中国糖尿病杂志
中國糖尿病雜誌
중국당뇨병잡지
CHINESE JOURNAL OF DIABETES
2001年
4期
195-199
,共5页
纪立农%周翔海%韩学尧%罗晏权%陈陵霞
紀立農%週翔海%韓學堯%囉晏權%陳陵霞
기립농%주상해%한학요%라안권%진릉하
2型糖尿病%胰岛素抵抗%胰岛素分泌%家系
2型糖尿病%胰島素牴抗%胰島素分泌%傢繫
2형당뇨병%이도소저항%이도소분비%가계
type 2 Insulin resistance insulin secretion Pedigree
目的研究胰岛素抵抗及胰岛紊分泌功能在2型糖尿病(DM)发生、发展中的作用.方法在2型DM家系成员中,对已诊断DM者按病程中位数分组,病程≤4年组153例,<4年组129例.经口服葡萄糖耐量试验(OGTT),按1999年WHO糖尿病诊断标准,新诊断DM组72例.非DM者按HbAlc分组,HbAlc≤5.5%组78例,HbAlc<5.5%组110例,计算各组HOMA模型胰岛素抵抗指数(HOMAIR)、β细胞功能指数(HOMAβ)及胰岛素敏感性指数(ISI),与无DM家族史的正常人98例比较.结果除HbAlc≤5.5%组外,家系各组HOMAIR均值高于正常对照,差异有显著性(P<0.01).家系非DM两组HOMA β高于正常对照(P<0.01),DM各组HOMAβ低于正常对照(P<0.01).结论北京地区2型DM家系中非DM一级亲属的胰岛素抵抗及糖耐量异常可能继发于胰岛素分泌功能异常增高,胰岛素分泌功能降低和胰岛素抵抗是发生糖尿病的主要机制.
目的研究胰島素牴抗及胰島紊分泌功能在2型糖尿病(DM)髮生、髮展中的作用.方法在2型DM傢繫成員中,對已診斷DM者按病程中位數分組,病程≤4年組153例,<4年組129例.經口服葡萄糖耐量試驗(OGTT),按1999年WHO糖尿病診斷標準,新診斷DM組72例.非DM者按HbAlc分組,HbAlc≤5.5%組78例,HbAlc<5.5%組110例,計算各組HOMA模型胰島素牴抗指數(HOMAIR)、β細胞功能指數(HOMAβ)及胰島素敏感性指數(ISI),與無DM傢族史的正常人98例比較.結果除HbAlc≤5.5%組外,傢繫各組HOMAIR均值高于正常對照,差異有顯著性(P<0.01).傢繫非DM兩組HOMA β高于正常對照(P<0.01),DM各組HOMAβ低于正常對照(P<0.01).結論北京地區2型DM傢繫中非DM一級親屬的胰島素牴抗及糖耐量異常可能繼髮于胰島素分泌功能異常增高,胰島素分泌功能降低和胰島素牴抗是髮生糖尿病的主要機製.
목적연구이도소저항급이도문분비공능재2형당뇨병(DM)발생、발전중적작용.방법재2형DM가계성원중,대이진단DM자안병정중위수분조,병정≤4년조153례,<4년조129례.경구복포도당내량시험(OGTT),안1999년WHO당뇨병진단표준,신진단DM조72례.비DM자안HbAlc분조,HbAlc≤5.5%조78례,HbAlc<5.5%조110례,계산각조HOMA모형이도소저항지수(HOMAIR)、β세포공능지수(HOMAβ)급이도소민감성지수(ISI),여무DM가족사적정상인98례비교.결과제HbAlc≤5.5%조외,가계각조HOMAIR균치고우정상대조,차이유현저성(P<0.01).가계비DM량조HOMA β고우정상대조(P<0.01),DM각조HOMAβ저우정상대조(P<0.01).결론북경지구2형DM가계중비DM일급친속적이도소저항급당내량이상가능계발우이도소분비공능이상증고,이도소분비공능강저화이도소저항시발생당뇨병적주요궤제.
Objective To investigate the roles of insulin resistance and insulin secretory function in the pathogenesis of type 2 diabetes mellitus (T2DM). Methods We recruited six groups of subjects. Individuas (n= 282) with previously diagnosed T2DM were selected from families included in our T2DM family study. They were divided according to the median duration of DM (4 years) into a group of 153 patients with duration 4 years or less and a group of 129 patients with duration more than 4 years. From the same families,we recruited 72 subjects with diabetes newly diagnosed by OGTT. Also from these same families,we recruited non-diabetic first-degree relatives (n=188) that we divided into the groups of 78 with HbAlc less than or equal 5. 5% and 110 with HbAlc over 5. 5%. In addition,we recruited 98 unrelated non-diabetic controls. In each group,we used the HOMA model to calculate HOMA-IR as an index of insulin resistance and HOMAβ as an index of beta-cell function. We also calculated the insulin sensitivity index (ISI). Results In all of the groups of subjects selected from the T2DM families,mean HOMA-IR was significantly (P<0.01) higher than that in non-diabetic controls,with the exception of the group of non-diabetic relatives with HbAlc less than 5. 5%. In both groups of relative without diabetes,mean HOMA β was significantly (P<0. 01 ) higher than that in normal controls,while in all 3 group of relatives with diabetes,mean HOMA β was significantly (P<0. 01 ) lower than that of normal controls. In conclusion,in the families of patients with type 2 diabetes in the Beijing area,first degree relatives with normal glucose tolerance and low HbAlc have higher insulin secretion (HOMAβ) than nondiabetic controls,despite having a mean HOMA-IR comparable to the nondiabetic controls. Conclusion This evidence of over-active insulin secretory function in some non-diabetic relatives in T2DM families may point to a role of insulin secretion in the induction of insulin resistance and to the’development of glucose intolerance and T2DM. Diabetes occurs when insulin resistance worsens and insulin secretion declines.