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Early life nutritional intervention results in hypothalamic neuronal malprogramming predispsoing to adult‐onset obesity
Author(s) -
Patel Mulchand S,
ShbeirElDika Suhad,
Srinivasan Malathi,
Bodiga Vijaya,
Thamotharan Shanthie,
Devaskar Sherin
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a522-b
Subject(s) - obesity , intervention (counseling) , medicine , gerontology , physiology , psychology , neuroscience , pediatrics , endocrinology , psychiatry
Altered nutritional experiences in early periods of life have been identified as causative factors in the etiology of the obesity epidemic observed in adults and children. We have shown that a high carbohydrate (HC) dietary treatment in neonatal rats resulted in chronic hyperinsulinemia (supported by functional adaptations in islets) and adult‐onset obesity (HC phenotype). Due to the aberration in the energy balance in the HC rats we have investigated the effects of the HC milk formula on neuronal signaling related to energy homeostasis in the hypothalamus. Immunohistochemical analyses of brain sections from 12 day‐old HC pups in comparison with age‐matched mother‐fed (MF) control pups showed significant increases in the immunoreactivity in arcuate nucleus of orexigenic peptides (neuropeptide Y, agouti‐related polypeptide) and decreases in immunoreactivity of insulin receptor β subunit, leptin receptor and α melanocortin‐stimulating hormone. These early hypothalamic changes persisted in adult HC rats despite weaning on to a rodent diet on day 24. The occurrence of the early hypothalamic adaptations in HC pups are likely due to the overlap of the HC dietary treatment with the period of developmental plasticity of hypothalamic neurons. Additionally, we have also observed that the hypothalamus of term fetuses of hyperinsulinemic/obese HC mothers depicted malprogramming of the neurons predisposing them for the development of obesity in their adulthood (Supported by NIH Grant DK 61518).