糖尿病
糖尿病
糖尿病是一种因体内胰岛素绝对或者相对不足所导致的一系列临床综合症，与遗传基因有着非常密切的关联。糖尿病的主要临床表现为多饮、多尿、多食和体重下降（―三多一少‖），以及血糖高、尿液中含有葡萄糖（正常的尿液中不应含有葡萄糖）等。
世界卫生组织将糖尿病分为四种类型：1型糖尿病、2型糖尿病、其他类型糖尿病和妊娠期糖尿病，虽然每种类型的糖尿病的症状都是相似甚至相同的，但是导致疾病的原因和它们在不同人群中的分布却不同。不同类型的糖尿病都会导致胰腺中的β细胞不能产生足量的胰岛素以降低血糖的浓度，导致高血糖症的发生。1型糖尿病一般是由于自体免疫系统破坏产生胰岛素的β细胞导致的；2型糖尿病是由于组织细胞的胰岛素抵抗（通俗地说，就是细胞不再同胰岛素结合，使得进入细胞内部参与生成热量的葡萄糖减少，留在血液中的葡萄糖增多）、β细胞功能衰退或其他多种原因引起的；妊娠期糖尿病则与2型糖尿病相似，也是源于细胞的胰岛素抵抗，不过其胰岛素抵抗是由于妊娠期妇女分泌的激素（荷尔蒙）所导致的。
目前，1、2型糖尿病尚不能完全治愈，但是自从1921年医用胰岛素发现以来，糖尿病得到了很好的治疗和控制。目前糖尿病的治疗主要是饮食控制配合降糖药物（对于2型糖尿病）或者胰岛素补充相结合治疗糖尿病。妊娠期糖尿病通常在分娩后自愈。
糖尿病可以引起多种并发症。如果糖尿病没有得到足够的控制，可以引起一些急性并发症，如低血糖症、酮症酸中毒、非酮高渗性昏迷。严重的长期并发症包括：心血管疾病、慢性肾衰竭（又称糖尿病肾病，是发展中国家成年人中血液透析的主要原因）、视网膜病变（又称糖尿病眼病，可致盲，是发展中国家非老龄成年人致盲的主要疾病）、神经病变及微血管病变。其中，微血管病变可能导致勃起功能障碍（阳痿）以及伤口难以愈合。而足部难以愈合的伤口则可能导致坏疽（俗称―糖尿病足‖），进而导致患者截肢。如果糖尿病得到了足够的控制，并且对血压充分控制并结合良好的生活习惯（如不吸烟，保持健康的体重等），则可以在有效的降低罹患上述并发症的危险。
世界卫生组织2011年的的报告指出全世界有3.46亿人患有糖尿病，2004年估计有340万人死于高血糖引起的后果，超过80%的糖尿病死亡发生在低收入和中等收入国家[1]。
有报道称，亚洲人（特别是东亚）更容易患糖尿病的一个重要原因，是以米饭为主粮太过精细、单一所造成的。[2]
目录
? 1 历史
? 2 病因及类型
o 2.1 糖代谢
? 3 糖尿病诊断标准
o 3.1 糖代谢状态分类
（WHO1999）
o 3.2 中国糖尿病诊断标准[7]
o 3.3 美国糖尿病诊断标准? 4 糖尿病之种类
o 4.1 1型糖尿病
o 4.2 2型糖尿病
o 4.3 妊娠期糖尿病
o 4.4 其他类型糖尿病? 5 糖尿病所引致之并发症? 6 治疗和控制
o 6.1 口服降糖药物[8]
o 6.2 胰岛素
o 6.3 饮食原则
o 6.4 中医
?7 糖尿病与感染
?8 糖尿病的自我检测
?9 参考文献
?10 外部链接
历史
糖尿病自古代就已被发现，最早记载于西元一千五百年前的古埃及[3][4][4]。在中世纪以后在世界各地出现了多种不同的有效的治疗方法，但是，直到1900年左右糖尿病的发病机理才被科学实验所证实。1889年，德国科学家约瑟夫·冯·梅林（Joseph von Mering）和俄裔德国科学家奥斯卡·明科夫斯基（Oskar Minkowski）发现摘除了胰腺的狗出现了糖尿病所有的症状并在不久后死亡。1910年，爱德华·阿尔伯特·沙比-谢弗爵士提出患有糖尿病的病人是因为缺少一种胰腺制造的
物质，他建议称这种物质为―insulin‖（源自拉丁文―insula‖，意为小岛，中文译为―胰岛素‖）。
直到1921年，胰脏在新陈代谢中的内分泌作用以及胰岛素是否真的存在才被进一步的研究所证实。1921年，弗雷德里克·格兰特·班廷爵士和查尔斯·赫伯特·贝斯特（Charles Herbert Best）重复了梅林和明科夫斯基的实验，然后，他们进一步证明，可以通过注射健康狗的胰岛提取物使患了糖尿病的狗恢复过来。班廷、贝斯特以及他们的同事，特别是化学家科利普（Collip）在多伦多大学继续从事提纯牛胰岛素的工作。直到1922年，第一位糖尿病患者得到了一种有效的治疗——胰岛素注射疗法。班廷和实验室主任约翰·麦克劳德因此获得了1923年的诺贝尔生理学和医学奖，这在诺贝尔奖历史上是最快的一次，从发现到获奖只有2年的时间。班廷和贝斯特为胰岛素注册了专利但是并没有收取专利许可费或控制商业生产，这使得胰岛素的生产和使用迅速的遍及全世界。
1936年1月哈罗德·珀西瓦尔·希姆斯沃斯爵士（Sir Harold Percival Himsworth）发表论文指出了1型糖尿病和2型糖尿病的区别。
其他的划时代的发现包括：
1.1942年，发明磺酰脲类药物（作用于胰岛的β细胞以增加胰岛素的分泌）
2.1955年，化学家弗雷德里克·桑格爵士（Sir Frederick Sanger）确定了胰岛
素中氨基酸的排列次序，他也因此而获得1958年诺贝尔化学奖；
3.胰岛素的放射性免疫测定（radioimmunoassay），由罗萨林·耶洛（Rosalyn
Yalow）和所罗门·伯森（Solomon Berson）发明，耶洛因此获得1977年
诺贝尔生理学和医学奖；
4.1969年，多萝西·克劳福特·霍奇金发现了胰岛素的三维空间结构；
5.1988年杰拉德·瑞文博士确认了代谢综合症（metabolic syndrome）
病因及类型
糖代谢
因为胰岛素是调节大多数组织细胞（主要是肌细胞和脂肪细胞，不包括中枢神经系统的神经元细胞）吸收葡萄糖的主要激素，所以胰岛素缺乏和细胞受体对胰岛素不敏感在所有类型的糖尿病中都扮演着重要的角色。
大多数食物中的碳水化合物在几个小时之内就会被转化成葡萄糖单糖——一种在血液中主要的碳水化合物。也有一些碳水化合物不能转化，例如果糖(fructose)，虽然其也能作为细胞能量来源，但是并不会转换为葡萄糖，也不参与胰岛素-葡萄糖调节机制。另外，纤维素也不能被转换成葡萄糖，虽然其是由许多葡萄糖分子组成的长链，这是因为人类和许多动物的消化道没有能力消化它。
当血液中葡萄糖的浓度升高时，比如饭后，β细胞就释放胰岛素到血液中。胰岛素使得大多数的细胞（通常的估计是全身2/3的细胞，包括肌细胞和脂肪组织）从血液中吸收葡萄糖作为他们的能量，或者转化成其它人体所需要的分子，或者储存起来。
胰岛素也是葡萄糖和储存于肝脏和肌肉细胞中的肝糖之间相互转换的主要控制信号，血糖浓度降低既会导致胰岛β细胞减少释放胰岛素，也会降低葡萄糖向肝糖的转化。
高胰岛素水平可以加速多种生化合成的过程，比如细胞的生长和分裂、蛋白质合成和脂肪形成等。
糖尿病诊断标准
世界卫生组织糖尿病诊断标准[5][6]
条件餐后两小时血糖空腹血糖HbA1c
mmol/l（mg/dl）mmol/l（mg/dl）% 正常<7.8（<140）<6.1（<110）<6.0
空腹血糖障碍(Impaired <7.8（<140）≥6.1（≥110）& <7.0（<126） 6.0–6.4
fasting glucose)
糖耐量受损(Impaired
glucose tolerance)
≥7.8（≥140）<7.0（<126） 6.0–6.4 糖尿病≥11.1（≥200）≥7.0（≥126）≥6.5糖代谢状态分类（WHO1999）
糖代谢分类
静脉血浆葡萄糖（mmol/L）
空腹血糖（FPG）糖负荷后2小时血糖（2hPPG）
正常血糖（NGR）<6.1 <7.8
空腹血糖受损（IFG） 6.1～<7.0 <7.8
糖耐量减低（IGT）<7.0 7.8～<11.1 糖尿病（DM）≥7.0≥11.1
中国糖尿病诊断标准[7]
诊断标准静脉血浆葡萄糖水平mmol/L
(1)糖尿病症状（高血糖所导致的多饮、多食、多尿、体重下
降、皮肤瘙痒、视力模糊等急性代谢紊乱表现）加随机血糖
≥11.1
或
(2)空腹血糖（FPG）≥7.0
或
(3)葡萄糖负荷后2 h血糖≥11.1
无糖尿病症状者，需改日重复检查
美国糖尿病诊断标准
根据美国糖尿病协会（ADA）2010年的推荐标准，满足以下任何一条即可诊断为糖尿病：
1.空腹血浆血糖在7.0毫摩尔/升（126 毫克/分升）或以上；
2.在口服糖耐量试验中，口服75克葡萄糖2小时后，血浆血糖在11.1毫摩尔/
升（200毫克/分升）或以上；
3.有高血糖症状，并且随机血浆血糖在11.1毫摩尔/升（200毫克/分升）或以上；
4.糖化血红蛋白（HbA1C）在6.5或以上。
不过一些标准会认为，如果空腹血糖高于100毫克/分升或糖化血色素大于5.7，就已经算是糖尿病前期，但很有机会透过饮食控制、健康减肥及充足运动来治愈。糖尿病之种类
1型糖尿病
主条目：1型糖尿病
也称为胰岛素依赖型糖尿病，患者病状通常出现在儿童或青少年时期。可能是一种自体免疫性疾病。在这情况下，身体的免疫系统对体内生产胰岛素的β细胞做出攻击，最终导致体内无法生产胰岛素。患者需要注射外源性的胰岛素来控制体内的血糖，这是一种由先天家族遗传的疾病。
2型糖尿病
主条目：2型糖尿病
也称非胰岛素依赖型糖尿病，常出现在成年人（特别是肥胖症患者）身上，其病症会导致消瘦。
病因包括：
?胰岛素抵抗，使到身体不能有效地使用胰岛素。
?胰岛素分泌的减少，无法满足身体所需。
早期第二类糖尿病患者可以通过改善生活方式(如健康饮食、适量运动、安全减肥、戒烟及避免二手烟暴露等)来控制、甚至治愈糖尿病。大多数患者可通过口服降糖药物来帮助控制体内血糖。一些第2类糖尿病患者需要胰岛素注射。
妊娠期糖尿病
主条目：妊娠期糖尿病
妊娠期糖尿病（Gestational Diebetes Mellitus，GDM），是围产期的主要并发症之一。可能导致胎儿发育畸形、胎儿宫内窘迫、胎死宫内新生儿低血糖、巨大儿以及难产或者死产等并发症。
诊断标准：妊娠24-28周时，若使用两阶段检测先进行50克的葡萄糖筛检（口服），若是异常则进行100克口服葡萄糖量（口服）试验，分别测量空腹、餐后1小时、2小时及3小时的血糖浓度，若
?空腹>95 mg/dL（5.28 mmol/L）；
?餐后1小时>180 mg/dL（10.00 mmol/L）；
?餐后2小时>155 mg/dL（8.61 mmol/L）；
?餐后3小时>140 mg/dL（7.78 mmol/L）
符合其中的两项或者两项以上，即可诊断妊娠糖尿病。
其他类型糖尿病
一些糖尿病导因有别于第一型，第二型和妊娠糖尿病，这包括：
?β细胞基因缺陷（β细胞分泌胰岛素）
?遗传性胰岛素抗拒
?胰脏疾病
?荷尔蒙失调
?化学或药物导致
糖尿病所引致之并发症
经过光凝治疗的糖尿病患的视网膜
糖尿病的并发症主要表现在全身微循环的障
碍，可以发生在心脏血管、脑血管、眼的视网
膜、四肢周边血管及肾脏，也可引起神经病变：
1.糖尿病视网膜病变：长期的高血糖环境会损伤视网膜血管的内皮，引起一系
列的眼底病变，如微血管瘤、硬性渗出、棉絮斑、新生血管、玻璃体增殖甚至视网膜脱离。一般糖尿病出现十年以上的病人开始出现眼底病变，但如果血糖控制差，或者是第一型糖尿病的患者则可能更早出现眼底病变，故糖尿病患者需要定期到眼科检查眼底。
2.糖尿病肾病：可分成五个阶段，最终可能引致肾衰竭。
3.糖尿病足：初期只是脚部伤口难于愈合，若处理不当可引致截肢。
治疗和控制
总的治疗原则是通过改变生活方式，包括饮食控制、体育锻炼、减轻体重，不吸烟及避免二手烟对预防及控制糖尿病也有一定的效果，并配合一定的药物治疗，以达到控制血糖、预防并发症的目的。
口服降糖药物[8]
1.双胍类药物:主要药理作用是通过减少肝葡萄糖的输出和改善外周胰岛素抵
抗而降低血糖。
2.磺脲类药物:属于促胰岛素分泌剂，主要药理作用是通过刺激胰岛β细胞分泌
胰岛素，增加体内的胰岛素水平而降低血糖。
3.噻唑烷二酮类药物（TZDs）:主要通过增加靶细胞对胰岛素作用的敏感性而
降低血糖。
4.格列奈类药物:为非磺脲类的胰岛素促泌剂，主要通过刺激胰岛素的早期分泌
而降低餐后血糖.
5.α-糖苷酶抑制剂:通过抑制碳水化合物在小肠上部的吸收而降低餐后血糖。
6.二肽基肽酶-4（DPP-4）抑制剂:通过抑制DPP-4而减少GLP-1在体内的失活，
增加GLP-1在体内的水平。
对于严重的第2型糖尿病且严重肥胖的患者，最近发展了一种胃绕道手术手术，可以显著改善其血糖水平。
胰岛素
根据来源和化学结构的不同，胰岛素可分为动物胰岛素、人胰岛素和胰岛素类似物。人胰岛素如诺和灵系列，胰岛素类似物如门冬胰岛素、门冬胰岛素30、地特胰岛素注射液。按作用时间的特点可分为：速效胰岛素类似物、短效胰岛素、中效胰岛素、长效胰岛素（包括长效胰岛素类似物）和预混胰岛素（预混胰岛素类似物），常见速效胰岛素类似物如门冬胰岛素，长效胰岛素类似物如地特胰岛素。临床试验证明，胰岛素类似物在模拟生理性胰岛素分泌和减少低血糖发生的危险性方面优于人胰岛素。[9]
饮食原则
1.避免肥胖，维持理想且合适的体重。
2.定时定量，每餐饮食按照计划份量进食，不可任意增减。
3.少吃油煎、炸、油酥及猪皮、鸡皮、鸭皮等含油脂高的食物。
4.烹调多采用清蒸、水煮、凉拌、涮、烧、炖、卤等方式。不可太咸，食盐摄
入量6克以下为宜
5.饮食不可太咸，少吃胆固醇含量高的食物，例如腰花、肝、肾等动物内脏类
食物。
6.烹调宜用植物性油脂。
7.配合长期性且适当的运动、药物、饮食的控制。
8.尽量减少赴宴，必要时，注意选择食物的种类及分量。
9.糖尿病[10]患者由于特殊的体征表现及病理情况，其在饮食上要有特别注意，
米饭水果要适当食用，尤其甜食要格外注意。宜吃五谷粗粮；豆类制品食物；
香菇、苦瓜等。不宜糖类、动物脂肪及高胆固醇食物；忌嗜酒。
10.忌辛辣；戒烟限酒、避免接触二手烟。
11.进餐时，要专心吃；咀嚼要细嚼慢咽，不可狼吞虎咽；不要用菜汁泡饭吃；
不要吃剩饭；饭后立即刷牙漱口。
中医
中医虽然没有血糖概念，但对水的概念很重视（比如，肾五行属水等等）。虽然没有糖尿病的这个名词，却有该病症—消渴。中医所说的消渴症分为三种：饥食百碗不解饥；渴饮千杯不解渴；性冷淡。比糖尿病的范围要广的多。
糖尿病与感染
糖尿病患者常见感染类型：泌尿系感染、肺炎、结核病、胆道感染、皮肤及软组织感染、外耳炎和口腔感染。
糖尿病的自我检测
糖尿病患者可采用血糖仪进行自我检测，准备工具：血糖仪、试纸、采血笔、采血针。方法：
1.消毒皮肤
2.使用采血笔采血
3.把血液放置试纸
4.把试纸放入血糖仪读取数据
参考文献
1.^糖尿病. 世卫组织. 2011年9月[2011-11-15].
2.^老虎索阮光锋. 亚洲人更易患糖尿病罪魁祸首竟是―白米饭‖. 羊城晚报.
2012年5月1日.
3.^ Ripoll, Brian C. Leutholtz, Ignacio. Exercise and disease management 2nd ed.
Boca Raton: CRC Press. : 25. ISBN978-1-4398-2759-8.
4.^ 4.04.1 editor, Leonid Poretsky,. Principles of diabetes mellitus 2nd ed. New York:
Springer. 2009: 3. ISBN978-0-387-09840-1.
5.^Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia:
report of a WHO/IDF consultation. Geneva: World Health Organization. 2006. 21.
ISBN978-92-4-159493-6.
6.^ Vijan, S. Type 2 diabetes. Annals of Internal Medicine. March 2010, 152 (5):
ITC31-15. doi:10.1059/0003-4819-152-5-201003020-01003. PMID20194231.
7.^中国2型糖尿病防治指南2010
8.^中国2型糖尿病防治指南2010
9.^新型胰岛素类似物的研究进展.《世界临床药物》2004年第12期.
10.^糖尿病食谱
外部链接
?糖尿病
?美国亚裔糖尿病研进会
?英国糖尿病协会
?香港糖尿联会
?北京协和医院糖尿病的自我检测
糖尿病藥物治療
糖尿病普遍分為一型和二型。一型糖尿是由於胰島素分泌不足或缺乏而形成；二型糖尿則是因為身體對胰島素出現抗拒，使肝臟、肌肉、和脂肪等組織不能對胰島素產生反應，而造成胰島素供不應求的情况。二型糖尿患者於後期也會出現胰島素分泌不足或缺乏的情況。
糖尿病一般須要靠藥物控制，一型糖尿患者必須注射胰島素，至於二型糖尿病人，在以下情況亦會需要注射胰島素；如病人出現急性併發症，嚴重感染，急性心臟病，腎功能衰竭，在手術前後，在懷孕期間或當口服降糖藥未能有效控制血糖時。
口服降糖藥則適用於二型糖尿患者。市面上有不同種類的降糖藥，它們是針對二型糖尿不同病理上的缺陷而設的，因此各藥物的功效和副作用也各不同。現在就讓我們嘗試解開降糖藥物之謎。
I. 口服降糖藥
1. 磺胺尿素劑(Sulphonylurea)
2. 雙胍類(Biguanides)
3. 葡萄糖甘酶抑制劑(α-glucosidase inhibitor)
4. 胰島素反應加强劑(Insulin sensitizer)
5. 餐時血糖調節劑(Prandial glucose regulator)
6. 二肽基肽IV抑制劑(DDP-IV inhibitor)
II. 胰島素
III. 甚麼人需要打胰島素?
I. 口服降糖藥
常見的口服降糖藥大致可分為五類：
1. 磺胺尿素劑(Sulphonylurea) 藥例：Glibenclamide (Daonil)，gliclazide (Diamicron)，glimepiride (Amaryl)，glipizide (Minidiab)
磺胺尿素劑的作用是增加胰臟細胞分泌和釋放胰島素，減少肝糖產生，從而降低血糖。飯前30分鐘服用效果佳，服藥後2到3小時可發揮最大治療效果，使飯後血糖值維持穩定。有部份磺胺尿素劑更能改善外周組織對胰島素的敏感度，尤其適用於較為肥胖的糖尿病患者。它或會有的副作用是會導致血糖過低，如有腎衰竭患者要小心使用。
2. 雙胍類(Biguanides) 藥例：甲福明Metformin (Glucophage)
雙胍類的作用是抑制肝臟釋放過量的糖份，增加機體組織對胰島素的敏感性，從而降低血糖。這藥應作為所有新二型糖尿病患者的首選藥物，因為二型糖尿患者有較大機會出現胰島素抗拒的現象。它的特點是單獨使用時，它能有效降低血糖水平導致至血糖過低的機會很微。它或會有的副作用是引致腸道不適，如嘔心、反胃、腹瀉等。但對於有嚴重心、肝、肺、腎功能不良的患者，不推薦使用。
3. 葡萄糖甘酶抑制劑(α-glucosidase inhibitor) 藥例：Acarbose (Glucobay)
葡萄糖甘酶抑制劑主要是抑制澱粉質、蔗糖和麥芽糖在小腸的分解，使葡萄糖的吸收減慢，從而降低餐後的血糖濃度，故適宜那些單純以餐後血糖升高爲主的患者。餐前即服或與第一口飯同服，且膳食中必須含有一定的碳水化合物（如大米、麵粉等）時才能發揮效果。它或會有的副作用是胃腸氣脹、腹瀉等。
4. 胰島素反應加強劑(Insulin sensitizer)藥例：Pioglitazone (Actos)
胰島素反應加强劑的主要作用是減低身體對胰島素的抗拒，增加肌肉細胞對胰島素的敏感，特別適合用於肥胖二型糖尿病患者。它或會有的副作用是水腫，體重上升。患有心臟衰竭或肝功能不正常的病人都不適合使用。
5. 餐時血糖調節劑(Prandial glucose regulator) 及仿腸降糖素(incretin mimetic)
a) 餐時血糖調節劑(Prandial glucose regulator) 藥例：Repaglinide (Novonorm) 及Nateglinide (Starlix)
餐時血糖調節劑的主要作用是增加胰島素的分泌，其功能與磺胺尿素劑相近，服藥後約30到60分鐘開始作用，建議飯前15到30分鐘或隨餐服用以減少餐後血糖過高和餐前血糖過低的機會。
b) 仿腸降糖素(incretin mimetic) 藥例：仿GLP-1 Exenatide (Byetta)
Glucagon-like peptide-1 (GLP1) 是其中一種已知擁有腸降糖素作用的荷爾蒙。Exenatide 則仿造人體腸道內天然GLP-1的作用，提升胰島素分泌，抑制體內的升糖素(glucagon)，降低血糖濃度。Exenatide需要經皮下進行注射，它的好處是不會導致血糖過低的情况和有助減低體重。它或會有的副作用是噁心，嘔吐及頭痛等。
6. 二肽基肽IV抑制劑(DDP-IV inhibitor) 藥例：Saxagliptin (Onglyza) ，Sitagliptin (Januvia)，Vildagliptin (Galvus)
DDP-IVinhibitor能減低腸降糖素的分解，使GLP-1和GIP (gastric inhibitory peptide) 的水平增加，進一步增加胰島素分泌和抑制升糖素，達到控制血糖的效果。Sitagliptin是新一代口服降糖藥，它能有效地控制血糖，亦可減少血糖過低的情况，適合二型糖尿的患者使用。
但是此類藥物應用的時間較短，它的副作用尚待觀察，因此它們暫時只被定為治療二型糖尿病的二線藥物，服用前應徵詢醫護人員意見。
II. 胰島素
胰島素(Insulin)是一種荷爾蒙，由胰臟內的β細胞製造並分泌。胰島素的工作是幫助血糖進入身體細胞，使血糖維持在正常水平。它是一種蛋白質，功效會被腸胃的消化液破壞，故不能口服，一般都以皮下注射的方式吸收。
胰島素可以按來源、生產方法、作用時間及純度來分類。從前我們用的動物胰島素較易引起過敏性反應及抗體的產生，現時市面上的胰島素大多是用科學方法仿人體的胰島素造成(Human HM)，近年還有幾種對原用胰島素的化學結構作改變的胰島素同類物(Insulin analogue)。
除以上種類外也有由不同長短性混合而成的混合劑，如Mixtard 30HM、Humalog Mix 75/25、Humalog Mix 50/50、Humulin 70/30、Novomix30等，為不同需要的病人調制。
III. 甚麼人需要打胰島素?
1. 所有一型糖尿病人
2. 在緊急情況下，如糖尿酮酸中毒症或高血糖昏迷症
3. 懷孕期間或患有其他嚴重疾病，如感染等
4. 部份二型糖尿病人，隨著病情的變化，雖然遵守飲食和運動治療後，仍未能令血糖受到控制。
估計現時半數患有二型糖尿病十年以上的人士需轉用胰島素來控制病情。
總括來說，糖尿病除了依靠藥物控制之外，更重要的是要病人配合，控制飲食習慣，進行適量運動，達到控制體重的目的。在醫生、糖尿專科護士、營養師和足病診療師的治療和護理下，糖尿病患者必定能有效地控制血糖水平，減少糖尿併發症的出現。
Diabetes mellitus
Diabetes mellitus (DM) or simply diabetes, is a group of metabolic diseases in which a person has high blood sugar.[2] This high blood sugar produces the symptoms of frequent urination, increased thirst, and increased hunger. Untreated, diabetes can cause many complications. Acute complications include diabetic ketoacidosis and nonketotic hyperosmolar coma. Serious long-term complications include heart disease, kidney failure, and damage to the eyes.
Diabetes is due to either the pancreas not producing enough insulin, or because cells
of the body do not respond properly to the insulin that is produced.[3] There are three main types of diabetes mellitus:[4]
?Type 1 DM results from the body's failure to produce insulin. This form was previously referred to as "insulin-dependent diabetes mellitus" (IDDM) or
"juvenile diabetes".[4]
?Type 2 DM results from insulin resistance, a condition in which cells fail to use insulin properly, sometimes also with an absolute insulin deficiency. This form was previously referred to as non insulin-dependent diabetes mellitus (NIDDM) or "adult-onset diabetes".
?Gestational diabetes, is the third main form and occurs when pregnant women without a previous diagnosis of diabetes develop a high blood glucose level.
Prevention and treatment often involve a healthy diet, physical exercise, not using tobacco, and being a normal body weight.[4]Blood pressure control and proper foot care are also important for people with the disease.[4] Type 1 diabetes must be managed with insulin injections.[4] Type 2 diabetes may be treated with medications with or without insulin.[4] Insulin and some oral medications can cause low blood sugar, which can be dangerous. Gastric bypass surgery has been successful in many with severe obesity and type 2 DM. Gestational diabetes usually resolves after the birth of the baby.
Globally, as of 2013, an estimated 382 million people have diabetes worldwide, with type 2 diabetes making up about 90% of the cases.[5][6] This is equal to 3.3% of the population, with equal rates in both women and men.[7] In 2011 diabetes resulted in 1.4 million deaths worldwide, making it the 8th leading cause of death.[4] The number of people with diabetes is expected to rise to 592 million by 2035.[6]
Contents
? 1 Signs and symptoms
o 1.1 Diabetic emergencies
o 1.2 Complications
? 2 Causes
o 2.1 Type 1
o 2.2 Type 2
o 2.3 Gestational diabetes
o 2.4 Other types
? 3 Pathophysiology
? 4 Diagnosis
? 5 Prevention
? 6 Management
o 6.1 Lifestyle
o 6.2 Medications
o 6.3 Pancreatic transplantation
o 6.4 Support
?7 Epidemiology
?8 History
o8.1 Etymology
?9 Society and culture
o9.1 Naming
?10 Other animals
?11 Research
?12 References
?13 Further reading
?14 External links
Signs and symptoms
Overview of the most significant symptoms of diabetes The classic symptoms of untreated diabetes
are weight loss, polyuria (frequent
urination), polydipsia (increased thirst), and
polyphagia (increased hunger).[8] Symptoms may develop rapidly (weeks or months) in
type 1 diabetes, while they usually develop much more slowly and may be subtle or absent in
type 2 diabetes.
Prolonged high blood glucose can
cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in
vision changes. Blurred vision is a common complaint
leading to a diabetes diagnosis. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes.
Diabetic emergencies
People (usually with type 1 diabetes) may also experience episodes of diabetic ketoacidosis, a type of metabolic problems characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness.[9]
A rare but equally severe possibility is hyperosmolar nonketotic state, which is more common in type 2 diabetes and is mainly the result of dehydration.[9] Complications
Main article: Complications of diabetes mellitus
All forms of diabetes increase the risk of long-term complications. These typically develop after many years (10–20), but may be the first symptom in those who have otherwise not received a diagnosis before that time.
The major long-term complications relate to damage to blood vessels. Diabetes doubles the risk of cardiovascular disease[10] and about 75% of deaths in diabetics are due to coronary artery disease.[11] Other "macrovascular" diseases are stroke, and peripheral vascular disease.
The primary microvascular complications of diabetes include damage to the eyes, kidneys, and nerves.[12] Damage to the eyes, known as diabetic retinopathy, is caused by damage to the blood vessels in the retina of the eye, and can result in gradual vision loss and potentially blindness.[12] Damage to the kidneys, known as diabetic nephropathy, can lead to tissue scarring, urine protein loss, and eventually chronic kidney disease, sometimes requiring dialysis or kidney transplant.[12] Damage to the nerves of the body, known as diabetic neuropathy, is the most common complication of diabetes.[12] The symptoms can include numbness, tingling, pain, and altered pain sensation, which can lead to damage to the skin. Diabetes-related foot problems (such as diabetic foot ulcers) may occur, and can be difficult to treat, occasionally requiring amputation. Additionally, proximal diabetic neuropathy causes painful muscle wasting and weakness.
There is a link between cognitive deficit and diabetes. Compared to those without diabetes, those with the disease have a 1.2 to 1.5-fold greater rate of decline in cognitive function.[13]
Causes
Comparison of type 1 and 2 diabetes[5]
Feature Type 1 diabetes Type 2 diabetes
Onset Sudden Gradual
Age at onset Mostly in children Mostly in adults
Body size Thin or normal[14]Often obese
Ketoacidosis Common Rare
Autoantibodies Usually present Absent
Endogenous insulin Low or absent Normal, decreased or increased Concordance in identical twins50% 90%
Prevalence ~10% ~90%
Diabetes mellitus is classified into four broad categories: type 1, type 2, gestational diabetes, and "other specific types".[3] The "other specific types" are a collection of a few dozen individual causes.[3] The term "diabetes", without qualification, usually refers to diabetes mellitus.
Type 1
Main article: Diabetes mellitus type 1
Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the islets of Langerhans in the pancreas, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of the immune-mediated nature, in which a T-cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin.[15] It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults, but was traditionally termed "juvenile diabetes" because a majority of these diabetes cases were in children.
"Brittle" diabetes, also known as unstable diabetes or labile diabetes, is a term that was traditionally used to describe the dramatic and recurrent swings in glucose levels, often occurring for no apparent reason in insulin-dependent diabetes. This term, however, has no biologic basis and should not be used.[16] Still, type 1 diabetes can be accompanied by irregular and unpredictable hyperglycemia, frequently with ketosis, and sometimes with serious hypoglycemia. Other complications include an impaired counterregulatory response to hypoglycemia, infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (e.g., Addison's disease).[16] These phenomena are believed to occur no more frequently than in 1% to 2% of persons with type 1 diabetes.[17]
Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people,
the onset of diabetes can be triggered by one or more environmental factors, such as a viral infection or diet. There is some evidence that suggests an association between type 1 diabetes and Coxsackie B4 virus. Unlike type 2 diabetes, the onset of type 1 diabetes is unrelated to lifestyle.
Type 2
Main article: Diabetes mellitus type 2
Type 2 diabetes mellitus is characterized by insulin resistance, which may be combined with relatively reduced insulin secretion.[3] The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus cases due to a known defect are classified separately. Type 2 diabetes is the most common type.
In the early stage of type 2, the predominant abnormality is reduced insulin sensitivity. At this stage, hyperglycemia can be reversed by a variety of measures and medications that improve insulin sensitivity or reduce glucose production by the liver.
Type 2 diabetes is due primarily to lifestyle factors and genetics.[18] A number of lifestyle factors are known to be important to the development of type 2 diabetes, including obesity (defined by a body mass index of greater than thirty), lack of physical activity, poor diet, stress, and urbanization.[5] Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60-80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders.[3] Those who are not obese often have a high waist–hip ratio.[3]
Dietary factors also influence the risk of developing type 2 diabetes. Consumption of sugar-sweetened drinks in excess is associated with an increased risk.[19][20] The type of fats in the diet is also important, with saturated fats and trans fatty acids increasing the risk and polyunsaturated and monounsaturated fat decreasing the risk.[18] Eating lots of white rice appears to also play a role in increasing risk.[21] A lack of exercise is believed to cause 7% of cases.[22]
Gestational diabetes
Main article: Gestational diabetes
Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2-10% of all pregnancies and may improve or disappear after delivery.[23] However, after pregnancy approximately 5-10% of women with gestational diabetes are found to have diabetes mellitus, most commonly type 2.[23] Gestational diabetes is fully treatable, but requires careful medical supervision
throughout the pregnancy. Management may include dietary changes, blood glucose monitoring, and in some cases insulin may be required.
Though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor induction may be indicated with decreased placental function. A Caesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
Other types
Prediabetes indicates a condition that occurs when a person's blood glucose levels are higher than normal but not high enough for a diagnosis of type 2 DM. Many people destined to develop type 2 DM spend many years in a state of prediabetes.
Latent autoimmune diabetes of adults (LADA) is a condition in which type 1 DM develops in adults. Adults with LADA are frequently initially misdiagnosed as having type 2 DM, based on age rather than etiology.
Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization when the current taxonomy was introduced in 1999.[24]
Other forms of diabetes mellitus include congenital diabetes, which is due to genetic defects of insulin secretion, cystic fibrosis-related diabetes, steroid diabetes induced by high doses of glucocorticoids, and several forms of monogenic diabetes.
The following is a comprehensive list of other causes of diabetes:[25]
?Genetic defects of β-cell function ?Endocrinopathies
o Maturity onset diabetes of the young
o Mitochondrial DNA mutations
? Genetic defects in insulin processing or insulin action
o Defects in proinsulin conversion
o Insulin gene mutations
o Insulin receptor mutations ? Exocrine pancreatic defects
o Chronic pancreatitis
o Pancreatectomy
o Pancreatic neoplasia
o Cystic fibrosis
o Hemochromatosis
o Fibrocalculous pancreatopathy o Growth hormone excess (acromegaly ) o Cushing syndrome o Hyperthyroidism
o Pheochromocytoma o Glucagonoma ? Infections o Cytomegalovirus infection
o Coxsackievirus B ? Drugs o Glucocorticoids o Thyroid hormone o β-adrenergic agonists o Statins [26]
Pathophysiology
The fluctuation of blood sugar (red) and the
sugar-lowering hormone insulin (blue) in humans
during the course of a day with three meals - one
of the effects of a sugar -rich vs a starch -rich meal
is highlighted.
Mechanism of insulin release in normal
pancreatic beta cells - insulin production is more or
less constant within the beta cells. Its release is
triggered by food, chiefly food containing
absorbable glucose. Insulin is the principal hormone that regulates the
uptake of glucose from the blood into most cells of the body,
especially liver, muscle, and adipose tissue. Therefore, deficiency of insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus.[27] The body obtains glucose from three main places: the intestinal absorption of food, the breakdown of glycogen , the storage form of glucose found in the liver, and gluconeogenesis , the generation of glucose from non-carbohydrate substrates in the body.[28] Insulin plays a critical role in balancing glucose levels in the body. Insulin can inhibit the breakdown of glycogen or the process of gluconeogenesis , it can stimulate the transport of glucose into fat and muscle cells, and it can stimulate the storage of glucose in the form of glycogen .[28]
Insulin is released into the blood by beta cells(β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.[29]
If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or insulin resistance), or if the insulin itself is defective, then glucose will not be absorbed properly by the body cells that require it, and it will not be stored appropriately in the liver and muscles. The net effect is persistently high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidosis.[28]
When the glucose concentration in the blood remains high over time, the kidneys will reach a threshold of reabsorption, and glucose will be excreted in the urine (glycosuria).[30] This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst (polydipsia).[28]
Diagnosis
See also: Glycated hemoglobin and Glucose tolerance test
WHO diabetes diagnostic criteria[31][32]edit
Condition 2 hour glucose Fasting glucose HbA1c
mmol/l(mg/dl) mmol/l(mg/dl) % Normal <7.8 (<140) <6.1 (<110) <6.0 Impaired fasting glycaemia<7.8 (<140) ≥ 6.1(≥110) & <7.0(<126) 6.0–6.4 Impaired glucose tolerance≥7.8 (≥140)<7.0 (<126) 6.0–6.4 Diabetes mellitus≥11.1 (≥200)≥7.0 (≥126)≥6.5
Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:[24]
?Fasting plasma glucose level ≥ 7.0 mmol/l (126 mg/dl)
?Plasma glucose≥ 11.1 mmol/l (200 mg/dL) two hours after a 75 g oral glucose load as in a glucose tolerance test
?Symptoms of hyperglycemia and casual plasma glucose ≥ 11.1 mmol/l (200 mg/dl)
Glycated hemoglobin(Hb A1C) ≥ 6.5%.[33]
A positive result, in the absence of unequivocal hyperglycemia, should be confirmed by a repeat of any of the above methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test.[34] According to the current definition, two fasting glucose measurements above 126 mg/dl (7.0 mmol/l) is considered diagnostic for diabetes mellitus.
Per the World Health Organization people with fasting glucose levels from 6.1 to
6.9 mmol/l (110 to 125 mg/dl) are considered to have impaired fasting glucose.[35] people with plasma glucose at or above
7.8 mmol/L (140 mg/dL), but not over
11.1 mmol/L (200 mg/dL), two hours after a 75 g oral glucose load are considered to have impaired glucose tolerance. Of these two prediabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus, as well as cardiovascular disease.[36] The American Diabetes Association since 2003 uses a slightly different range for impaired fasting glucose of 5.6 to 6.9 mmol/l (100 to
125 mg/dl).[37]
Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.[38]
The rare disease diabetes insipidus has similar symptoms to diabetes mellitus, but without disturbances in the sugar metabolism (insipidus means "without taste" in Latin) and does not involve the same disease mechanisms.
Prevention
There is no known preventive measure for type 1 diabetes.[4] Type 2 diabetes can often be prevented by a person being a normal body weight, physical exercise, and following a healthy diet.[4] Dietary changes known to be effective in helping to prevent diabetes include a diet rich in whole grains and fiber, and choosing good fats, such as polyunsaturated fats found in nuts, vegetable oils, and fish.[39] Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help in the prevention of diabetes.[39] Active smoking is also associated with an increased risk of diabetes, so smoking cessation can be an important preventive measure as well.[40]
Management
Main article: Diabetes management
Diabetes mellitus is a chronic disease, for which there is no known cure except in very specific situations. Management concentrates on keeping blood sugar levels as close to normal ("euglycemia") as possible, without causing hypoglycemia. This can