Garofalo Robert S
Dept Cardiovascular and Metabolic Diseases, Pfizer Global Research and Development, MS-3220-3082, Groton, CT 06340, USA.
Trends Endocrinol Metab. 2002 May-Jun;13(4):156-62. doi: 10.1016/s1043-2760(01)00548-3.
Studies in the fruit fly Drosophila melanogaster and the nematode Caenorhabditis elegans have revealed that components of the insulin signaling pathway have been highly conserved during evolution. Genetic analysis in Drosophila suggests that structural conservation also extends to the functional level. Flies carrying mutations that reduce insulin signaling have a growth deficiency phenotype similar to that seen in mice with disruptions of genes encoding insulin-like growth factors (IGFs) or the IGF-I receptor. Recent studies in flies have demonstrated a role for the insulin signaling pathway in the regulation of metabolism, reproduction and lifespan via modulation of central neuroendocrine pathways. Similarly, mice with loss of brain insulin receptors or insulin receptor substrate 2 deficiency exhibit neuroendocrine defects and female infertility. These parallels suggest that the insulin system has multiple conserved roles, acting directly to modulate growth and indirectly, via the neuroendocrine system, to modulate peripheral physiology in response to changes in nutrient availability.
对果蝇黑腹果蝇和线虫秀丽隐杆线虫的研究表明,胰岛素信号通路的组成部分在进化过程中高度保守。果蝇的遗传分析表明,结构保守性也延伸到功能水平。携带降低胰岛素信号突变的果蝇具有生长缺陷表型,类似于编码胰岛素样生长因子(IGF)或IGF-I受体的基因被破坏的小鼠。最近对果蝇的研究表明,胰岛素信号通路通过调节中枢神经内分泌通路在代谢、繁殖和寿命调节中发挥作用。同样,脑胰岛素受体缺失或胰岛素受体底物2缺乏的小鼠表现出神经内分泌缺陷和雌性不育。这些相似之处表明,胰岛素系统具有多种保守作用,直接调节生长,间接通过神经内分泌系统,根据营养可用性的变化调节外周生理。