Nicolaidis S, Even P
Laboratoire de Neurobiologie des Régulations, UA 637, CNRS, Institut de Biologie du Collège de France, Paris.
Int J Obes Relat Metab Disord. 1992 Dec;16 Suppl 3:S31-41.
Hunger is elicited by the depletion of available macronutrients to the cells. The question is how the depletion is sensed and transduced into a biologically meaningful signal of hunger. Accumulating data show that the signal comes not from depletion of carbohydrates alone or from one of the other major macronutrients. Instead, the signal is generated by the overall cellular power production that induces hunger when it decreases and satiety when it increases. As for satiation, i.e. the state that causes the termination of a meal before nutrients cross the intestinal barrier, it is induced by early metabolic events elicited reflexly from orogastric afferences and tuning the preprandial metabolism towards the level of the postprandial metabolism. Neuronal responses from the medial hypothalamus suggest that they may integrate information on the degree of utilization of glucose and of lipids. Some of the pharmacological agents that reduce feeding seem to operate by increasing the metabolic rate in a way similar to that induced by a meal. These pharmacological agents are active because they mobilize endogenous metabolites, such as lipids, so inducing a sort of 'autocanibalic' meal.
饥饿是由细胞可用的大量营养素耗尽引发的。问题在于这种耗尽是如何被感知并转化为具有生物学意义的饥饿信号的。越来越多的数据表明，该信号并非仅来自碳水化合物的耗尽，也不是来自其他主要大量营养素中的某一种。相反，该信号是由整体细胞能量产生所生成的，当能量产生减少时引发饥饿，而当能量产生增加时则引发饱腹感。至于饱腹感，即营养物质穿过肠屏障之前导致进食终止的状态，它是由口胃传入神经反射引发的早期代谢事件所诱导的，并将餐前代谢调节至餐后代谢水平。来自下丘脑内侧的神经元反应表明，它们可能整合有关葡萄糖和脂质利用程度的信息。一些减少进食的药物似乎通过以类似于进食所诱导的方式提高代谢率来发挥作用。这些药物之所以有效，是因为它们调动内源性代谢物，如脂质，从而引发一种“自身消耗”式的进食。
