Should Prevention of Childhood Obesities Start In The Womb?Monday, March 14, 2011
Regular readers will recall the accumulating evidence that maternal health and weight before and during pregnancy may have a substantial influence on the risk of excessive weight gain in their offspring, most likely resulting from epigenetic programming in utero.
A study by Mina Desai and colleagues from the University of California Los Angeles, just published in Brain Research, now suggests that intra-uterine genetic adaptation may have a substantial influence on the growth and development neurons that regulate appetite and energy homeostasis.
The researchers examined the hypothesis that a programmed impairment of neural progenitor cells (NPC) may contribute to altered hypothalamic neural pathways that control feeding behaviours in the development of low-birth-weight (LBW) offspring.
In their study, they examined hypothalamic NPCs in the brains of pups born to food restricted and unrestricted mice and showed that the LBW offspring born to the former had impaired in vivo evidence of NPC division and migration, and reduced in vitro evidence of proliferation and differentiation to neurons and astrocytes, under basal and when stimulated with the appetite-regulating hormones insulin and leptin.
These studies show that the environmental exposure of the mother can significantly affect the brain development of offspring in areas essential for appetite and energy control.
Although these findings come from animal studies, the association between adverse in utero factors, resulting in either low or too-high birth weight babies, and excess weight gain in kids, youth and adults has been accumulating in human studies.
Thus, these findings, add considerable plausibility to the postulated relationship between maternal health and fetal programming of appetite and energy regulation increasing the propensity to obesity later in life.
Desai M, Li T, & Ross MG (2011). Hypothalamic neurosphere progenitor cells in low birth-weight rat newborns: Neurotrophic effects of leptin and insulin. Brain research, 1378, 29-42 PMID: 21215735