Differential brain responses to satiation in obese and lean men.

Abstract

Knowledge of how the brain contributes to the regulation of food intake in humans is limited. We used positron emission tomography and measures of regional cerebral blood flow (rCBF) (a marker of neuronal activity) to describe the functional anatomy of satiation (i.e., the response to a liquid meal) in the context of extreme hunger (36-h fast) in 11 obese (BMI ≥35 kg/m 2 , age 27 ± 5 years, weight 115 ± 11 kg, 38 ± 7% body fat; mean ± SD) and 11 lean (BMI ≤25 kg/m 2 , age 35 ± 8 years, weight 73 ± 9 kg, 19 ± 6% body fat) men. As in lean men, satiation in obese men produced significant increases in rCBF in the vicinity of the ventromedial and dorsolateral prefrontal cortex and significant decreases in rCBF in the vicinity of the limbic/paralimbic areas (i.e., hippocampal formation, temporal pole), striatum (i.e., caudate, putamen), precuneus, and cerebellum. However, rCBF increases in the prefrontal cortex were significantly greater in obese men than in lean men (P < 0.005). rCBF decreases in limbic/paralimbic areas, temporal and occipital cortex, and cerebellum were also significantly greater in obese men than in lean men (P < 0.005), whereas rCBF decreases in the hypothalamus and thalamus were attenuated in obese men compared with lean men (P < 0.05). This study raises the possibility that the brain responses to a meal in the prefrontal areas (which may be involved in the inhibition of inappropriate response tendencies) and limbic/paralimbic areas (commonly associated with the regulation of emotion) may be different in obese and lean men. Additional studies are required to investigate how these differential responses are related to the pathophysiology of obesity. Diabetes 49:838-846, 2000 O besity is a chronic relapsing disease with a prevalence reaching epidemic proportions in most industrialized countries (1,2). Whereas the exact pathophysiology of this disease remains unclear, studies in animals (3,4) and numerous reports in humans (5-10) indicate that eating behavior disorders (i.e., hyperphagia) and the resulting excessive energy intake play a major role in the development of obesity.The role of the brain (especially the hypothalamus) in the regulation of body weight is well established in animals (11). In humans, substantial molecular (12) and neuropharmacologic evidence (13) attest to the importance of the central nervous system in maintaining energy balance. However, the neuroanatomical correlates of human feeding behavior are largely unknown. Some information comes from pathological conditions associated with hyperphagia and obesity such as hypothalamic tumors (14) and Prader-Willi syndrome, the most common type of inherited human hypothalamic disorder (15). In addition, patients with frontal lobe dementia with computerized tomography documented prefrontal atrophy frequently present with hyperphagia (16). Furthermore, seizures of the opercula (including the insular cortex) induce mastication, salivation, swallowing, and gustatory hallucinations (17). Finally, in 1 study, 50% of patients with eating epi...

Brain Activation by Visual Food-Related Stimuli and Correlations with Metabolic and Hormonal Parameters: A fMRI Study

“…In contrast to the findings of Gautier et al, we did not find correlations between postprandial FFA and activation in hippocampal and parahippocampal regions [28]. Also, there were no significant correlations between glucose and the activation in the limbic system during the fasting and satiated condition when viewing food vs nonfood food pictures.…”

“…extremely long fasting period as used by others [28]. Also, we performed a second measurement one hour after ingestion of a standardized meal, expecting the acute metabolic and hormonal changes following a meal to be effective in producing a satiated state.…”

Neural mechanisms underlying food motivation in children and adolescents

“…Previous findings in adults with obesity indicate greater increases in the PFC and greater decreases in the OFC, amygdala, hippocampus, insula, and temporal lobe during satiation compared to lean individuals Gautier et al, 2000). While these studies examining food motivation in overweight adults aid in the overall understanding of neural mechanisms of overeating and obesity, none have been performed in groups of children and adolescents.…”

“…It has been hypothesized that these neural systems also play an important role in controlling hyperphagia in obese individuals (e.g., Tataranni and DelParigi, 2003). Though still in its infancy, neuroimaging research on obese and overweight adults has shown differential patterns of neural activity in obese compared to lean individuals, including abnormal functioning in the hypothalamus (Matsuda et al, 1999), insula Gautier et al, 2000), hippocampus Gautier et al, 2000), and OFC (Gautier et al, 2000). These findings offer evidence for discrepancies in neural circuits involved in food motivation between obese and lean adults.…”

Obese children show hyperactivation to food pictures in brain networks linked to motivation, reward and cognitive control

“…Differential activations (hyperactivation) have been found in the hypothalamus, 29,30 OFC, 19,30 dorsal striatum, 17 insula 31,32 and hippocampus 31 in obese individuals. Obese adults also show a smaller decrease in hypothalamic activity after a meal when compared with HW individuals.…”