Abstract:
Hunger and satiety drive eating behaviours via changes in brain function. The hypothalamus is a central component of the brain networks that regulate food intake. Animal research parsed the roles of the lateral hypothalamus (LH) and medial hypothalamus (MH) in hunger and satiety, respectively. Here, we examined how hunger and satiety change information flow between human LH and MH brain networks, and how these interactions are influenced by body mass index (BMI). Forty participants (16 overweight/obese) underwent two resting-state functional MRI scans while being fasted and sated. The excitatory/inhibitory influence of information flow between the MH and LH was modelled using spectral dynamic causal modelling. Our results revealed two core networks interacting across homeostatic state and weight: subcortical bidirectional connections between the LH, MH and the substantia nigra pars compacta (prSN), and cortical top-down inhibition from fronto-parietal and temporal areas. During fasting, we found higher inhibition between the LH and prSN, whereas the prSN received greater top-down inhibition from across the cortex. Individuals with higher BMI showed that these network dynamics occur irrespective of homeostatic state. Our findings reveal fasting affects brain dynamics over a distributed hypothalamic-midbrain-cortical network. This network is less sensitive to state-related fluctuations among people with obesity.
The hypothalamus is a central component of the brain networks regulating food intake. Animal research subdivided the hypothalamus anatomically and functionally into lateral hypothalamus (LH) and medial hypothalamus (MH). This is the first study showing how the LH and MH causally interact with other neural regions and how their dynamics change with weight and homeostasis in humans. Adopting state-of-the-art spectral dynamic causal modelling of resting-state fMRI data, we provide new insights into how homeostasis affect hypothalamic circuit dynamics, which involve a distributed network of midbrain and cortical areas with a key role of the substantia nigra. We identified unique aspects of network organisation associated with obesity involving reciprocal connections between the LH and MH, and input from the substantia nigra to the MH.
摘要:
饥饿和饱腹感通过大脑功能的变化来驱动饮食行为。下丘脑是调节食物摄入的大脑网络的中心组成部分。动物研究分析了外侧下丘脑(LH)和内侧下丘脑(MH)在饥饿和饱腹感,分别。这里,我们研究了饥饿和饱腹感如何改变人类LH和MH大脑网络之间的信息流,以及这些相互作用如何受到体重指数(BMI)的影响。40名参与者(16名超重/肥胖)在禁食和禁食的同时进行了两次静息状态功能MRI扫描。使用光谱动态因果模型对MH和LH之间的信息流的兴奋/抑制影响进行建模。我们的结果揭示了两个核心网络在体内平衡状态和体重之间相互作用:LH之间的皮质下双向连接,MH和黑质致密部(prSN),以及来自额顶叶和颞叶区域的皮质自上而下的抑制。在禁食期间,我们发现LH和prSN之间有更高的抑制作用,而prSN从整个皮质受到更大的自上而下的抑制。BMI较高的个体表明,这些网络动力学的发生与稳态无关。我们的发现表明,禁食会影响分布的下丘脑-中脑-皮层网络的大脑动力学。该网络对肥胖人群中与状态相关的波动不太敏感。
下丘脑是调节食物摄入的大脑网络的中心组成部分。动物研究在解剖学和功能上将下丘脑细分为下丘脑外侧(LH)和下丘脑内侧(MH)。这是第一项研究,显示了LH和MH如何与其他神经区域发生因果关系,以及它们的动力学如何随着人类的体重和稳态而变化。采用最先进的静息状态fMRI数据的频谱动态因果建模,我们提供了关于稳态如何影响下丘脑回路动力学的新见解,其中涉及中脑和皮质区域的分布式网络,黑质起着关键作用。我们确定了与肥胖相关的网络组织的独特方面,涉及LH和MH之间的相互联系,从黑质输入到MH。