26 research outputs found

    Specific [<sup>123</sup>I]β-CIT SERT binding ratios in saline and MDMA-treated rats.

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    <p>Specific [<sup>123</sup>I]β-CIT SERT binding ratios in saline and MDMA-treated rats.</p

    Demographics, characteristics of MDMA use and exposure to other recreational drugs.

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    <p>Demographics, characteristics of MDMA use and exposure to other recreational drugs.</p

    <sup>18</sup>F-FDG uptake in the colon is modulated by metformin but not associated with core body temperature and energy expenditure

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    <div><p>Purpose</p><p>Physiological colonic <sup>18</sup>F-fluorodeoxyglucose (<sup>18</sup>F-FDG) uptake is a frequent finding on <sup>18</sup>F-FDG positron emission tomography computed tomography (PET-CT). Interestingly, metformin, a glucose lowering drug associated with moderate weight loss, is also associated with an increased colonic <sup>18</sup>F-FDG uptake. Consequently, increased colonic glucose use might partly explain the weight losing effect of metformin when this results in an increased energy expenditure and/or core body temperature. Therefore, we aimed to determine whether metformin modifies the metabolic activity of the colon by increasing glucose uptake.</p><p>Methods</p><p>In this open label, non-randomized, prospective mechanistic study, we included eight lean and eight overweight males. We measured colonic <sup>18</sup>F-FDG uptake on PET-CT, energy expenditure and core body temperature before and after the use of metformin. The maximal colonic <sup>18</sup>F-FDG uptake was measured in 5 separate segments (caecum, colon ascendens,—transversum,—descendens and sigmoid).</p><p>Results</p><p>The maximal colonic <sup>18</sup>F-FDG uptake increased significantly in all separate segments after the use of metformin. There was no significant difference in energy expenditure or core body temperature after the use of metformin. There was no correlation between maximal colonic <sup>18</sup>F-FDG uptake and energy expenditure or core body temperature.</p><p>Conclusion</p><p>Metformin significantly increases colonic <sup>18</sup>F-FDG uptake, but this increased uptake is not associated with an increase in energy expenditure or core body temperature. Although the colon might be an important site of the glucose plasma lowering actions of metformin, this mechanism of action does not explain directly any associated weight loss.</p></div

    Relative increase of <sup>18</sup>F-FDG uptake.

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    <p>The relative increase in 18F-FDG uptake in the separate segments of the colon in lean (left panel) and overweight (right panel) subjects. The relative increase was calculated as (<sup>18</sup>F-FDG uptake post-exposure * 100%) / <sup>18</sup>F-FDG uptake pre-exposure.</p

    Consort flowchart.

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    <p>Flow chart of subjects completing each stage of the study. We screened and included 16 subjects (eight overweight (body mass index [BMI], > 28 kg/m<sup>2</sup>) and eight lean (BMI, <24 kg/m<sup>2</sup>). All 16 subjects completed the study and were included in the analysis.</p

    Correlations.

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    <p>Correlations between the difference in energy expenditure pre and post administration and the difference in core body temperature.</p

    Transversal images of D2/3R availability.

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    <p>Transversal [123I]IBZM SPECT slices at the level of the striatum showing D2/3 receptor availability in a TRD patient, a TRD patient on antipsychotics (TRD AP), and a healthy control subject.</p

    Striatal D2/3R availability for TRD, TRD AP and healthy control subjects.

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    <p>Striatal D2/3 receptor (D2/3R) availability of TRD patients, TRD patients with antipsychotics (TRD AP) and healthy control subjects. The black dots represents the striatal D2/3R availability of each subject. The horizontal lines indicate the mean D2/3R availability of each group which is 0.84 for the TRD, 0.50 for the TRD AP and 0.81 for the healthy control subjects.</p
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