第二型糖尿病病程中造成胰臟β細胞功能受損的病因及治療

第二型糖尿病被稱為二十一世紀盛行率最高的文明病之一，對職場勞工健康產生非常重大的危害。第二型糖尿病的臨床併發症歸因於組織的胰島素抗性和β細胞凋亡兩大關鍵病因，而其中β細胞凋亡在其病程發展中扮演非常重要的角色，它是決定糖尿病病人血糖高低和葡萄糖耐受性的關鍵因素如何預防或改善此一疾病的併發症。高血糖是第二型糖尿病程的主要病徵，而產生的葡萄糖毒性會造成β細胞受損，此惡性循環會加速β細胞的功能惡化，再則，大部分第二型糖尿病患都伴隨有肥胖和高血脂，當脂肪增加與高血糖惡化情形一樣時，其蘭氏小島堆積的脂肪會使β細胞功能減弱，故不正常的脂肪堆積跟長期高血糖一樣會使β細胞功能惡化，而不論是高血糖或高血脂造成的β細胞功能受損都與其造成β細胞的長期氧化壓力增加有關，其中特別是高血糖誘發β細胞的葡萄糖毒性反應被認為是造成其胰島素分泌功能受損的主要原因。是故，如何降低第二型糖尿病病人的血糖濃度並改善其體內的氧化壓力和高血脂症，是避免其病程惡化及改善糖尿病控制的重要治療策略。

關鍵字

第二型糖尿病； β細胞；胰島素分泌；高血糖；高血脂；氧化壓力；勞工健康

並列摘要

Type 2 diabetes is generally viewed as a clinical syndrome with variable phenotypic expression rather than a single disease with a specific etiology. Phenotypic elements of the syndrome include β-cell insufficiency and insulin resistance. The relentless decline in β-cell function frequently observed in type 2 diabetic patients, despite optimal drug management, has variously been ascribed to glucose toxicity and lipotoxicity. Recent reports suggested that hyperglycemia, an outcome of the disease, acts as a secondary force that further damages B-cells and often-accompanied hyperlipidemia is also considered as a primary cause of β-cell dysfunction. Recent studies also demonstrated that the patients with type 2 diabetes continually undergo oxidative stress, that elevated glucose concentrations increase levels of reactive oxygen species in β-cells, that islets have intrinsically low antioxidant enzyme defense, that antioxidant drugs and hypoglycemic agents may protect β-cells from glucose toxicity, and that lipotoxicity attributable to hyperlipidemia ocurres only in the context of preexisting hyperglycemia, wherea glucose toxicity can occur in the absence of hyperlipidemia. This review may be of clinical importance for providing possible therapeutic strategies to improve and retard the development of T2DM.

並列關鍵字

type 2 diabetes mellitus ； β-cell ； insulin secretion ； hyperglycemia ； hyperlipidemia ； oxidative stress ； health promotion

國際替代計量

第二型糖尿病病程中造成胰臟β細胞功能受損的病因及治療

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