Mitochondrial signaling in adipose tissue

肥胖已成为全球医疗保健的一个重大问题。当大量的注意力被投入到控制这种情况时，相对较少的注意力被投入到理解肥胖的生化起源上。当身体开始以脂肪的形式积累多余的卡路里时，决定健康与疾病之间平衡的生化信号的性质发生了变化。理解这些变化的意义是很重要的。这些信号的主要来源之一是脂肪或脂肪组织。脂肪组织释放一种叫做脂肪因子的分子，这种分子与包括胰腺和心脏在内的全身组织进行交流。其中一些分子引起炎症，有些可能导致II型糖尿病。这项研究将解决的重要问题是“脂肪组织的什么特性导致它释放这些分子？”我们认为，脂肪通过其线粒体（细胞中产生能量的成分）感知代谢压力，并使用自由基（由线粒体产生）作为释放这些脂肪因子的信号。我们将试图通过改变脂肪细胞线粒体产生的自由基水平并确定对这些信号分子释放的影响来证明这一点。

Obesity has become a significant health care concern globally. While a great deal of attention is being devoted to managing this condition, relatively little attention is devoted to understanding the biochemical origins of obesity. As the body begins to accumulate excess calories in the form of fat, the nature of the biochemical signals that dictate the balance between health and disease change. It is important to understand the significance of these changes. One of the major sources of these signals is fat or adipose tissue. Adipose tissue releases molecules, called adipokines, which communicate with a number of tissues throughout the body including the pancreas and heart. Some of these molecules cause inflammation and some may be responsible for causing type II diabetes. The important question that will be addressed in this research is "what properties of adipose tissue cause it to release these molecules?" We believe the fat senses metabolic stress from its mitochondria, the components of the cell that produce energy, and uses free radicals (produced by the mitochondria) as a means to signal the release of these adipokines. We will try to prove this by altering the level free radicals produced by fat cell mitochondria and determining the effect on the release of these signaling molecules.