Abstract
Body weight (BW) is regulated in age-dependent manner; it continues to increase during growth period, and reaches a plateau once reaching adulthood. However, its underlying mechanism remains unknown. Regarding such mechanisms in the brain, we here report that neural circuits from the hypothalamus (paraventricular nucleus: PVN) to the brainstem (dorsal vagal complex: DVC) suppress late-onset BW gain without affecting food intake. The genetic suppression of the PVN-DVC circuit induced BW increase only in aged rats, indicating that this circuit contributes to suppress the BW at a fixed level after reaching adulthood. PVN neurons in the hypothalamus were inactive in younger rats but active in aged rats. The density of neuropeptide Y (NPY) terminal/fiber is reduced in the aged rat PVN area. The differences in neuronal activity, including oxytocin neurons in the PVN, were affected by the application of NPY or its receptor inhibitor, indicating that NPY is a possible regulator of this pathway. Our data provide new insights into understanding age-dependent BW regulation.
Highlights
Body weight (BW) is regulated in age-dependent manner; it continues to increase during growth period, and reaches a plateau once reaching adulthood
We previously reported on a projection from the paraventricular nucleus (PVN) in the hypothalamus to the nucleus of the solitary tract (NTS), which is a component of the dorsal vagal complex (DVC) in the brainstem that regulates energy homeostasis, including food intake[14,15,21]
We found a significant reduction of neuropeptide Y (NPY) IR terminal/fiber density of approximately 10% in the PVN of the 40-week-old rats compared to the 20-week-old rats (Fig. 3a–c), whereas α-melanocyte stimulating hormone (α-MSH) IR terminals/fibers in the PVN tended to decrease but not significantly different in the 40-week-old rats compared to the 20-week-old rats
Summary
Body weight (BW) is regulated in age-dependent manner; it continues to increase during growth period, and reaches a plateau once reaching adulthood. Regarding such mechanisms in the brain, we here report that neural circuits from the hypothalamus (paraventricular nucleus: PVN) to the brainstem (dorsal vagal complex: DVC) suppress late-onset BW gain without affecting food intake. Neuropeptide Y (NPY) and α-melanocyte stimulating hormone (α-MSH), derived from the precursor proopiomelanocortin (POMC), are major neuronal peptides for regulating appetite in the ARC as orexigenic and anorexigenic peptides, respectively. These two neuronal species in the ARC provide inhibitory or stimulatory signals to the PVN neurons, thereby integrating energy state information from peripheral signals
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