22895731)
Diabetes. 2001 Aug;50(8):1714-9. (PMID: 11473029)
J Physiol Pharmacol. 2005 Dec;56(4):555-70. (PMID: 16391414)
Neuroreport. 2004 Dec 22;15(18):2801-5. (PMID: 15597058)
Nature. 2000 Oct 19;407(6806):908-13. (PMID: 11057670)
Proc Natl Acad Sci U S A. 2013 Jan 22;110(4):1512-7. (PMID: 23297228)
J Neurosci. 2004 Mar 17;24(11):2797-805. (PMID: 15028773)
Annu Rev Nutr. 2005;25:435-68. (PMID: 16011474)
Endocrinology. 2004 Jun;145(6):2607-12. (PMID: 14962995)
Neuroendocrinology. 2003 Feb;77(2):91-9. (PMID: 12624530)
Neurosci Lett. 2000 Oct 20;293(1):21-4. (PMID: 11065128)
J Comp Neurol. 2014 Nov 1;522(16):3644-66. (PMID: 24825838)
J Clin Invest. 2015 Feb;125(2):846-58. (PMID: 25607843)
Trends Endocrinol Metab. 2013 Oct;24(10):525-35. (PMID: 23791137)
Am J Clin Nutr. 2013 Dec;98(6):1395-401. (PMID: 24108786)
Cell Metab. 2014 Feb 4;19(2):293-301. (PMID: 24506870)
Nat Med. 1996 May;2(5):589-93. (PMID: 8616722)
Cell Metab. 2013 Apr 2;17(4):607-17. (PMID: 23562080)
PLoS One. 2009 Jun 11;4(6):e5870. (PMID: 19516909)
Front Neuroendocrinol. 2010 Jul;31(3):270-83. (PMID: 20206200)
Lancet. 1996 Jul 20;348(9021):159-61. (PMID: 8684156)
Peptides. 2011 Nov;32(11):2362-6. (PMID: 21736909)
PLoS One. 2011;6(11):e25726. (PMID: 22073140)
Nat Med. 2002 Jul;8(7):643-4. (PMID: 12091883)
Int J Obes Relat Metab Disord. 2003 Jul;27(7):755-77. (PMID: 12821960)
Diabetes. 2001 Apr;50(4):707-9. (PMID: 11289032)
Endocrinology. 2008 Feb;149(2):470-5. (PMID: 18006626)
Cell Metab. 2005 Jun;1(6):371-8. (PMID: 16054086)
Obesity (Silver Spring). 2008 Oct;16(10):2323-30. (PMID: 18719634)
Am J Physiol Regul Integr Comp Physiol. 2009 Mar;296(3):R537-48. (PMID: 19158409)
Exp Physiol. 2007 Mar;92(2):287-98. (PMID: 17170060)
J Endocrinol. 2002 May;173(2):239-45. (PMID: 12010631)
Endocrinology. 2010 Oct;151(10):4745-55. (PMID: 20826561)
Endocrinology. 2004 Aug;145(8):3813-20. (PMID: 15142981)
Am J Physiol Endocrinol Metab. 2012 Jun 15;302(12):E1586-98. (PMID: 22510708)
Horm Res. 2006;65 Suppl 3:83-9. (PMID: 16612119)
Diabetes. 2001 Nov;50(11):2540-7. (PMID: 11679432)
Front Neuroendocrinol. 2013 Jan;34(1):18-26. (PMID: 23357643)
Neuron. 2003 Feb 20;37(4):649-61. (PMID: 12597862)
Endocrinology. 2010 Feb;151(2):702-13. (PMID: 20016030)
J Clin Endocrinol Metab. 2008 Jul;93(7):2800-5. (PMID: 18460565)
Cell Metab. 2008 Feb;7(2):179-85. (PMID: 18249177)
J Neurosci. 2004 Nov 17;24(46):10353-63. (PMID: 15548649)
Mol Metab. 2013 Oct 17;3(1):64-72. (PMID: 24567905)
Science. 1988 Jun 3;240(4857):1328-31. (PMID: 3131879)
J Comp Neurol. 2006 Jan 20;494(3):528-48. (PMID: 16320257)
Endocrinology. 2010 Sep;151(9):4270-9. (PMID: 20668022)
Endocrinology. 2005 Oct;146(10):4211-6. (PMID: 16020474)
Endocrinology. 2010 Apr;151(4):1598-610. (PMID: 20194730)
Endocrinology. 2013 Feb;154(2):709-17. (PMID: 23307790)
J Clin Invest. 1997 Feb 1;99(3):385-90. (PMID: 9022070)
معلومات مُعتمدة: P01 ES022845 United States ES NIEHS NIH HHS; R01 DK084142 United States DK NIDDK NIH HHS
فهرسة مساهمة: Keywords: ARH, arcuate nucleus; AgRP, agouti-related peptide; DMH, dorsomedial nucleus; GHSR, growth hormone secretagogue receptor; GOAT, ghrelin O-acyltransferase; Ghrelin; HFHS, high-fat/high-sucrose diet; Hormone; Hypothalamus; LHA, lateral hypothalamic area; MBH, mediobasal hypothalamus; ME, median eminence; NL, normal litters; NPY, neuropeptide Y; Nutrition; P, postnatal day; POMC, pro-opiomelanocortin; PVH, paraventricular nucleus; Programming; SL, small litter; Tanycytes
تواريخ الأحداث: Date Created: 20150217 Date Completed: 20150216 Latest Revision: 20181113
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC4314535
DOI: 10.1016/j.molmet.2014.10.003
PMID: 25685686
قاعدة البيانات: MEDLINE
الوصف
تدمد:2212-8778
DOI:10.1016/j.molmet.2014.10.003