Influence of Diabetic Neuropathy on Activation of Brown Adipose Tissue
赞助:
Doctor Giacomo Gastaldi
合作者:
信息的提供 (责任方):
Doctor Giacomo Gastaldi，University Hospital, Geneva
| 追踪信息 | |||
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| 首次提交日期 ICMJE | September 26, 2018 | ||
| 首次发布日期e ICMJE | October 4, 2018 | ||
| 最后更新发布日期 | October 4, 2018 | ||
| 预计研究开始日期 ICMJE | October 15, 2018 | ||
| 预计主要完成日期 | October 15, 2019 (主要结果测量的最终数据收集日期) | ||
| 目前主要观察指标 ICMJE |
brown adipose tissue activation[ Time Frame: 120 minutes after cold exposure ] PET- MRI measurement (SUVR) |
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| 原始主要观察测量 ICMJE | 与当前相同 | ||
| 目前的二级观察 ICMJE |
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| 描述性信息 | |||
| 简略标题 ICMJE | Influence of Diabetic Neuropathy on Activation of Brown Adipose Tissue | ||
| 正式标题 ICMJE | Influence of Diabetic Neuropathy on Activation of Brown Adipose Tissue | ||
| 简要概况 | Influence of diabetic neuropathy on cold induced brown adipose tissue in type 1 diabetic patients. |
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| 详细说明 | The prevalence of type 1 diabetes has been steadily increasing for about 20 years. Despite therapeutic progress, between 20 and 65% of people with diabetes develop diabetic neuropathy, resulting in increased morbidity and mortality. Diabetic neuropathy is not limited to sensitive pain in the lower limbs. It also affects the fibres of the autonomic nervous system (ANS), which results in systemic complications, often disabling (erectile dysfunction, dysidrosis, gastroparesis, orthostatism, etc.) and a probable alteration in the body's thermogenic capacities, although this possibility has not been studied in humans. In rodents, it is possible to activate induced thermogenesis via central stimulation of the ANS or to inactivate it, which promotes the development of obesity and greater insulin resistance. This knowledge is based on cellular and animal models that have identified the bio-molecular mechanisms that give brown adipose tissue (BAT) the ability to dissipate energy in the form of heat. Induced thermogenesis is mediated by decoupling proteins 1 (DCS-1) located on the mitochondrial inner membrane of the TAB. DCS-1 decouple oxidative phosphorylation from ATP production, dissipating the proton gradient. The activation of UCP1 is particularly influenced by the sympathetic system and more particularly by catecholamines which will bind to ß3 adrenergic receptors (Rß3). In humans, the persistence of active areas of TAB has recently been demonstrated by positron emission tomography (PET) imaging using a glucose analogue radiotracer, 18F-Fluoro-Deoxy-Glucose (18F-FDG), coupled with the scanner (CT). Recently, it has been shown that the use of 18F-FDG PET coupled with magnetic resonance (MRI) is equally effective in differentiating TAB from white fat tissue with less patient irradiation. The activity of the TAB is estimated using the measurement of SUV (standard uptake value) which represents the total glycolytic activity of the tissue and is also commonly referred to as the total metabolic volume. It has been shown in humans that TAB activity is inversely correlated with body mass index and age and positively correlated with exposure to cold and stress levels[6]. Among diabetics, the data are disparate but the spontaneous prevalence of TAB appears to be reduced compared to the general population (1.1% vs 7.5%). To date, no studies have investigated a possible link between the decrease in TAB activity observed in diabetics and the presence of autonomic neuropathy, which is a common and often under-diagnosed complication of diabetes. The main purpose of this study is to evaluate whether the activity and distribution of TAB in patients with diabetes is influenced by the presence of diabetic neuropathy. On the other hand, if the existence of diabetic neuropathy influences energy expenditure in the event of exposure to cold. Finally, whether any differences in the activity and distribution of TAB could be related to changes in the central nervous system. The investigators plan to include a total of 24 patients with type 1 diabetes and separate them into 2 groups: group A; no neuropathic complications and group B; presence of neuropathy. All patients will be characterized in terms of clinical, metabolic and energy expenditure. The activity of the TAB will be evaluated through the use of 18F-FDG PET/IRM imaging, after a cold stimulation protocol (refrigerated jacket) in order to activate the TAB in a homogeneous manner among the participants. | ||
| 研究类型 ICMJE | Interventional | ||
| 研究阶段 | N/A | ||
| 研究设计 ICMJE | 分配: Non-Randomized 干预模型: Parallel Assignment 干预模型描述: 盲法: Interventional 盲法描述: 主要目的: Basic Science |
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| 适用条件 ICMJE | |||
| 干预项目 ICMJE |
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| 研究工具 |
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| 招募信息 | |||
| 招募状态 ICMJE | Not yet recruiting | ||
| 预计入组 ICMJE |
24 | ||
| 原始预计入组 ICMJE | 与当前相同 | ||
| 预计研究完成日期 | October 15, 2019 | ||
| 预计主要完成日期 | October 15, 2019 (主要结果测量的最终数据收集日期) | ||
| 合格标准 ICMJE | Inclusion Criteria: 1. Type 1 diabetes 2. Patients who can understand the issue of this study and who are able to decide for themselves whether or not to participate in the study. 3. Adult patient (>18 years old) 4. Informed Consent form signed 5. Differentiated inclusion: - Group A: absence of neuropathy - Group B: significant neuropathy Exclusion Criteria: 1. Treatment with beta-blockers 2. Alcohol consumption(> 50 gr/week) 3. Allergy to 18F-FDG 4. Participation in another clinical study (4 weeks prior to entry) that may influence the activity of brown adipose tissue 5. Pregnancy 6. Exposure to ionizing radiation greater than or equal to 5 mSv during the year preceding the PET-RMI planned in the study | ||
| 性别 |
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| 年龄 | 最小年龄：18 Years ，最大年龄：N/A | ||
| 接受健康的志愿者 | 没有 | ||
| 可入组国家 ICMJE | |||
| 管理信息 | 数据检测委员会 | No | |
| 研究涉及美国FDA监管的产品 |
研究美国FDA监管的药品: No 研究涉及美国FDA监管的设备产品: No |
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| IPD 共享声明 |
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| 责任方 | Doctor Giacomo Gastaldi，University Hospital, Geneva | ||
| 研究赞助商 ICMJE | Doctor Giacomo Gastaldi | ||
| 合作者 ICMJE | |||
| 研究员 ICMJE |
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| PRS 账户 | University Hospital, Geneva | ||
| 验证日期 | October 2018 | ||
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ICMJE 国际医学期刊编辑委员会和 世界卫生组织 ICTRP 要求的元素 |
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