Mechanism of Anorexia in Vitamin-deficient Hyperphagic Animals

Abstract

RECENT findings¹ have demonstrated that the ventromedial hypothalamic nuclei act as ‘satiety’ brakes which, in response to certain stimuli (particularly metabolic), inhibit a constantly activated ‘feeding’ mechanism. This mechanism, in turn, appears to be initiated at the level of the anterolateral nuclei². Destruction of the ventromedial nuclei does not increase hunger (as measured by rate of ingestion); it shortens the pauses between ‘meals’ which, in normal animals, steadily increase during the day so as to constitute a 24-hr, feeding cycle marked with a definite ‘satiety’ pattern¹. A method for the destruction of these centres in the rat³, the mouse⁴ and other species is through the use of stefeotaxic instruments. In the mouse, it has also been shown recently⁵ that administration of gold thioglucose leads to obesity through injury to the ventromedial nuclei. Such mice and ‘hypothalamic’ rats and mice can thus be used for elucidating whether vitamin deficiencies act by permanently activating the ‘satiety’ mechanism or by inactivating the ‘feeding’ mechanism. For example, one could visualize that thiamine deficiency, the anorexic effect of which is classic, permanently activates the ventromedial nuclei because of the constant elevation of blood concentration of intermediaries of carbohydrate metabolism, or inactivates the feeding mechanism through the action of toxic accumulation of noxious products or because of the lack of carboxylase per se.