IN VIVO 23NA NMR SPECTROSCOPY & IMAGING

体内 23NA 核磁共振波谱

• 批准号: 6335266
• 负责人: NAVIN BANSAL
• 金额: $ 0.7万
• 依托单位: UT SOUTHWESTERN MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-08-15 至 2001-08-14
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6335266
• 关键词: Mammalia; bioimaging /biomedical imaging; biomedical resource; carbohydrates; diabetes mellitus; endocrine gland /system; female; genetics; hormones; human subject; lipids; magnetic resonance imaging; male; musculoskeletal system

The Zucker diabetic fatty rat is a well accepted model of human obesity and NIDDM. Animals inheriting a defect in the leptin receptor (fa/fa) develop early obesity insulin resistance and in males, NIDDM due to their leptin resistance. We have demonstrated that spectral analysis of whole body fat content detects the pre-obese (fa/fa) genotype before gross obesity and other metabolic derangements develop. In addition, this analysis provides a measure of lean body mass using our previous validated technique of fat and whole body water detection. We are finding that this animal model has a co-existent defect in lean body mass accumulation. Paradoxically in a second model using i.c.v. leptin infusion into normal rats, we are observing accelerated lean body mass loss in addition to augmented fat oxidation mediated by the central effects of leptin. Hyperinsulinemic glucose clamp studies in these two animal models suggest that there is strong correlation between intramyocellular triglyceride content and insulin sensitivity. We have been able to specifically monitor intramyocellular lipids through the use of proton spectroscopy and have previously validated its use in dogs and rabbits using the 1.5T clinical MR system at the Rogers MR Center. Studies are currently in progress to better understand the relationship between amounts and types of dietary fats, leptin, leptin resistance, intra-myocellular triglyceride stores and the development of insulin resistance and impaired insulin secretory response. (Service 5) REPORT PERIOD: (09/01/97-08/31/98)

Zucker糖尿病肥胖大鼠是公认的人类 肥胖和非胰岛素依赖型糖尿病。遗传性瘦素受体缺陷的动物 (FA/FA)发展为早期肥胖的胰岛素抵抗，在男性中，NIDDM 因为他们对瘦素有抵抗力。我们已经证明了这种光谱 分析全身脂肪含量检测肥胖前期(FA/FA) 严重肥胖和其他代谢紊乱之前的基因型别 发展。此外，这一分析还提供了一种瘦身的衡量标准 使用我们之前验证的脂肪和全身技术进行质量 水检测。我们发现这个动物模型有一个 瘦体质量积聚并存缺陷。矛盾的是，在一个 使用I.C.V.的第二种模型。给正常大鼠注射瘦素，我们正在 在增加脂肪的同时观察瘦身质量的加速下降 瘦素的中枢作用所介导的氧化。高胰岛素血症 在这两种动物模型中进行的葡萄糖钳夹研究表明 心肌细胞内甘油三酯含量与 胰岛素敏感性。我们已经能够专门监控 通过使用质子光谱分析和细胞内脂肪 之前已经使用1.5T在狗和兔子身上验证了它的使用 罗杰斯磁共振中心的临床磁共振系统。研究目前正在进行中 在更好地理解数量和 膳食脂肪类型、瘦素、瘦素抵抗、心肌细胞内 甘油三酯储存与胰岛素抵抗的发展和 胰岛素分泌反应受损。(服务5)报告期： (09/01/97-08/31/98)