Koike G, Van Vooren P, Shiozawa M, Galli J, Li L S, Glaser A, Balasubramanyam A, Brown L J, Luthman H, Szpirer C, MacDonald M J, Jacob H J
Cardiovascular Research Center, Massachusetts General Hospital-East, Charlestown 02129-2060, USA.
Genomics. 1996 Nov 15;38(1):96-9. doi: 10.1006/geno.1996.0599.
The mitochondrial FAD-dependent glycerol-3-phosphate dehydrogenase (mtGPD) plays an important role in the regulation of insulin secretion and has been postulated as a candidate responsible for the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM) in humans as well as in rodent models of NIDDM. Recent molecular genetic studies of the Goto-Kakizaki (GK) rat model of NIDDM have identified loci linked to NIDDM. To elucidate whether rat mtGPD might play a role in the pathogenesis of NIDDM, the rat mtGPD gene (Gpd2) was cloned, and a genetic marker for Gpd2 was developed. The gene mapped to the region of rat chromosome 3 that contains a region linked to NIDDM in the GK rat. Fluorescence in situ hybridization was also carried out to verify the map position.
线粒体FAD依赖的甘油-3-磷酸脱氢酶(mtGPD)在胰岛素分泌调节中起重要作用,并且在人类非胰岛素依赖型糖尿病(NIDDM)以及NIDDM啮齿动物模型的发病机制中被认为是一个候选因素。最近对NIDDM的Goto-Kakizaki(GK)大鼠模型的分子遗传学研究已经确定了与NIDDM相关的基因座。为了阐明大鼠mtGPD是否可能在NIDDM的发病机制中起作用,克隆了大鼠mtGPD基因(Gpd2),并开发了Gpd2的遗传标记。该基因定位于大鼠3号染色体区域,该区域在GK大鼠中包含一个与NIDDM相关的区域。还进行了荧光原位杂交以验证图谱位置。