Lean M E, Jennings G
Dunn Nutrition Laboratory, Cambridge.
J Clin Pathol. 1989 Nov;42(11):1153-6. doi: 10.1136/jcp.42.11.1153.
Brown adipose tissue was investigated in two cases of cot death in which core temperatures were above 40 degrees C on arrival at the mortuary. Evidence was obtained from mitochondrial (8-3H) guanosine diphosphate (GDP) binding and oxygen uptake of active thermogenesis with uncoupled mitochondrial respiration which was recoupled by GDP. Thermogenic capacity of brown adipose tissue, estimated by radioimmunoassay of the specific mitochondrial membrane "uncoupling protein" responsible for heat production, was similar to that measured in other infants or in experimental animals acclimated to moderately warm conditions (23 degrees C). Brown adipose tissue thermogenesis, occurring inappropriately in a warm, well insulated infant, could be a cause of some cases of cot death.
对两例婴儿猝死病例的棕色脂肪组织进行了研究,这两例病例在送到停尸房时核心体温均高于40摄氏度。通过线粒体(8-3H)鸟苷二磷酸(GDP)结合以及活性产热的氧摄取实验获取了证据,该活性产热是通过未偶联的线粒体呼吸进行的,而这种呼吸可被GDP重新偶联。通过对负责产热的特定线粒体膜“解偶联蛋白”进行放射免疫测定来估计棕色脂肪组织的产热能力,其与在其他婴儿或适应适度温暖条件(23摄氏度)的实验动物中测得的产热能力相似。在温暖且保暖良好的婴儿身上不恰当地发生的棕色脂肪组织产热,可能是某些婴儿猝死病例的一个原因。