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1、此处替换为文档标题Review Article评论文章Banting Memorial Lecture 2012班廷纪念讲座2012Reversing the twin cycles of Type 2 diabetes逆转2型糖尿病的双周期R. Taylor泰勒Magnetic Resonance Centre, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK磁共振中心，纽卡斯尔大学医学院，蜂窝，泰恩河畔纽卡斯尔，英国Accepted 12 October 2012接受12十月2012
2、1. Abstract 摘要It has become widely accepted that Type 2 diabetes is inevitably life-long, with irreversible and progressive beta cell damage. However, the restoration of normal glucose metabolism within days after bariatric surgery in the majority of people with Type 2 diabetes disproves this concep
3、t. There is now no doubt that this reversal of diabetes depends upon the sudden and profound decrease in food intake, and does not relate to any direct surgical effect. The Counterpoint study demonstrated that normal glucose levels and normal beta cell function could be restored by a very low calori
4、e diet alone. Novel magnetic resonance methods were applied to measure intra-organ fat.它已成为被广泛接受，2型糖尿病是不可避免的终身，具有不可逆的和渐进的细胞损伤。然而，恢复正常糖代谢在几天内，在2型糖尿病患者反驳这个概念大多数人减肥手术后。毫无疑问，这种逆转的糖尿病取决于食物摄入量的突然和深刻的下降，并没有涉及到任何直接的手术效果。对位的研究表明，正常的血糖水平与正常细胞的功能可以由一个非常低热量饮食恢复。新的磁共振方法应用于测量器官内的脂肪The results showed two different
5、 time courses: a) resolution of hepatic insulin sensitivity within days along with a rapid fall in liver fat and normalisation of fasting glucose levels; and b) return of normal beta cell insulin secretion over weeks in step with a fall in pancreas fat. Now that it has been possible to observe the p
6、athophysiological events during reversal of Type 2 diabetes, the reverse time course of events which determine the onset of the condition can be identified. The twin cycle hypothesis postulates that chronic calorie excess leads to accumulation of liver fat with eventual spill over into the pancreas.
7、 These selfreinforcing cycles between liver and pancreas eventually cause metabolic inhibition of insulin secretion after meals and onset of hyperglycaemia. It is now clear that Type 2 diabetes is a reversible condition of intra-organ fat excess to which some people are more susceptible than others.
8、结果显示两个不同的课程：一）分辨率的肝脏胰岛素敏感性的几天内随着空腹血糖水平与正常肝脏脂肪快速下降；b）与胰腺脂肪下降一周正常细胞胰岛素分泌功能恢复。现在，它已经可以观察到逆转2型糖尿病的病理生理事件，事件的反向时间过程中确定的情况下，可以识别。双周期假说认为，慢性热量过剩导致最终泄漏的肝脏脂肪堆积在胰腺。这些selfreinforcing周期肝脏和胰腺之间最终导致胰岛素分泌代谢抑制餐后高血糖的发生。现在已经清楚了，2型糖尿病是一个可逆的内器官脂肪的条件，有些人比其他人更容易受到影响Diabet. Med. 30, 267275 (2013)糖尿病。基础教学法硕士30，267 - 275（20
9、13）2. Introduction 简介What is the basic nature of Type 2 diabetes? What causes it? It is associated with obesity, and both insulin resistance and a bcell defect are involved. After diagnosis blood glucose levels rise steadily whether or not treatment is intensive 1. By 10 years after diagnosis, the r
10、ate of rise in HbA1c decreases, because by that stage 50% of all people with Type 2 diabetes are on insulin therapy. This steady deterioration has been observed in many studies and underpins the belief that Type 2 diabetes is an inexorably progressive disease. It is widely acknowledged as a lifelong
11、 condition and, in order to maximize coping, those with the disease are advised to come to terms with the notion that they have an incurable condition 2.2型糖尿病的基本性质是什么？是什么原因造成的？它是与肥胖和胰岛素抵抗，与B细胞缺陷有关。确诊后血糖水平稳步上升，无论治疗是否密集 1 。在诊断后10年，在HbA1c降低增长速度，因为所有的2型糖尿病患者对胰岛素治疗的50%阶段。这种恶化已在许多研究中观察到，是认为2型糖尿病是一种无情的疾病进展
12、。它被广泛认为是一个终身的条件，为了最大限度地应对，那些与疾病的建议，他们有一个不可治愈的条件的概念 2 。3. What causes the deterioration in control?3.1. 是什么导致了控制的恶化？The major pathophysiological change underlying the steady worsening of blood glucose control is a steady decrease in b-cell function, as shown by modelling b-cell function from the UK P
13、rospective Diabetes Study (UKPDS) data set 3. Indeed, at the time of diagnosis, it is already down to 50% of normal. Then it deteriorates in a depressingly linear fashion. The rate of decline in glucose tolerance is strongly related to the loss of b-cell function, whilst insulin resistance in muscle
14、 changes little 4,5. This mirrors observations on populations with high incidence of Type 2 diabetes, in which transition from hyperinsulinaemic normal glucose tolerance to overt diabetes involved a further loss of acute b-cell competence 6,7.主要的病理生理变化基本稳定恶化血糖控制在B细胞功能的持续下降，如B细胞功能建模从英国前瞻性糖尿病研究（UKPDS）
15、数据集 3 。事实上，在诊断的时候，它已经下降到正常的50%。然后它恶化的一个令人沮丧的线性方式。在糖耐量下降速度是B细胞功能丧失密切相关，肌肉的变化不大，而胰岛素抵抗4,5。这反映在与2型糖尿病的发病率高的人群的观察，其中高胰岛素正常糖耐量过渡到显性糖尿病的急性B细胞能力6,7进一步亏损。Direct observation of the 13-year period leading up to diagnosis of Type 2 diabetes has recently provided insight into the time course of changes leading
16、to diagnosis. The Whitehall II Study has shown that plasma glucose levels are very slightly elevated years before diagnosis, although well within the normal range, but that the onset of distinct hyperglycaemia occurs over only 2 years (Fig. 1) 8. What could underlie this relatively rapid failure of insulin secretion? Does this reflect a process such as amyloid deposition or oxidative stress leading to b-cel
