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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neurological mechanisms associated with weight gain in animals have been extensively studied in mammals, but relatively little investigation has been carried out in birds. As in mammals, it has been shown that lesion of the ventromedial nucleus of the hypothalamus leads to hyperphagia and obesity in several species of birds. Likewise, bilateral lesions of the lateral hypothalamus result in aphagia and weight loss. Therefore, at the level of the hypothalamus, control of body weight appears to be controlled by similar neurological mechanisms in all homeothermic species via modulation of the sympathetic nervous system. Because of the role of the mammalian striatum in body weight regulation, body weight data from various manipulative studies in chickens were analyzed to see if these areas play a role in avian body weight regulation. In the first study, cycloheximide, glutamate, or saline was injected intracerebrally into 1-day-old chicks. In the second study, 3-day-old chicks received surgical ablation of the neocortex or kainic acid-induced lesions of the paleostriatum. Decreased body weight was noted in chicks that received injections of cycloheximide or glutamate, or kainic acid-induced lesions. The disruption in body weight in Experiment 1 might have been due to neurochemical pathology thought to occur in the paleostriatum. In the second experiment, lesions of the neostriatum or hyperstriatum, analogous to the neocortex in mammals, did not produce a difference in weight gain compared to controls. This preliminary work with kainic acid lesions in the chicken paleostriatum demonstrates a significant long-term decrease in body weight. As in mammals, the basal ganglia may have a role in body weight regulation.
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PMID:Avian telencephalon and body weight. 791 25

Feeding is a complex process responsive to sensory information related to sight and smell of food, previous feeding experiences, satiety signals elicited by ingestion and hormonal signals related to energy balance. Dopamine released in specific brain regions is associated with pleasurable and rewarding events and may reinforce positive aspects of feeding. Dopamine also influences initiation and coordination of motor activity and is required for sensorimotor functions. Thus, dopamine may facilitate integration of sensory cues related to hunger, initiating the search for food and its consumption. Dopaminergic neurons in the substantia nigra and ventral tegmental area project to the caudate putamen and nucleus accumbens, where they modulate movement and reward. There are projections from the nucleus accumbens to the lateral hypothalamus that regulate feeding. Dopamine-deficient mice (Dbh(Th/+), Th-/-; hereafter DD mice) cannot synthesize dopamine in dopaminergic neurons. They gradually become aphagic and die of starvation. Daily treatment of DD mice with L-3,4-dihydroxyphenylalanine (L-DOPA) transiently restores brain dopamine, locomotion and feeding. Leptin-null (Lep(ob/ob)) mice exhibit obesity, decreased energy expenditure and hyperphagia. As the hypothalamic leptin-melanocortin pathway appears to regulate appetite and metabolism, we generated mice lacking both dopamine and leptin (DD x Lep(ob/ob)) to determine if leptin deficiency overcomes the aphagia of DD mice. DD x Lep(ob/ob) mice became obese when treated daily with L-DOPA, but when L-DOPA treatment was terminated the double mutants were capable of movement, but did not feed. Our data show that dopamine is required for feeding in leptin-null mice.
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PMID:Dopamine is required for hyperphagia in Lep(ob/ob) mice. 1080 66


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