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      Sweet Dopamine: Sucrose Preferences Relate Differentially to Striatal D 2 Receptor Binding and Age in Obesity

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          Abstract

          Alterations in dopaminergic circuitry play a critical role in food reward and may contribute to susceptibility to obesity. Ingestion of sweets releases dopamine in striatum, and both sweet preferences and striatal D 2 receptors (D2R) decline with age and may be altered in obesity. Understanding the relationships between these variables and the impact of obesity on these relationships may reveal insight into the neurobiological basis of sweet preferences. We evaluated sucrose preferences, perception of sweetness intensity, and striatal D2R binding potential (D2R BP ND) using positron emission tomography with a D2R-selective radioligand insensitive to endogenous dopamine, ( N-[ 11C] methyl)benperidol, in 20 subjects without obesity (BMI 22.5 ± 2.4 kg/m 2; age 28.3 ± 5.4 years) and 24 subjects with obesity (BMI 40.3 ± 5.0 kg/m 2; age 31.2 ± 6.3 years). The groups had similar sucrose preferences, sweetness intensity perception, striatal D2R BP ND, and age-related D2R BP ND declines. However, both striatal D2R BP ND and age correlated with sucrose preferences in subjects without obesity, explaining 52% of their variance in sucrose preference. In contrast, these associations were absent in the obese group. In conclusion, the age-related decline in D2R was not linked to the age-related decline in sweetness preferences, suggesting that other, as-yet-unknown mechanisms play a role and that these mechanisms are disrupted in obesity.

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          Most cited references24

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          Whole brain segmentation: automated labeling of neuroanatomical structures in the human brain.

          We present a technique for automatically assigning a neuroanatomical label to each voxel in an MRI volume based on probabilistic information automatically estimated from a manually labeled training set. In contrast to existing segmentation procedures that only label a small number of tissue classes, the current method assigns one of 37 labels to each voxel, including left and right caudate, putamen, pallidum, thalamus, lateral ventricles, hippocampus, and amygdala. The classification technique employs a registration procedure that is robust to anatomical variability, including the ventricular enlargement typically associated with neurological diseases and aging. The technique is shown to be comparable in accuracy to manual labeling, and of sufficient sensitivity to robustly detect changes in the volume of noncortical structures that presage the onset of probable Alzheimer's disease.
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            Psychophysics of sweet and fat perception in obesity: problems, solutions and new perspectives.

            Psychophysical comparisons seem to show that obese individuals experience normal sweet and fat sensations, they like sweetness the same or less, but like fat more than the non-obese do. These psychophysical comparisons have been made using scales (visual analogue or category) that assume intensity labels (e.g. extremely) which denote the same absolute perceived intensity to all. In reality, the perceived intensities denoted by labels vary because they depend on experiences with the substances to be judged. This variation makes comparisons invalid. Valid comparisons can be made by asking the subjects to rate their sensory/hedonic experiences in contexts that are not related to the specific experiences of interest. Using this methodology, we present the evidence that the sensory and hedonic properties of sweet and fat vary with body mass index. The obese live in different orosensory and orohedonic worlds than do the non-obese; the obese experience reduced sweetness, which probably intensifies fat sensations, and the obese like both sweet and fat more than the non-obese do. Genetic variation as well as taste pathology contribute to these results. These psychophysical advances will impact experimental as well as clinical studies of obesity and other eating disorders.
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              "Nonhedonic" food motivation in humans involves dopamine in the dorsal striatum and methylphenidate amplifies this effect.

              The drive for food is one of the most powerful of human and animal behaviors. Dopamine, a neurotransmitter involved with motivation and reward, its believed to regulate food intake in laboratory animals by modulating its rewarding effects through the nucleus accumbens (NA). Here we assess the involvement of dopamine in "nonhedonic" food motivation in humans. Changes in extracellular dopamine in striatum in response to nonhedonic food stimulation (display of food without consumption) were evaluated in 10 food-deprived subjects (16-20 h) using positron emission tomography (PET) and [11C]raclopride (a D2 receptor radioligand that competes with endogenous dopamine for binding to the receptor). To amplify the dopamine changes we pretreated subjects with methylphenidate (20 mg p.o.), a drug that blocks dopamine transporters (mechanism for removal of extracellular dopamine). Although the food stimulation when preceded by placebo did not increase dopamine or the desire for food, the food stimulation when preceded by methylphenidate (20 mg p.o.) did. The increases in extracellular dopamine were significant in dorsal (P < 0.005) but not in ventral striatum (area that included NA) and were significantly correlated with the increases in self-reports of hunger and desire for food (P < 0.01). These results provide the first evidence that dopamine in the dorsal striatum is involved in food motivation in humans that is distinct from its role in regulating reward through the NA. In addition it demonstrates the ability of methylphenidate to amplify weak dopamine signals. Copyright 2002 Wiley-Liss, Inc.
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                Author and article information

                Journal
                Diabetes
                Diabetes
                diabetes
                diabetes
                Diabetes
                Diabetes
                American Diabetes Association
                0012-1797
                1939-327X
                September 2016
                15 June 2016
                : 65
                : 9
                : 2618-2623
                Affiliations
                [1] 1Atkins Center of Excellence in Obesity Medicine, Center for Human Nutrition, Washington University School of Medicine in St. Louis, St. Louis, MO
                [2] 2Department of Psychiatry, Washington University School of Medicine in St. Louis, St. Louis, MO
                [3] 3Department of Radiology, Washington University School of Medicine in St. Louis, St. Louis, MO
                [4] 4Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine in St. Louis, St. Louis, MO
                [5] 5Department of Neurology, Washington University School of Medicine in St. Louis, St. Louis, MO
                [6] 6Department of Neuroscience, Washington University School of Medicine in St. Louis, St. Louis, MO
                [7] 7Department of Occupational Therapy, Washington University School of Medicine in St. Louis, St. Louis, MO
                [8] 8Department of Physical Therapy, Washington University School of Medicine in St. Louis, St. Louis, MO
                Author notes
                Corresponding author: Marta Y. Pepino, pepinodegruevmy@ 123456wustl.edu .
                Article
                0407
                10.2337/db16-0407
                5001180
                27307220
                92bb7705-045b-4fce-a321-2155fe30a672
                © 2016 by the American Diabetes Association.

                Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at http://diabetesjournals.org/site/license.

                History
                : 28 March 2016
                : 31 May 2016
                Page count
                Figures: 3, Tables: 1, Equations: 0, References: 24, Pages: 6
                Funding
                Funded by: National Institutes of Health
                Award ID: R01 DK085575
                Award ID: P30 DK056341
                Award ID: UL1 TR000448
                Categories
                Obesity Studies

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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