--临床研究显示,慢性感染和二型糖尿病有很深的联系,最近来自美国国家健康中心的研究人员在认识这一问题上又向前迈了一步。研究人员发现人体内产生的内源性大麻素可能引发了体内的炎症进程并促使免疫系统作出反应,导致分泌胰岛素的胰岛B细胞死亡进而导致二型糖尿病的发生。研究人员在小鼠实验中观察到如果抑制免疫系统或者内源性大麻素,小鼠的二型糖尿病症状有明显缓解。这一研究被发表在Nature Medicine上。同时,也为二型糖尿病提供新的药物靶点。
详细英文报道:
Chronic inflammation has long been thought to have ties to Type 2 diabetes, and now researchers at the National Institutes of Health (NIH) believe they have discovered what that connection may be. The findings also point to a possible molecular target for treating the disease, which is a growing epidemic in the U.S.
Scientists found that endocannabinoids, natural messenger chemicals in the body that help regulate many biological functions, are also involved in an inflammatory chain that can kill cells in the pancreas, where insulin is produced. Recent research has found a connection between endocannabinoids--which are chemically similar to the active compound in marijuana--to metabolic problems that induce diabetes.
"To understand Type 2 diabetes, a public health threat that affects young and old alike, we need to consider all the factors at play," said co-author Dr. Monica Skarulis, staff clinician at the National Institute of Diabetes and Digestive and Kidney Diseases. "We hope that what we've learned from this research will help us develop new strategies to prevent and treat the condition."
In a Type 2 diabetes rat model, researchers found that when they activated the endocannabinoids of immune system cells called macrophages that rid the body of cellular waste and pathogens located in the pancreas, a protein complex within the macrophages called the Nlrp3 inflammasome also became activated. This led to the release of molecules from the inflammasome that killed pancreatic beta cells in rats, spurring the progression of Type 2 diabetes in the animals.
Conversely, when the rats were treated with compounds that deplete macrophages or block the peripheral cannabinoid receptors, beta cell function was restored and the severity of the animals' disease was reduced. The research was published Aug. 18 in the journal Nature Medicine.