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Review
, 65 (5), 699-713

Central Nervous System Regulation of Eating: Insights From Human Brain Imaging

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Review

Central Nervous System Regulation of Eating: Insights From Human Brain Imaging

Olivia M Farr et al. Metabolism.

Abstract

Appetite and body weight regulation are controlled by the central nervous system (CNS) in a rather complicated manner. The human brain plays a central role in integrating internal and external inputs to modulate energy homeostasis. Although homeostatic control by the hypothalamus is currently considered to be primarily responsible for controlling appetite, most of the available evidence derives from experiments in rodents, and the role of this system in regulating appetite in states of hunger/starvation and in the pathogenesis of overeating/obesity remains to be fully elucidated in humans. Further, cognitive and affective processes have been implicated in the dysregulation of eating behavior in humans, but their exact relative contributions as well as the respective underlying mechanisms remain unclear. We briefly review each of these systems here and present the current state of research in an attempt to update clinicians and clinical researchers alike on the status and future directions of obesity research.

Keywords: Brain; CNS; Eating; MRI; Obesity.

Conflict of interest statement

Conflicts of Interest: The authors have no conflicts to disclose.

Figures

Figure 1
Figure 1
Control of eating in human brain is regulated by several systems including the homeostatic brain systems (hypothalamus), attention systems (including the parietal and visual cortices), emotion and memory systems (such as the amygdala and hippocampus), cognitive control (including the prefrontal cortex), and the reward network (including the VTA and striatum).
Figure 2
Figure 2
Schematic of nuclei in the hypothalamus which contribute to the control of eating as well as inputs from the periphery. The arcuate (ARC) nucleus contains NPY/AgRP neurons which are orexigenic and POMC/CART neurons which are anorexigenic. These neurons communicate with the other nuclei and neurons which release other orexigenic or anorexigenic peptides. Please note that the neurons may not release all anorexigenic or orexigenic peptides shown (e.g. a single neuron may not release TRH, Oxytocin, AVP and CART in the PVN), but are shown in groups by whether they are anorexigenic or orexigenic in each nucleus. AgRP, agouti-related peptide; ARC, arcuate nucleus; AVP, arginine-vasopressin; BDNF, brain-derived neurotrophic factor; CART, cocaine- and amphetamine regulated transcript; DMH, dorsomedial hypothalamus; LH, lateral hypothalamus; MCH, melanin-concentrating hormone; NPY, neuropeptide Y; NTS, nucleus of the solitary tract; POMC, proopiomelanocortin; PVN, paraventricular nucleus; PYY, peptide YY; TRH, thyroid-releasing hormone; VMH, ventromedial nucleus.
Figure 3
Figure 3
General map of connectivity of the hypothalamus to other CNS centers important for energy intake. These areas communicate with each other and the hypothalamus to control energy intake. Importantly, the hypothalamus also receives key inputs from the periphery regarding available energy (recent intake and storage). NAcc, nucleus accumbens; OFC, orbitofrontal cortex; SN, substantia nigra; VTA, ventral tegmental area.
Figure 4
Figure 4
The reward system mainly consists of the dopaminergic projections from the ventral tegmental area (VTA) and substantia nigra (SN) to the orbitofrontal cortex (OFC) and striatum, particularly the Nucleus Accumbens (NAcc).
Figure 5
Figure 5
Theories of how reward responsivity is affected in obesity: hyperresponsivity (a) and hyporesponsivity (b). The first theory suggests that obese individuals have a heightened reward response to food cues but after increased food consumption, this leads to a decreased response to reward to actual food consumption (but not food cues), and this disconnect leads to greater food intake over time. The second theory posits that individuals with a natural hyposensitivity for rewards consume more food because they require more food consumption and more high calorie or high fat foods to achieve the same level of reward.
Figure 6
Figure 6
Memory influences eating behaviors in a cyclical manner. Decreased hippocampal activity leads to decreased memory of meals and increased response to food cues. This leads to increased caloric consumption and obesity, which in turn leads to increased inflammation and cardiometabolic dysfunction which in turn decreases hippocampal function.
Figure 7
Figure 7
A theory of how cognitive control may interact with reward and food consumption is that in typical cases, heightened cognitive control may decrease the reward system's activation to food cues and thus decrease food consumption (a). This may be altered in obesity, where cognitive control is impaired, and the reward system may be heightened, leading to increased food consumption (b).

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