Maternal PUFA Supplementation and Epigenetic Influences on Fat Tissue

Abstract

Brown adipose tissue (BAT) has the unique ability amongst fat cells of generating heat without causing muscular movement (i.e. shivering). It achieves this by converting surplus chemical energy into heat via UCP1 (uncoupling protein 1), located within mitochondria. At present, research is focusing on BAT due to its essential role in regulating energy balance through the consumption of calories to generate body heat. Although the majority of children, adolescents and healthy adults have extensive deposits of BAT [1–4], adults suffering from obesity do not possess this tissue, which implies a role in how individuals become obese. Children who are obese and are susceptible to metabolic disorders are at risk of continuing to be obese in adulthood and of developing type 2 diabetes mellitus. Accordingly, ways to prevent children becoming obese and a knowledge of the factors governing the development of an excessive body mass index are vital for interventions to halt the vast numbers of adults who are now obese. How BAT grows in utero and shortly after birth is crucial to the longer term persistence of BAT in children and adults [5, 6]. Up to now, however, researchers have not addressed in detail how the mother’s diet may affect the maturation of foetal BAT. Although it is clear that the presence or absence of BAT has a major impact on the development of obesity, the relationship between the quantity of BAT present neonatally, the speed with which BAT is lost and the risk of becoming obese at a later stage has not yet been elucidated. It is known, however, that BAT is lost either through degeneration or a switch in phenotype to white adipose. Specifically, the potential for reducing obesity in her children by manipulating the mother’s diet in pregnancy remains unknown [6–9].