Neuroanatomical correlates of hunger and satiation in humans using positron emission tomography

Abstract

The central role of the hypothalamus in the origination and͞or processing of feeding-related stimuli may be modulated by the activity of other functional areas of the brain including the insular cortex (involved in enteroceptive monitoring) and the prefrontal cortex (involved in the inhibition of inappropriate response tendencies). Regional cerebral blood f low (rCBF), a marker of neuronal activity, was measured in 11 healthy, normal-weight men by using positron emission tomography in a state of hunger (after 36-h fast) and a state of satiation (after a liquid meal). Hunger was associated with significantly increased rCBF in the vicinity of the hypothalamus and insular cortex and in additional paralimbic and limbic areas (orbitofrontal cortex, anterior cingulate cortex, and parahippocampal and hippocampal formation), thalamus, caudate, precuneus, putamen, and cerebellum. Satiation was associated with increased rCBF in the vicinity of the ventromedial prefrontal cortex, dorsolateral prefrontal cortex, and inferior parietal lobule. Changes in plasma insulin concentrations in response to the meal were negatively correlated with changes in rCBF in the insular and orbitofrontal cortex. Changes in plasma free fatty acid concentrations in response to the meal were negatively correlated with changes in rCBF in the anterior cingulate and positively correlated with changes in rCBF in the dorsolateral prefrontal cortex. In conclusion, these findings raise the possibility that several regions of the brain participate in the regulation of hunger and satiation and that insulin and free fatty acids may be metabolic modulators of postprandial brain neuronal events. Although exploratory, the present study provides a foundation for investigating the human brain regions and cognitive operations that respond to nutritional stimuli.

Preliminary fMRI findings concerning the influence of 5‐HTP on food selection

“…Tataranni et al. (1999) have also shown the insular cortex to be associated with conditions of hunger. Also within the limbic system, the amygdala and cingulate cortex not only show a positive correlation with hunger but they also display sensitivity to food desirability (Arana et al., 2003; Shin, Zheng, & Berthoud, 2009).…”

“…Consideration of the brain's reactions to food stimuli demonstrates that responses are not restricted to a single area but rather a complex network of structures that participate in the evaluation of calories, nutrients, hunger, or satiety (Tataranni et al., 1999). Functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) illustrate that responses to food cues depend highly on an individual's physiological brain states.…”

“…Cortical regions responsive to food images include the limbic and paralimbic areas (Tataranni et al., 1999). Part of this system is the prefrontal cortex (PFC) which by receiving inputs from the hypothalamus, is implicated in food‐seeking behaviors as well as acting as a “regulating valve” for food consumption.…”

“…Part of this system is the prefrontal cortex (PFC) which by receiving inputs from the hypothalamus, is implicated in food‐seeking behaviors as well as acting as a “regulating valve” for food consumption. Neuroimaging studies argue that the ventromedial PFC (VMPFC) and dorsolateral PFC (DLPFC) in particular, exhibit an increased BOLD response during satiation in comparison to hunger (Del Parigi et al., 2002; Simmons, Martin, & Barsalou, 2005; Tataranni et al., 1999). …”

“…The insula, characterized by neurological studies as the site of the primary taste cortex, is of considerable interest since it connects the hypothalamus, OFC, the limbic system, and the occipital cortex (Cerf‐Ducastel, Van de Moortele, MacLeod, Le Bihan, & Faurion, 2001; Schienle et al., 2002; Tataranni et al., 1999). Individuals treated with monotonous diets when presented with non‐diet food stimuli demonstrated more activity in the left insula signifying craving and food desirability‐related activation (Pelchat et al., 2004).…”