Abstract
Puberty generally occurs when an individual has stored a sufficient amount of energy. Previous reports have shown that postnatal overfeeding, induced by a small litter size or maternal high fat diet (HFD) feeding during gestation and lactation increases body weight (BW), body fat, plasma leptin levels, and induces precocious puberty. The role of BW, body fat, and leptin in postnatal HFD-induced precocious puberty is poorly understood. In this study, we investigated if postnatal HFD feeding induces precocious puberty independent of BW, body fat, and leptin levels. Different litter sizes and different exposure time to HFD were used to produce HFD feeding pups with different BW and body fat. BW, body fat, and plasma hormones levels were checked at different time points to test their relation with HFD-induced precocious puberty. Our results showed that postnatal HFD feeding increases BW, body fat, adipocyte size, and induces precocious puberty. HFD-induced precocious puberty was independent of BW, body fat, and plasma leptin levels. Plasma gonadotrophin, estradiol, testosterone and insulin levels were comparable in most of the groups. Our results collectively suggest that postnatal HFD feeding induces precocious puberty independent of BW, body fat and plasma leptin levels. Our results also suggest that HFD feeding acts as a stimulator for puberty onset but further studies are needed to understand how it induces precocious puberty.
Highlights
Puberty is an important developmental stage of the life span when an individual achieves somatic and reproductive maturity [1,2,3]
To check whether postnatal high fat diet (HFD) feeding induces obesity before puberty onset in female C57BL/6J mouse pups, we provided a HFD to dams after delivery and to pups post-weaning and checked body weight, body fat and day of Vaginal Canalization (VC)
Our results demonstrate that postnatal HFD feeding induces obesity and precocious puberty in C57BL/6J mouse pups
Summary
Puberty is an important developmental stage of the life span when an individual achieves somatic and reproductive maturity [1,2,3]. Neurohormones, and environmental cues integrate on the hypothalamic-pituitary-gonadal axis (HPG-axis) and regulate reproduction and puberty onset [2, 4, 5]. The HPG-axis is activated by GnRH neurons during puberty, which results in gonadal maturation and function [2, 6]. Nutritional status including overnutrition, undernutrition, and overall metabolic alterations during perinatal stages affect puberty onset. Postnatal overnutrition and HFD feeding induce earlier puberty onset [11,12,13]; undernutrition delays puberty onset [13].
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