据英国《每日电讯报》近日报道，美国科学家发现，高脂肪食物会让身体内一个能诱发糖尿病的遗传开关犯错，让人罹患糖尿病。这一发现有助于科学家解释Ⅱ型糖尿病与肥胖的关系，并据此开发出新疗法。相关研究发表在《自然•医学》杂志上。
科学家们对老鼠和人进行了研究，结果发现高浓度脂肪会瓦解打开和关闭基因的两个关键蛋白FOXA2和HNF1A。这两个蛋白会激活胰腺酶，预防人罹患糖尿病。
当这两个蛋白停止工作，这种酶就关闭了，反过来则会扰乱胰腺中的胰岛素分泌β细胞监控血糖浓度的能力。如果人体和动物缺乏这种葡萄糖感应机制，就无法正确地调控血糖，β细胞的葡萄糖感应减少是导致糖尿病恶化的重要因素。
领导该研究的加州大学圣地亚哥分校细胞与分子学教授、桑福德-伯纳姆医学研究所的詹米•马斯表示：“新研究有助于我们更深地了解营养过度如何导致Ⅱ型糖尿病，我们能据此研制出干预过程和疗法以治疗糖尿病。我们或许可以通过β细胞基因治疗或干扰这种路径的药物来维持正常的β细胞功能。”
科学家在老鼠身上进行的实验表明，维持这种被FOXA2和HNF1A影响的胰腺酶的功能可阻止它们罹患糖尿病。马斯团队正在想方设法增强这种酶在人体内的活性。
糖尿病分Ⅰ型糖尿病、Ⅱ型糖尿病、妊娠糖尿病以及其他特殊类型的糖尿病。其中Ⅱ型糖尿病所占比例约为95%，而Ⅰ型糖尿病多发生于青少年，是一种自体免疫失调引发的疾病。
生物探索推荐英文论文摘要：
Pathway to diabetes through attenuation of pancreatic beta cell glycosylation and glucose transport
A connection between diet, obesity and diabetes exists in multiple species and is the basis of an escalating human health problem. The factors responsible provoke both insulin resistance and pancreatic beta cell dysfunction but remain to be fully identified. We report a combination of molecular events in human and mouse pancreatic beta cells, induced by elevated levels of free fatty acids or by administration of a high-fat diet with associated obesity, that comprise a pathogenic pathway to diabetes. Elevated concentrations of free fatty acids caused nuclear exclusion and reduced expression of the transcription factors FOXA2 and HNF1A in beta cells. This resulted in a deficit of GnT-4a glycosyltransferase expression in beta cells that produced signs of metabolic disease, including hyperglycemia, impaired glucose tolerance, hyperinsulinemia, hepatic steatosis and diminished insulin action in muscle and adipose tissues. Protection from disease was conferred by enforced beta cell–specific GnT-4a protein glycosylation and involved the maintenance of glucose transporter expression and the preservation of glucose transport. We observed that this pathogenic process was active in human islet cells obtained from donors with type 2 diabetes; thus, illuminating a pathway to disease implicated in the diet- and obesity-associated component of type 2 diabetes mellitus.
