美国科研人员最近发现，人体中的一种基因在糖尿病的发展过程中发挥着重要作用。这一发现有望为预防和治疗糖尿病找到新方法。
美国得克萨斯农作物生命研究所科研人员在12月份的《生物化学》上报告说，代谢炎症是导致糖尿病或使其恶化的主要“元凶”。他们发现，一种名为PFKFB3的基因正是人体新陈代谢的“调节器”，它在糖尿病的发展过程中发挥着重要作用。
研究人员认为，增加营养可以激活这种基因，从而可以起到预防或遏制糖尿病发展的作用。为此，研究人员正在与营养学家合作，以确定是通过改变饮食还是通过服用补充剂来向这种基因提供营养，从而获得更有效的防治效果。（生物谷Bioon.com）
生物谷推荐原始出处：
JBC November 30, 2009, doi: 10.1074/jbc.M109.058446
Disruption of inducible 6-phosphofructo-2-kinase ameliorates diet-induced adiposity but exacerbates systemic insulin resistance and adipose tissue inflammatory response
Yuqing Huo1, Xin Guo2, Honggui Li2, Huan Wang1, Weiyu Zhang1, Ying Wang2, Huaijun Zhou3, Zhanguo Gao4, Sucheta Telang5, Jason Chesney5, Y. Eugene Chen6, Jianping Ye4, Robert S. Chapkin2 and Chaodong Wu2,*
1 University of Minnesota, United States;
2 Texas A&M University;
4 Pennington Biomedical Research Center, United States;
5 University of Louisville, United States;
6 University of Michigan, United States
Adiposity is commonly associated with adipose tissue dysfunction and many overnutrition-related metabolic diseases including type 2 diabetes. Much attention has been paid to reducing adiposity as a way to improve adipose tissue function and systemic insulin sensitivity. PFKFB3/iPFK2 is a master regulator of adipocyte nutrient metabolism. Using PFKFB3+/- mice, the present study investigated the role of PFKFB3/iPFK2 in regulating diet-induced adiposity and systemic insulin resistance. On a high-fat diet (HFD), PFKFB3+/- mice gained much less body weight than did wild-type littermates. This was attributed to a smaller increase in adiposity in PFKFB3+/- mice than in wild-type controls. However, HFD-induced systemic insulin resistance was more severe in PFKFB3+/- mice than in wild-type littermates. Compared to wild-type littermates, PFKFB3+/- mice exhibited increased severity of HFD-induced adipose tissue dysfunction, as evidenced by increased adipose tissue lipolysis, inappropriate adipokine expression, and decreased insulin signaling, as well as increased levels of proinflammatory cytokines in both isolated adipose tissue macrophages and adipocytes. In an in vitro system, knockdown of PFKFB3/iPFK2 in 3T3-L1 adipocytes caused a decrease in the rate of glucose incorporation into lipid but an increase in the production of reactive oxygen species. Furthermore, knockdown of PFKFB3/iPFK2 in 3T3-L1 adipocytes inappropriately altered the expression of adipokines, decreased insulin signaling, increased the phosphorylation states of JNK and NFκB p65, and enhanced the production of proinflammatory cytokines. Together, these data suggest that PFKFB3/iPFK2, although contributing to adiposity, protects against diet-induced insulin resistance and adipose tissue inflammatory response.
