Identifying neurological mechanisms that regulate feeding behaviour could help to advance the treatment and prevention of obesity and eating disorders. New research in mice has identified and localized a population of neurons that promotes eating to satiate hunger and reduces the desire to eat simply for pleasure.

One subset of these DBB^PENK neurons projects from the DBB to the paraventricular nucleus of the hypothalamus (PVH) and another subset projects to the lateral nucleus of the hypothalamus (LH). The researchers hypothesized that these two neuronal subpopulations have different roles in feeding control. To test this hypothesis, the researchers compared how strongly PVH-projecting DBB^PENK neurons and LH-projecting DBB^PENK neurons responded when fasted or fed mice were given either normal chow or fatty, sugary food. They demonstrate that PVH-projecting DBB^PENK neurons are more responsive to food presentation in fasted mice than in satiated mice. This was true whether the researchers gave the mice normal chow or fatty, sugary food. LH-projecting DBB^PENK neurons, on the other hand, were more active when mice were presented with sugary, fatty food than when they were given normal chow. This response was seen in both fasted and fed mice. The investigators also showed that optogenetic stimulation of PVH-projecting DBB^PENK neurons promoted increased feeding in mice, whereas stimulating LH-projecting DBB^PENK neurons caused the animals to eat less than wild-type controls.

确定调节喂养行为的神经机制可能有助于推进肥胖和饮食失调的治疗和预防。对小鼠的新研究已经确定并定位了一个神经元群，这些神经元促进进食以填补饥饿感，并减少仅仅为了娱乐而吃东西的欲望。

这些 DBB^PENK 神经元的一个子集从 DBB 投射到下丘脑的室旁核 （PVH），另一个子集投射到下丘脑的外侧核 （LH）。研究人员假设这两个神经元亚群在摄食控制中具有不同的作用。为了检验这一假设，研究人员比较了当给禁食或喂食小鼠正常食物或高脂肪、含糖食物时，PVH 投射的 DBB^PENK 神经元和 LH 投射的 DBB^PENK 神经元的反应强度。他们证明，与饱腹小鼠相比，空腹小鼠中投射 PVH 的 DBB^PENK 神经元对食物呈现的反应更敏感。无论研究人员给老鼠喂正常的食物还是高脂肪、含糖的食物，都是如此。另一方面，当小鼠接受含糖、高脂肪的食物时，LH 投射的 DBB^PENK 神经元比给予正常食物时更活跃。这种反应在禁食和进食小鼠中都可见。研究人员还表明，投射 PVH 的 DBB^PENK 神经元的光遗传学刺激促进了小鼠进食的增加，而刺激投射 LH 的 DBB^PENK 神经元会导致动物吃得比野生型对照少。