Abstract
The etiology of pathological eating in anorexia nervosa (AN) remains poorly understood. Cerebral blood flow (CBF) is an indirect marker of neuronal function. In healthy adults, fasting increases CBF, reflecting increased delivery of oxygen and glucose to support brain metabolism. This study investigated whether women remitted from restricting-type AN (RAN) have altered CBF in response to hunger that may indicate homeostatic dysregulation contributing to their ability to restrict food. We compared resting CBF measured with pulsed arterial spin labeling in 21 RAN and 16 healthy comparison women (CW) when hungry (after a 16-h fast) and after a meal. Only remitted subjects were examined to avoid the confounding effects of malnutrition on brain function. Compared to CW, RAN demonstrated a reduced difference in the Hungry − Fed CBF contrast in the right ventral striatum, right subgenual anterior cingulate cortex (pcorr < 0.05) and left posterior insula (punc < 0.05); RAN had decreased CBF when hungry versus fed, whereas CW had increased CBF when hungry versus fed. Moreover, decreased CBF when hungry in the left insula was associated with greater hunger ratings on the fasted day for RAN. This represents the first study to show that women remitted from AN have aberrant resting neurovascular function in homeostatic neural circuitry in response to hunger. Regions involved in homeostatic regulation showed group differences in the Hungry − Fed contrast, suggesting altered cellular energy metabolism in this circuitry that may reduce motivation to eat.
Highlights
The motivation to eat in humans is a complex process influenced by intrinsic mechanisms relating to hunger and satiety, and extrinsic mechanisms based on the appetitive incentive value of food [1]
The purpose of this study was to determine whether women with a prior history of Anorexia nervosa (AN) have a diminished Cerebral blood flow (CBF) response when hungry, suggesting that altered homeostatic regulation might contribute to reduced motivation to eat in AN
Using pulsed arterial spin labeling (ASL), we reproduced previous positron emission tomography (PET) findings [12] in a larger sample of healthy women and found that hunger was associated with increased CBF in regions involved in appetite regulation, including the right ventral striatum (VST), subgenual anterior cingulate cortex (ACC), and left posterior insula
Summary
The motivation to eat in humans is a complex process influenced by intrinsic mechanisms relating to hunger and satiety, and extrinsic mechanisms based on the appetitive incentive value of food [1]. Homeostatic and hedonic brain regions, including the hypothalamus, amygdala, striatum, orbitofrontal cortex, insula, and anterior cingulate cortex (ACC), are tightly interconnected and form a network that controls feeding behavior [1, 11, 12]. The hypothalamus, a homeostatic center, regulates metabolic processes, including hunger and food intake, with motivation-reward systems associated with the hedonic drive to eat [1, 11]. The insula, a key area in the neural control of intrinsic homeostatic processes, serves as the primary gustatory and interoceptive region in the human cortex [13]. Together in a coordinated effort, these brain regions interpret the metabolic state of an individual and regulate appetite, motivation, and reward processing [11]
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