Obesity and Brain Positron Emission Tomography

Abstract

Obesity, an increasingly common problem in modern societies, results from energy intake chronically exceeding energy expenditure. This imbalance of energy can be triggered by the internal state of the caloric equation (homeostasis) and non-homeostatic factors, such as social, cultural, psychological, environmental factors or food itself. Nowadays, positron emission tomography (PET) radiopharmaceuticals have been examined to understand the cerebral control of food intake in humans. Using ¹⁵O-H₂ PET, changes in regional cerebral blood flow (rCBF) coupled to neuronal activity were reported in states of fasting, satiation after feeding, and sensory stimulation. In addition, rCBF in obese subjects showed a greater increase in insula, the primary gustatory cortex. ¹⁸F-fluorodeoxyglucose PET showed higher metabolic activity in postcentral gyrus of the parietal cortex and lower in prefrontal cortex and anterior cingulate cortex in obese subjects. In addition, dopamine receptor (DR) PET demonstrated lower DR availability in obese subjects, which might lead to overeating to compensate. Brain PET has been utilized to reveal the connectivity between obesity and brain. This could improve understanding of obesity and help develop a new treatment for obesity.

Keywords: Brain; Obesity; Positron-emission tomography.

Fig. 1

Brain areas involved in the regulation of eating behavior: amygdala (behavioral salience and stress responses), anterior cingulate cortex (regulation of autonomic function of the body, reward anticipation, and decision making), brainstem (blood–brain barrier crossing of peripheral peptide hormones and binding to intracerebral receptors), dorsolateral prefrontal cortex (goal-directed behavior), fusiform gyrus (visual association cortex), hypothalamus (integration of homoeostatic information from the body), insula (interoception, homoeostasis, and integration of sensory signals across modalities), nucleus accumbens (reward prediction and conditioning), nucleus caudatus (feedback processing), and the orbitofrontal cortex (valuation and secondary gustatory cortex). Reprinted from Functional neuroimaging in obesity and the potential for development of novel treatments, Lancet Diabetes Endocrinology, 4(8), Schlögl H et al., 695–705, 2016, with permission from Elsevier

Fig. 2

Transaxial FDG PET images of a subject during food presentation and during neutral intervention at levels of postcentral gyrus, superior temporal cortex, insula, and orbitofrontal cortex. Reprinted from Exposure to appetitive food stimuli markedly activates the human brain, Neuroimage, 21(4), Wang GJ et al., 1790–1797, 2004, with permission from Elsevier

Fig. 3

Group average images of ¹¹C–Raclopride (distribution volume image) PET for controls (left) and obese (right) individuals at the level of the basal ganglia. Reprinted from Brain dopamine and obesity, Lancet, 357(9253), Wang GJ et al., 354–357, 2001, with permission from Elsevier