Fetal and neonatal pathways to obesity

Gluckman, P.D., Hanson, M.A., Beedle, A.S. and Raubenheimer, D. (2008) Fetal and neonatal pathways to obesity Frontiers of Hormone Research. Glucocorticoid-Induced Osteoporosis, 36, pp. 61-72. (doi:10.1159/000115337). (PMID:18230894).


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Evolutionary and developmental perspectives add considerably to our understanding of the aetiology of obesity and its related disorders. One pathway to obesity represents the maladaptive consequences of an evolutionarily preserved mechanism by which the developing mammal monitors nutritional cues from its mother and adjusts its developmental trajectory accordingly. Prediction of a nutritionally sparse environment leads to a phenotype that promotes metabolic parsimony by favouring fat deposition, insulin resistance, sarcopenia and low energy expenditure. But this adaptive mechanism evolved to accommodate gradual changes in nutritional environment; rapid transition to a situation of high energy density results in a mismatch between predicted and actual environments and increased susceptibility to metabolic disease. This pathway may also explain why breast and bottle feeding confer different risks of obesity. We discuss how early environmental signals act through epigenetic mechanisms to alter metabolic partitioning, glucocorticoid action and neuroendocrine control of appetite. A second pathway involves alterations in fetal insulin levels, as seen in gestational diabetes, leading to increased prenatal fat mass which is subsequently amplified by postnatal factors. Both classes of pathway may coexist in an individual. This developmental approach to obesity suggests that potential interventions will vary according to the target population.

Item Type: Article
Digital Object Identifier (DOI): doi:10.1159/000115337
ISSNs: 0301-3073 (print)
Keywords: evolution, insulin, female, environment, review, consequences, infant, overnutrition, complications, human, embryology, epigenetic, phenotype, obesity, glucocorticoids, physiology, adipose tissue, resistance, insulin resistance, risk, insulin-resistance, cues, environmental, disease, humans, pregnancy, infant nutrition disorders, metabolic disease, genetic predisposition to disease, prediction, fetal, etiology, diabetes, mass
ePrint ID: 61167
Date :
Date Event
Date Deposited: 11 Sep 2008
Last Modified: 16 Apr 2017 17:31
Further Information:Google Scholar
URI: http://eprints.soton.ac.uk/id/eprint/61167

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