The John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia.
Int J Obes (Lond). 2012 Oct;36(10):1366-9. doi: 10.1038/ijo.2011.267. Epub 2012 Jan 17.
Glutathione transferase Kappa (GSTK1-1) also termed disulfide bond-forming oxidoreductase A-like protein (DsbA-L) has been implicated in the post-translational multimerization of adiponectin and has been negatively correlated with obesity in mice and humans. We investigated adiponectin in Gstk1(-/-) mice and surprisingly found no difference in the levels of total serum adiponectin or the level of high molecular weight (HMW) multimers when compared with normal controls. Non-reducing SDS-polyacrylamide gel electrophoresis and western blotting also showed a similar distribution of low, middle and HMW multimers in normal and Gstk1(-/-) mice. Variation in adiponectin has been correlated with glucose tolerance and with the levels of phosphorylated AMP-kinase but we found similar glucose tolerance and similar levels of phospho 5-AMP-activated protein kinase in normal and Gstk1(-/-) mice. Consequently, our findings suggest that GSTK1-1 is not absolutely required for adiponectin multimerization in vivo and alternate pathways may be activated in GSTK1-1 deficiency.
谷胱甘肽转移酶 Kappa（GSTK1-1）也被称为二硫键形成氧化还原酶 A 样蛋白（DsbA-L），它参与了脂联素的翻译后多聚化，并且与小鼠和人类的肥胖呈负相关。我们在 Gstk1（-/-）小鼠中研究了脂联素，令人惊讶的是，与正常对照组相比，总血清脂联素水平或高分子量（HMW）多聚体水平没有差异。非还原 SDS-聚丙烯酰胺凝胶电泳和 Western blot 也显示正常和 Gstk1（-/-）小鼠中低、中、HMW 多聚体的分布相似。脂联素的变异与葡萄糖耐量和磷酸化 AMP 激酶水平相关，但我们发现正常和 Gstk1（-/-）小鼠的葡萄糖耐量和磷酸化 5-AMP 激活蛋白激酶水平相似。因此，我们的研究结果表明，GSTK1-1 并非体内脂联素多聚化所必需，在 GSTK1-1 缺乏时可能会激活替代途径。
