REGULATION OF GENE EXPRESSION RELEVANT TO THE ADIPOSE CELL AND OBESITY

我们正在研究能量的生理学 动态平衡及其在肥胖和糖尿病中的作用。我们整合了 生理学的分子生物学，主要是利用老鼠作为 模型系统。其中一个研究重点是瘦素，一种在 脂肪细胞对适应饥饿和营养不良非常重要 能量消耗与肥胖的反馈调节。我们是 控制瘦素表达的转录因子的特征 以及细胞类型、脂肪储存水平和荷尔蒙环境 调节瘦素转录。由于能源消耗对 对肥胖的防御，能量消耗也是一种兴趣。 我们发现了一种名为解偶联蛋白3(UCP3)的基因 在肌肉和脂肪组织中表达。UCP3与 UCP1，它负责将能量浪费为热量。UCP3是 受甲状腺激素、β3-肾上腺素能激动剂和空腹的调节 因此可能会调节能量消耗的一些变化 由这些因素/条件引起的。第三条调查路线是 缺乏白色脂肪的转基因小鼠。这只老鼠是一个很好的模型 患有脂肪萎缩性糖尿病的人。我们正在研究这些老鼠以 试着了解脂肪缺乏是如何导致糖尿病的，这是一种 与更多研究的情况形成了耐人寻味的对比 会导致糖尿病。

We are investigating the physiology of energy homeostasis and its role in obesity and diabetes. We integrate molecular biology with physiology, chiefly using the mouse as a model system. One research focus is on leptin, a hormone made in adipose cells that is important for adaptation to starvation and in feedback regulation of energy expenditure and adiposity. We are characterizing the transcription factors controlling leptin expression and how the cell type, level of adipose stores, and hormonal milieu regulate leptin transcription. Since energy expenditure is crucial to the defense against obesity, energy expenditure is also an interest. We discovered a gene, uncoupling protein-3 (ucp3) that is expressed in muscle and adipose tissue. Ucp3 is homologous to ucp1, which is responsible for 'wasting' energy as heat. Ucp3 is regulated by thyroid hormone, beta3-adrenergic agonist, and fasting and thus may mediate some of the changes in energy expenditure caused by these agents/conditions. A third line of investigation is a transgenic mouse lacking white fat. This mouse is a good model of humans with lipoatrophic diabetes. We are studying these mice to try to understand how the lack of fat causes diabetes, which is an intriguing contrast to the more studied situation in which excess fat causes diabetes.