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The hormone leptin, secreted from fat cells, binds to neurons in the arcuate nucleus to suppress the release of peptides NPY an AGRP while augmenting the release of α-MSH in the paraventricular nucleus. These changes in brain peptides converge to suppress feeding. As leptin levels fall, NPY and AGRP stimulation of the paraventricular nucleus increases while α-MSH stimulation declines, inducing hunger. Powerful genetic and seasonal factors influence body weight, and body weight is very tightly regulated around a set zone, despite extensive dietary, behavioral, or surgical interventions. See You Next Week ! Have a Good Day ! * * * * * * * Is There a Single Satiety or Hunger Center in the Brain The Ventromedial Hypothalamus Appeared for a Time to Be the Satiety Center The Lateral Hypothalamus Appeared for a Time to Be the Hunger Center Satiety and Hunger Functions Are Spread across Several Brain Regions Leptin Helps Regulate Body Weight Brain Peptides, in Response to Leptin, Mediate Some of the Signals for Hunger Brain Peptides, in Response to Leptin, Mediate Some of the Signals for Hunger 1. Fat cells secret leptin into circulation. The more and larger the fat cells, the more leptin is released 2. Leptin reaches leptin receptors in hypothalamus regions, including the LH, and the arcuate, supraoptic, and paraventricular nuclei 3. Leptin receptor activation suppresses neuropeptide production and release Brain Peptides, in Response to Leptin, Mediate Some of the Signals for Hunger 4. Leptin inhibits arcuate neurons releasing NPY and AGRP, but excites neurons releasing αMSH. NPY-receptive neurons in those regions normally trigger feeding, while the melancortin-receptive neurons (which are excited by αMSH and inhibited by AGRP) normally inhibit eating. As leptin levels fall, the circuits will induce hunger. NPY: neuropeptide Y AGRP: agouti-related peptide αMSH: α-melanocyte (黑素细胞) stimulating hormone MRC: melanocortin receptor Brain Peptides, in Response to Leptin,
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