Abstract
It is currently accepted that ambient, non-genetic factors influence perinatal development and evoke structural and functional changes that may persist throughout life. Overfeeding and androgenization after birth are two of these key factors that could result in “metabolic imprinting” of neuronal circuits early in life and, thereby, increase the body weight homeostatic “set point”, stimulate appetite, and result in obesity. Our aim was to determine the influence of these obesogenic factors on the response to ghrelin. We observed the expected orexigenic effect of ghrelin regardless of the nutritional or hormonal manipulations to which the animals were subjected to at early postnatal development and this effect remained intact at later stages of development. In fact, ghrelin responses increased significantly when the animals were subjected to one of the two manipulations, but not when both were combined. An increased response to ghrelin could explain the obese phenotype displayed by individuals with modified perinatal environment.
Highlights
It is currently accepted that ambient, non-genetic factors influence perinatal development and evoke structural and functional changes that may persist throughout life
Ghrelin-response studies were carried out in newly-weaned animals, postnatal day (PND) 24 (Fig 1A), and in adult animals, PND 90 (Fig 1B). As it was expected, according to data published by our group[2,4,7], animals treated with ghrelin increased food intake significantly, both at PND 24 and 90, regardless of whether they had been androgenized or not
Androgenized animals at PND 24 displayed basal levels of food intake that were similar to those of non-androgenized animals treated with ghrelin (Fig. 1A)
Summary
It is currently accepted that ambient, non-genetic factors influence perinatal development and evoke structural and functional changes that may persist throughout life. Pups are exposed to many environmental factors that can ‘‘programme’’ the energy regulatory system and have deleterious effects, such as hyperphagia, obesity and/or insulin resistance, among others[22,23,24] In this regard, there are several studies showing that transient exposure to androgens during late gestation[25] or an injection of exogenous testosterone after birth[26,27,28] in female rats or female mice[29,30] can cause metabolic imprinting. Hypothalamic KiSS1 neurons are crucial targets and transmitters of the regulatory actions of sex steroids and metabolic cues during early organizing periods and adulthood[33] In this context, it has been reported that perinatal testosterone excess modifies kisspeptin response impairing puberty and energy homeostasis both in female mice[29] as in male mice[31]. Postnatal overfeeding might modify the response to ghrelin after weaning
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