Regional cerebral glucose metabolism in bulimia nervosa.
ABSTRACT The authors' purpose in this study was to further delineate the character of cerebral metabolism in bulimia nervosa and to determine if functional links could be made between regional cerebral metabolism and the symptoms of depression, obsessive-compulsive disorder, and bulimia nervosa.
Regional cerebral glucose metabolism was measured by using positron emission tomography in 11 inpatients with bulimia nervosa and 18 normal comparison subjects matched in sex (all were women), age, and educational level. The bulimic patients were also tested for symptoms of major depression and obsessive-compulsive disorder.
The patients with bulimia showed a correlation between lower left anterolateral prefrontal regional cerebral glucose metabolism and greater depressive symptoms. However, the orbitofrontal regional cerebral glucose metabolism of patients with bulimia was not greater than that of comparison subjects, nor was higher orbitofrontal metabolism correlated with greater obsessive-compulsive disorder symptoms.
These findings lead to the conclusion that left anterior lateral prefrontal cortex hypometabolism varies with the depressive symptoms observed in bulimia but that temporal lobe hypermetabolism and asymmetries appear to be independent of the mood state.
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ABSTRACT: Objectives. Bulimia nervosa (BN) is associated with abnormalities of serotoninergic system. Functional or ligand specific brain imaging studies revealed abnormalities in non-overlapping regions. [(18)F]MPPF (4-(2-methoxyphenyl)-1-[2-(N-2-pyridinyl)-p-fluorobenzamido]-ethylpiperazine) is a selective 5-HT1A receptor antagonist with a serotonin-like affinity, capable to assess changes of brain serotoninergic activity in BN patients. Methods. [(18)F]MPPF cerebral binding potential (BPND) was measured by positron emission tomography scan in nine purging-type BN patients and eleven age-matched controls. Voxel-based statistical parametric mapping (SPM) analyses were performed to assess BPND differences between the two groups and between each BN patient and controls group. Results. Mean [(18)F]MPPF BPND was overall increased in BN patients. SPM analysis with revealed symmetrical large clusters of increased [(18)F]MPPF binding in insula, temporo-parietal cortex, prefrontal cortex, in limbic, paralimbic cortex and raphe nuclei. SPM individual analysis indicated significant heterogeneity of [(18)F]MPPF mapping within BN group, including cases with isolated up to widespread increased binding. [(18)F]MPPF BPND did not covariate with depression or eating behaviour-related scores. Conclusions. Large clusters of increased [(18)F]MPPF binding in severe BN overlap previous results, separately described within fMRI or PET studies. The relationship between the inter-individual [(18)F]MPPF binding heterogeneity and serotoninergic modulators efficacy in these patients remains to be assessed.The World Journal of Biological Psychiatry 07/2014; DOI:10.3109/15622975.2014.942358 · 4.23 Impact Factor
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ABSTRACT: BackgroundA high-fat diet (HFD) is a well-known risk factor for cardio-cerebrovascular disease but the relationship between a HFD and depressive symptoms remains unknown.ObjectiveCompare changes in behavioral and measures of brain glucose metabolism in rats fed a HFD to those of rats fed a standard diet.MethodsTwenty male Sprague-Dawley rats were randomly assigned to a study group (n=10) that received a high fat diet for 9 weeks or a control group (n=10) that received a standard diet for 9 weeks. At baseline and at the end of the 9-week trial assessments included body weight, serum lipids (total cholesterol, triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol), the sucrose preference test, and the open field test. The rate of brain glucose metabolism in different brain regions (assessed using micro-positron emission tomography) at the end of the trial was also compared between the two groups of rats.ResultsNine weeks of a HFD in rats resulted in the expected increase in weight and changes in serum lipid levels, but it was also associated with a decreased preference for sucrose (which may be due to a loss of interest in pleasurable activities), increased weight-adjusted water intake, and a significant deactivation of the right thalamus and right striatum (based on decreased rates of glucose metabolism). In the HFD group the magnitude of the drop in the sucrose preference was strongly correlated to the magnitude of the deactivation of the right thalamus (r=0.78) and the right striatum (r=0.81).ConclusionsThese findings support hypotheses about the role of a HFD in the causal pathway for depressive symptoms. Further work is needed to clarify the underling mechanism, but it appears that the interaction between the content of the diet and the limbic system-striatum-thalamus circuit plays a role in both eating behavior and depressive symptoms.06/2014; 26(3):129-137. DOI:10.3969/j.issn.1002-0829.2014.03.004