Relationship between Poor Fetal Growth and the Subsequent...

Epidemiological and animal studies have shown a relationship between poor fetal growth with the subsequent development of obesity, type 2 diabetes, and metabolic syndrome (Ravelli et al. 1976; Hales Ozanne 2003; Painter et al. 2008; Pembrey 2010). Such developmental programming has been explained by the â€Å"thrifty phenotype† hypothesis, which proposes that poor fetal nutrition can result in reprogramming of the fetus, which allows the offspring to maximize the bodys capacity for energy storage under conditions of poor nutrition once out of the womb. However, this phenotype would be detrimental under conditions where normal or excessive nutrition are present and would thus promote obesity (Hales Ozanne 2003). Body weight, food intake and metabolism are regulated by the hypothalamus that processes central and peripheral signals. Within the hypothalamus, neurons residing in the ARC (arcuate nucleus) – PVN (paraventricular) –PF/LH (perifornical/lateral hypothalamus) axis communicate with each other and are subjected to the influence of several peripheral factors, including leptin and insulin (Davis et al. 2010). The action of these hormones on food intake occurs in part by convergence on a specific set of neurons within the ARC (Elmquist et al. 1998, Abizaid Horvath 2008) that contains neuronal populations expressing orexigenic neuropeptide Y (NPY) and agouti-related peptide (AgRP) and the anorectic pro- opiomelanocortin (POMC). NPY synthesis and secretion have been found