Cardiometabolic Risk Factors in Experimental Spinal Cord Injury
Cardiometabolic Risk Factors in Experimental Spinal Cord Injury
复制标题
DOI：
10.1089/neu.2009.1064
复制
发表时间：
2010-01-01
影响因子：
4.2
通讯作者：
Krassioukov, Andrei
中科院分区：
文献类型：
--
作者：
Inskip, Jessica;Plunet, Ward;Krassioukov, Andrei
脊髓损伤（SCI）后的心脏代谢危险因素被严重低估，尽管在这一人群中代谢紊乱和心血管死亡率很高。身体成分分析和血清脂质分析是两种开始被广泛用于记录临床SCI后代谢变化的评估方法。据报道，SCI患者内脏脂肪增加，血清脂质水平改变。然而，对这些心脏代谢危险因素在动物模型中的发展知之甚少。使用磁共振成像（MRI）和脂肪组织解剖相结合，我们发现，内脏和皮下脂肪组织都增加了1个月，但不是在1周后，完全T3 SCI大鼠。此外，在损伤后1个月，T3 SCI大鼠表现出非空腹血清高胆固醇血症，这是使用标准临床方法和家用胆固醇监测装置（CHEMICAL CHEK）获得的结果。有趣的是，在损伤后1个月，完全T10 SCI的大鼠没有显示内脏脂肪或血清甘油三酯水平的增加。事实上，完全高胸脊髓损伤破坏脂质代谢和扰乱脂肪储存在亚急性期，而低胸脊髓损伤没有，表明脂肪组织的下行交感神经控制的差异可能在这些变化中发挥作用。这些结果提供了SCI实验动物心脏代谢危险因素的第一个证据，并且是研究经常伴随SCI的肥胖和代谢功能障碍的病因学的起点。
Cardiometabolic risk factors are sorely underreported after spinal cord injury (SCI), despite the high prevalence of metabolic disorders and cardiovascular mortality in this population. Body-composition analysis and serum-lipid profiling are two assessments that are beginning to be more widely used to document metabolic changes after clinical SCI. Individuals with SCI have been reported to carry increased visceral fat and to exhibit altered serum-lipid levels. However, little is known about the development of these cardiometabolic risk factors in animal models. Using a combination of magnetic resonance imaging (MRI) and adipose tissue dissection, we show that visceral and subcutaneous adipose tissue were both increased at 1 month, but not at 1 week, after complete T3 SCI in rats. Additionally, at 1 month post injury, T3 SCI rats exhibited nonfasting serum hypertriglyceridemia, a result obtained using both standard clinical methods and a home cholesterol monitoring device (CardioChek). Interestingly, at 1 month post injury, rats with complete T10 SCI did not show an increase in either visceral adiposity or serum triglyceride levels. The fact that complete high-thoracic SCI disrupts lipid metabolism and perturbs fat storage in the subacute period, while low-thoracic SCI does not, suggests that differences in descending sympathetic control of adipose tissue might play a role in these changes. These results provide the first evidence of cardiometabolic risk factors in experimental animals with SCI, and are a starting point for investigations of the etiology of obesity and metabolic dysfunctions that often accompany SCI.