美研究人员发现高胆固醇症发病原因
美国华盛顿大学的研究人员最近发现了遗传性高胆固醇症的原因。高胆固醇血症又叫家族性高血脂症，病人体内脂蛋白代谢缺陷，造成高胆固醇、高甘油三酯，或两者都高。据估计，在美国，每10个早期心脏病患者中就有一个患有此病。
新的研究发现，家族性高血脂症患者体内过多的产生一种叫做apoB(载脂蛋白B)的物质。载脂蛋白B是肝脏用来合成胆固醇的组成部份。
医学界对家族性高血脂症的研究已经有30年了，但是还存在很多未知数。在这项新研究中，研究人员通过测量血液中的总胆固醇、甘油三酯、载脂蛋白B(apoB)水平、腹部脂肪和胰岛素抵抗力，将家族性高血脂症患者和正常人进行对比。
研究结果发现，家族性高血脂症患者的总胆固醇、甘油三酯、极低密度脂蛋白、低密度脂蛋白以及apoB水平都比其他的研究对象要高。该研究结果促使研究员转而去寻找导致apoB水平增加的基因或基因组，他们希望借此可以发现减少心脏病危险的新的治疗方法。
, 百拇医药
与此同时，研究者还认为降低体重、低脂饮食、规律运动以及在必要时服用降低胆固醇的药物对家族性高血脂症患者非常重要。该研究报告发表在4月12日美国心脏协会主办的杂志《动脉硬化、血栓和血管生物学》上。
Genetic Cause of High Cholesterol Discovered
Researchers from the University of Washington may have found the cause behind genetically linked high cholesterol, a condition known as familial combined hyperlipidemia (FCHL).
Familial combined hyperlipidemia (FCHL) affects an estimated 1 in 10 Americans with premature heart disease. FCHL results from defects in the metabolism of lipoproteins that leads to high cholesterol, high triglycerides or both.
, 百拇医药
FCHL has been studied for 30 years, but many aspects of it remain a mystery. New research finds people with FCHL overproduce a substance called apolipoprotein (apoB). This substance is a component of cholesterol-containing particles made by the liver.
Researchers studied participants with FCHL and without FCHL. The investigators measured total cholesterol, triglycerides, apoB, abdominal fat and insulin resistance in all participants.
, 百拇医药
Researchers found that the FCHL participants had significantly higher levels of total cholesterol, triglycerides, very-low and low-density lipoproteins, and apoB compared with the other participants.
Researchers say their study has made them shift their investigation into looking for the gene or genes responsible for the increases in apoB. They hope that in turn could lead to new treatments aimed at reducing heart disease.
In the meantime, researchers say weight loss, a low-fat diet, regular exercise, as well as cholesterol lowering drugs if necessary are important for people with FCHL.
This study was reported in the April 12 issue of Arteriosclerosis, Thrombosis and Vascular Biology: Journal of the American Heart Association., http://www.100md.com
新的研究发现，家族性高血脂症患者体内过多的产生一种叫做apoB(载脂蛋白B)的物质。载脂蛋白B是肝脏用来合成胆固醇的组成部份。
医学界对家族性高血脂症的研究已经有30年了，但是还存在很多未知数。在这项新研究中，研究人员通过测量血液中的总胆固醇、甘油三酯、载脂蛋白B(apoB)水平、腹部脂肪和胰岛素抵抗力，将家族性高血脂症患者和正常人进行对比。
研究结果发现，家族性高血脂症患者的总胆固醇、甘油三酯、极低密度脂蛋白、低密度脂蛋白以及apoB水平都比其他的研究对象要高。该研究结果促使研究员转而去寻找导致apoB水平增加的基因或基因组，他们希望借此可以发现减少心脏病危险的新的治疗方法。
, 百拇医药
与此同时，研究者还认为降低体重、低脂饮食、规律运动以及在必要时服用降低胆固醇的药物对家族性高血脂症患者非常重要。该研究报告发表在4月12日美国心脏协会主办的杂志《动脉硬化、血栓和血管生物学》上。
Genetic Cause of High Cholesterol Discovered
Researchers from the University of Washington may have found the cause behind genetically linked high cholesterol, a condition known as familial combined hyperlipidemia (FCHL).
Familial combined hyperlipidemia (FCHL) affects an estimated 1 in 10 Americans with premature heart disease. FCHL results from defects in the metabolism of lipoproteins that leads to high cholesterol, high triglycerides or both.
, 百拇医药
FCHL has been studied for 30 years, but many aspects of it remain a mystery. New research finds people with FCHL overproduce a substance called apolipoprotein (apoB). This substance is a component of cholesterol-containing particles made by the liver.
Researchers studied participants with FCHL and without FCHL. The investigators measured total cholesterol, triglycerides, apoB, abdominal fat and insulin resistance in all participants.
, 百拇医药
Researchers found that the FCHL participants had significantly higher levels of total cholesterol, triglycerides, very-low and low-density lipoproteins, and apoB compared with the other participants.
Researchers say their study has made them shift their investigation into looking for the gene or genes responsible for the increases in apoB. They hope that in turn could lead to new treatments aimed at reducing heart disease.
In the meantime, researchers say weight loss, a low-fat diet, regular exercise, as well as cholesterol lowering drugs if necessary are important for people with FCHL.
This study was reported in the April 12 issue of Arteriosclerosis, Thrombosis and Vascular Biology: Journal of the American Heart Association., http://www.100md.com