The influence of leptin on early life programming of obesity.
Epidemiological evidence together with experimental models shows a direct relationship between fetal and early postnatal growth patterns and an increased risk of adult metabolic disease. Maternal health and nutrition are key determinants in influencing infant growth but the precise molecular mechanisms underlying this relationship are unclear, although it is evident that there are critical time windows when these effects are important. Animal models show mechanistic parallels with human populations and highlight that the early environment represents a therapeutic window for protection from obesity and metabolic disease. The observation that developmental programming can be reversed has been demonstrated in studies in which both maternal and neonatal leptin treatment prevents the induction of the adverse metabolic phenotype. Given that orally administered peptides are absorbed intact by the new born, the prospect of providing supplemental leptin either as drops or in milk deserves serious consideration as a means of reducing or reversing the obesity and type 2 diabetes epidemic.
Stocker
Claire J
CJ
Clore Laboratory, University of Buckingham, Buckingham MK18 1EG, UK.
Cawthorne
Michael A
MA
D000328:Adult; D000818:Animals; D004195:Disease Models, Animal; D005247:Feeding Behavior / Q000502:physiology*; D005260:Female; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D020738:Leptin / Q000378:metabolism* / Q000627:therapeutic use; D024821:Metabolic Syndrome / Q000503:physiopathology; D009765:Obesity / Q000503:physiopathology* / Q000517:prevention & control; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000503:physiopathology / Q000517:prevention & control
D020738:Leptin