PurposeBrown adipose tissue (BAT) is considered a potential target for combatting obesity, as it produces heat instead of ATP in cellular respiration due to uncoupling protein-1 (UCP-1) in mitochondria. However, BAT-specific thermogenic capacity, in comparison to whole-body thermogenesis during cold stimulus, is still controversial. In our present study, we aimed to determine human BAT oxygen consumption with [15O]O2 positron emission tomography (PET) imaging. Further, we explored whether BAT-specific energy expenditure (EE) is associated with BAT blood flow, non-esterified fatty acid (NEFA) uptake, and whole-body EE.MethodsSeven healthy study subjects were studied at two different scanning sessions, 1) at room temperature (RT) and 2) with acute cold exposure. Radiotracers [15O]O2, [15O]H2O, and [18F]FTHA were given for the measurements of BAT oxygen consumption, blood flow, and NEFA uptake, respectively, with PET-CT. Indirect calorimetry was performed to assess differences in whole-body EE between RT and cold.ResultsBAT-specific EE and oxygen consumption was higher during cold stimulus (approx. 50 %); similarly, whole-body EE was higher during cold stimulus (range 2–47 %). However, there was no association in BAT-specific EE and whole-body EE. BAT-specific EE was found to be a minor contributor in cold induced whole-body thermogenesis (almost 1 % of total whole-body elevation in EE). Certain deep muscles in the cervico-thoracic region made a major contribution to this cold-induced thermogenesis (CIT) without any visual signs or individual perception of shivering. Moreover, BAT-specific EE associated with BAT blood flow and NEFA uptake both at RT and during cold stimulus.ConclusionOur study suggests that BAT is a minor and deep muscles are a major contributor to CIT. In BAT, both in RT and during cold, cellular respiration is linked with circulatory NEFA uptake.Electronic supplementary materialThe online version of this article (doi:10.1007/s00259-016-3364-y) contains supplementary material, which is available to authorized users.
Objective: The reduced risk for Alzheimer's disease (AD) in high-educated individuals has been proposed to reflect brain cognitive reserve, which would provide more efficient compensatory mechanisms against the underlying pathology, and thus delayed clinical expression. Our aim was to find possible differences in brain amyloid ligand 11 C-labeled Pittsburgh Compound B ([ 11 C]PIB) uptake and glucose metabolism in high-and low-educated patients with mild AD. Methods: Twelve high-educated and 13 low-educated patients with the same degree of cognitive deterioration were studied with PET using [ 11 C]PIB and 18 F-fluorodeoxyglucose as ligands. The between-group differences were analyzed with voxel-based statistical method, and quantitative data were obtained with automated region-of-interest analysis. Results: High-educated patients showed increased [11 C]PIB uptake in the lateral frontal cortex compared with low-educated patients. Moreover, high-educated patients had significantly lower glucose metabolic rate in the temporoparietal cortical regions compared with low-educated patients. Interpretation: Our results suggesting more advanced pathological and functional brain changes in high-educated patients with mild AD are in accordance with the brain cognitive reserve hypothesis and point out the importance of development of reliable markers of underlying AD pathology for early AD diagnostics. Neurol 2008;63:112-118 Several epidemiological studies have found a lower incidence of Alzheimer's disease (AD) in high-educated populations, suggesting that education provides protection against the disease. Ann1 This reduced risk for AD in high-educated individuals is proposed to reflect brain cognitive reserve that provides greater brain capacity to compensate for disruption caused by disease pathology, and thus delays the clinical expression of AD.2 At a particular level of AD pathology, highly educated individuals are less likely to manifest clinical symptoms of dementia as compared with less educated individuals.3 After the diagnosis of AD, higheducated individuals show more rapid progression of dementia and lower survival compared with loweducated AD patients. 4 -6 The different course of the disease between these groups has been hypothesized to reflect a more advanced AD pathology at the time of diagnosis in high-educated patients, and a rapid cognitive deterioration after the compensatory capacity becomes insufficient.The association of educational level with the severity of brain damage in AD has been evaluated in vivo with positron emission tomography (PET) and singlephoton emission computed tomography by using the brain glucose metabolism or cerebral blood flow as measures of brain functional changes.7-12 These studies have shown an inverse relation between the level of education and brain glucose metabolism or blood flow after adjusted for the dementia severity. This relation was evident especially in brain regions typically affected in AD, such as temporal and parietal cortices. The effect of education on the ...
Obesity and insulin resistance are associated with altered brain glucose metabolism. Here, we studied brain glucose metabolism in 22 morbidly obese patients before and 6 months after bariatric surgery. Seven healthy subjects served as control subjects. Brain glucose metabolism was measured twice per imaging session: with and without insulin stimulation (hyperinsulinemic-euglycemic clamp) using [18F]fluorodeoxyglucose scanning. We found that during fasting, brain glucose metabolism was not different between groups. However, the hyperinsulinemic clamp increased brain glucose metabolism in a widespread manner in the obese but not control subjects, and brain glucose metabolism was significantly higher during clamp in obese than in control subjects. After follow-up, 6 months postoperatively, the increase in glucose metabolism was no longer observed, and this attenuation was coupled with improved peripheral insulin sensitivity after weight loss. We conclude that obesity is associated with increased insulin-stimulated glucose metabolism in the brain and that this abnormality can be reversed by bariatric surgery.
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