Proteins activate satiety-related neuronal pathways in the brainstem and hypothalamus of rats.

Our objective was to study the relationship between the satiety induced by high-protein meals and the activation of brain areas involved in the onset of satiety. In rats, we used immunohistochemistry to monitor brain centers activated by a meal by receiving information from the gastrointestinal tract or via humoral pathways. In the nucleus of the solitary tract (NTS), the acute or chronic intake of high-protein meals led to increased activation of the noradrenergic/adrenergic neurons involved in cholecystokinin-induced satiety.

Fos-positive neurons are increased in the nucleus of the solitary tract and decreased in the ventromedial hypothalamus and amygdala by a high-protein diet in rats.

Transition from a normal- (NP) to a high-protein (HP) diet induces a rapid depression in food intake and a progressive but incomplete return to the initial intake during the succeeding days. The aim of this study was to determine which CNS regions are involved in the HP diet-induced satiety in rats. Brains were collected from 3 groups of adult rats after habituation to an NP diet (21 d), during the transition phase to a HP diet (2 d), or after habituation to the HP diet (21 d).

Presence of the N-methyl-D-aspartic acid R1 glutamatergic receptor subunit in the lumbosacral spinal cord of male rats.

The lumbosacral spinal cord contains neurones that control the lower urogenital and digestive tracts. Spinal neurones respond to activation from the periphery and supraspinal nuclei. Glutamate, acting through a variety of receptors, is an established transmitter of excitatory pathways to the spinal cord.