Non-alcoholic fatty liver disease (NAFLD) is associated with obesity, insulin resistance, type 2 diabetes and cardiovascular disease and can be considered the hepatic manifestation of the metabolic syndrome. NAFLD represents a spectrum of disease, from the relatively benign simple steatosis to the more serious non-alcoholic steatohepatitis, which can progress to liver cirrhosis, hepatocellular carcinoma and end-stage liver failure, necessitating liver transplantation. Although the increasing prevalence of NAFLD in developed countries has substantial implications for public health, many of the precise mechanisms accounting for the development and progression of NAFLD are unclear. The environment in early life is an important determinant of cardiovascular disease risk in later life and studies suggest this also extends to NAFLD. Here we review data from animal models and human studies which suggest that fetal and early life exposure to maternal under- and overnutrition, excess glucocorticoids and environmental pollutants may confer an increased susceptibility to NAFLD development and progression in offspring and that such effects may be sex-specific. We also consider studies aimed at identifying potential dietary and pharmacological interventions aimed at reducing this risk. We suggest that further human epidemiological studies are needed to ensure that data from animal models are relevant to human health.

Egg fat is of considerable importance in the nutrition of the developing chick as a source of energy and essential fatty acids such as linoleic (18:2 n-6) and α-linolenic (18:3 n-3) acids. During incubation, yolk lipids provide fatty acids that are utilized for energy, synthesis of polyunsaturated fatty acids (PUFA)-rich membrane phospholipids, and eicosanoids by the embryo. Eicosanoids derived from n-6 fatty acid are more potent and pro-inflammatory than eicosanoids derived from n-3 fatty acids.

Two models of early life programming as affected by n-3 PUFA are investigated. Egg PUFA enrichment through breeder hen diet (pre-hatch or in ovo) or early post-hatch (within first 5 hours) feeding is investigated. Early access to nutrients (pre- and early post-hatch) is important because in broiler hatchlings that are selected for rapid early growth much of the immune system development occurs early in life. However, the current industry practice of feeding breeding hens diets high in n-6 fatty acids, limits the supply of essential n-3 PUFA in the hatchling. Early access to n-3 PUFA through in ovo or early post-hatch diet led to: (1) increase in the retention of n-3 PUFA in cell membranes, (2) reduction in plasma non-esterified fatty acids, (3) reduced production of pro-inflammatory eicosanoids, (4) suppression of cell-mediated immunity, and (5) alteration in cyclooxygenase-2 protein expression. The effects of an early exposure persisted from 14 to 35 days in different tissues and cells.

Given the fact that broiler birds are raised for 39 to 56 days, and that the effect of pre-hatch and early post-hatch nutrition persists for up to and over 36-47% of post-hatch life, using an early life programming approach will generate new knowledge about the role of maternal and early post-hatch diet in enhancing bird health and welfare.