美國(guó)科研人員最近發(fā)現(xiàn),，人體中的一種基因在糖尿病的發(fā)展過程中發(fā)揮著重要作用。這一發(fā)現(xiàn)有望為預(yù)防和治療糖尿病找到新方法,。
美國(guó)得克薩斯農(nóng)作物生命研究所科研人員在12月份的《生物化學(xué)》上報(bào)告說,，代謝炎癥是導(dǎo)致糖尿病或使其惡化的主要“元兇”。他們發(fā)現(xiàn),，一種名為PFKFB3的基因正是人體新陳代謝的“調(diào)節(jié)器”,，它在糖尿病的發(fā)展過程中發(fā)揮著重要作用。
研究人員認(rèn)為,，增加營(yíng)養(yǎng)可以激活這種基因,，從而可以起到預(yù)防或遏制糖尿病發(fā)展的作用。為此,，研究人員正在與營(yíng)養(yǎng)學(xué)家合作,，以確定是通過改變飲食還是通過服用補(bǔ)充劑來向這種基因提供營(yíng)養(yǎng),，從而獲得更有效的防治效果,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
