The effect of diet control on puberty onset and immunoreactivity of kisspeptin and neurokinin B in female rats

Early onset puberty and irregular estrous cycles occur more frequently in rats which are fed a high-fat diet. Kisspeptin is an essential factor for the regulation of sexual maturation and is co-expressed with neurokinin B in neurons in the hypothalamic arcuate nucleus. However, the effects of a diet change on kisspeptin neuronal signaling are not well-understood. Therefore, in this study, we examined the immunoreactivity pattern of the kisspeptin/kiss1-receptor (KISS1R) and neurokinin B/ineurokinin3-receptor (R). Pups born to high-fat diet rats were exposed to a high-fat diet until the onset of puberty. From puberty, the offspring originally exposed to a high-fat diet were fed a normal diet up to 85 postnatal days (PND 85). We examined kisspeptin/Kissl-receptor and neurokinin B/neurokinin3-receptor immunoreactivity (IR) in the arcuate nucleus of the pups. The onset of puberty in the high-fat group was significantly earlier than the control group. At the onset of puberty, the densities of kisspeptin and neurokinin B IR cells were significantly higher in the high-fat diet group than in the control group; however, the densities of KISS1 and neurokinin 3-receptor IR cells did not differ between the two groups. At PND 85, the density of kisspeptin and neurokinin B IR cells did not differ between control and high fat group. The density of densities of KISS! and neurokinin 3-receptor IR cells also did not differ between groups at this stage. These data suggest that a high-fat diet can influence puberty onset and the immunoreactivity of kisspeptin and neurokinin B. These effects can be modified by dietary control.