Increasing evidence suggests that early nutrition has programming effects on adult health.
We determined the potential programming effects of maternal obesity and high-fat (HF) diet during pregnancy and/or lactation on offspring metabolic syndrome.
These programming effects on the fetus would be physiologically mediated through heightened and/or abnormal activity of the maternal sympathetic-adrenal-medullary system (SAM) and especially of her hypothalamic-pituitary-adrenocortical axis (HPA-axis).
Mechanisms involved in these programming effects, apart from those described in central nervous system development, have not been established.
Several studies have demonstrated that early life growth patterns exert programming effects on disease risk in later life, highlighting the key role played by early nutrition [1], [2].
We have previously shown that this protocol normalizes the blood pressure of the resulting offspring of protein restricted rats, strongly suggesting that steroids play a key role in mediating the programming effects of undernutrition [24], [27].
Over the past decade a considerable body of evidence has emerged showing that circumstances during gestation may have lifelong programming effects on the offspring in both humans and animal models.
Woods and colleagues have asserted that rather than glucocorticoids mediating programming effects of undernutrition, all effects of steroid treatment in rodent pregnancy are related to associated reductions in food intake [31].
To begin to understand the long-term metabolic programming effects that a maternal high-fat diet has on the offspring, it is necessary to separate effects that occur in-utero from changes that occur after parturition.
However, apart from the effects on the central nervous system (CNS), there is little information on possible programming effects of perinatal conditions on the peripheral nervous system structures involved in the control of energy metabolism and adipose tissue growth.
Therefore, the potential exists for separate control by the CNS of the SNS drive on WAT at these distal levels of the neuroaxis and thus a possible neuroanatomical basis for the differential programming effects of perinatal conditions as well as on the inhibition of WAT cell proliferation.
