The hypothalamic syndrome in rats.
The original conception of the hypothalamus controlling feeding by the activity of two specific and reciprocally inhibitory centers has now been largely abandoned. Detailed neural research using a wide variety of methods has demonstrated the complex morphological and functional organization of this part of the brain and has modified the earlier simplistic approach. However, examination of the feeding responses to a variety of stimuli that represent components of control of feeding indicates that much or even most feeding control is extrahypothalamic. As demonstrated by the obesity or aphagia resulting from hypothalamic damage or from reversible hypothalamic interference, the hypothalamus influences or modulates feeding control, possibly by an enabling action, but it does not itself substantially control food intake either in the short or the long term. In the cachaxia of cancer, which can tentatively be regarded as a negative obesity, and which is closely reproducible in a rat model, the decline of food intake can be attributed to failure of control components that are all extrahypothalamic, and the deterioration of control of feeding appears to be quite independent of the hypothalamus. The very detailed reconstruction of intrahypothalamic circuitry that has been developed in recent years has not yet had any real impact on the problem of where or how the active control of food intake is generated or the way in which the hypothalamus influences this control.
D000818:Animals; D001069:Appetite Regulation / Q000187:drug effects; D002100:Cachexia / Q000503:physiopathology; D004195:Disease Models, Animal; D002149:Energy Intake; D005247:Feeding Behavior / Q000187:drug effects; D006801:Humans; D007031:Hypothalamus / Q000503:physiopathology*; D007328:Insulin / Q000494:pharmacology; D009369:Neoplasms / Q000503:physiopathology; D009765:Obesity / Q000503:physiopathology*; D051381:Rats; D013577:Syndrome
D007328:Insulin