Neonatal overnutrition, but not neonatal undernutrition, disrupts CCK-induced hypophagia and neuron activation of the nucleus of the solitary tract and paraventricular nucleus of hypothalamus of male Wistar rats
Hypophagia
Area postrema
Solitary tract
Overnutrition
Lateral hypothalamus
DOI:
10.1016/j.brainresbull.2023.02.012
Publication Date:
2023-02-20T17:39:20Z
AUTHORS (9)
ABSTRACT
Metabolic programming may be induced by reduction or enhancement of litter size, which lead to neonatal over undernutrition, respectively. Changes in nutrition can challenge some regulatory processes adulthood, such as the hypophagic effect cholecystokinin (CCK). In order investigate effects nutritional on anorexigenic function CCK pups were raised small (SL, 3 per dam), normal (NL, 10 large litters (LL, 16 and postnatal day 60, male rats treated with vehicle (10 µg/Kg) for evaluation food intake c-Fos expression area postrema (AP), nucleus solitary tract (NTS), paraventricular (PVN), arcuate (ARC), ventromedial (VMH), dorsomedial (DMH) nuclei hypothalamus. Overnourished showed increased body weight gain that was inversely correlated neuronal activation PaPo, VMH, DMH neurons, whereas undernourished had lower gain, PaPo only. SL no response neuron NTS PVN CCK. LL exhibited preserved hypophagia AP, NTS, immunoreactivity ARC, any litter. These results indicate actions, associated PVN, impaired overnutrition. However, these responses not disrupted undernutrition. Thus, data suggest an excess poor supply nutrients during lactation display divergent satiation signaling adult rats.
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