Metabolic programming of long-term outcomes due to fatty acid nutrition in early life

Abstract

Understanding of the importance of dietary fatty acids has grown beyond a simple source of energy to complex roles in regulating gene expression and cell and intracellular communication. This is important because the metabolic and neuroendocrine environment of the fetus and infant plays a key role in guiding the set point of neural receptors that regulate energy homeostasis and expression of genes that control energy storage and oxidation. Early deviations in these pathways have the potential to lead to lasting adaptations, termed metabolic programming, which may combine to increase the risk of metabolic syndrome in later life. The quality of fatty acids in human diets has undergone major changes in the last 50 years, characterized by an increase in ω-6 and decrease in ω-3 fatty acids. Evidence is accumulating to support the concept that the maternal intake of ω-6 and ω-3 fatty acids in gestation and lactation, possibly involving both excess ω-6 and inadequate ω-3 fatty acids, can impact the developing infant tissue lipids and neuroendocrine and metabolic pathways relevant to metabolic programming. Further work is needed to understand the needs for different ω-6 and ω-3 fatty acids during fetal and infant life, and their roles with respect to development of energy homeostasis and metabolism.

Figure 1

Schematic to illustrate the concept that deficiency, excesses or imbalances in fatty acids at key stages of development may have lasting consequences due to alterations in cellular development, gene expression or the metabolic and neuroendocrine response to the fatty acid supply. Effects are expected to involve multiple mechanisms and organs and cross‐talk among organs and mechanisms. Adapted from Symonds et al. (2009).

Figure 2

Per capita intakes of fats from vegetable oils and animal fats in developed and developing nations. Redrawn using data from Wolmarans (2009).