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Emerging evidence suggests that maternal obesity may programme offspring obesity and dysmetabolism [4] such that the phenomenal rises in the rates of obesity within the last few decades may not just be due to the ready availability of cheap energy dense foods but may also be due to transgenerational amplification of obesity through epigenetic mechanisms [5 7].
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This is an important observation, as pregnancy and the early postnatal period represent critical stages of development for the offspring and may "programme" the risk of metabolic disorders later in life [ 36, 37].
Adverse events in pregnancy may 'programme' offspring for the later development of cardiovascular disease and hypertension.
27 It is possible that the determination of the T cell balance in pregnancy may also programme long term immune responses in offspring.
This finding suggests that the quality of the food eaten in pregnancy may in some way pre-programme offspring to over consume.
Maternal water restriction (WR) may induce offspring plasma hypertonicity and enhanced vasopressin secretory responses.
Prenatal environment may increase offspring's risk for obesity.
Additionally, in these rats, postnatal leptin treatment of offspring from normally-nourished mothers programmes their male offspring to develop obesity in later life, while there is no comparable effect in their female offspring.
The male may pull the offspring from the birth canal, clean them, or collect food for the mother and offspring.
Adult males may kill dependent offspring that are not theirs so the female will return to estrus and thus they can sire offspring of their own.
This may substantially reduce offspring survival chances in the wild.
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Justyna Jupowicz-Kozak
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