成都地區2型糖尿病患者糖耐量正常一級親屬代謝紊亂的臨床研究_《華西醫學》

作者：

劉宋芳 ¹ , 龔媛 ¹ , 劉圓圓 ¹ , 宋潔 ¹ , 田浩明 ^1,2 , 陳濤 ¹ , 冉興無 ¹ , 喻紅玲 ² , 張祥迅 ² , 龍洋 ² ,  任艷 ¹

四川大學華西醫院（成都，610041）1 內分泌代謝科，2 內分泌及代謝病實驗室;

關鍵詞：

2型糖尿病代謝異常糖耐量正常一級親屬

視頻：

導出 下載 收藏 掃碼 引用

摘要 全文 圖表 視頻 參考文獻 施引文獻 補充材料

【摘要】　目的　調查成都地區2型糖尿病患者糖耐量正常一級親屬的代謝狀態及與胰島素抵抗、胰島β細胞功能的相關性。　方法　 2007年7-9月共納入糖耐量正常的一級親屬312例（NGT-FDR組），無家族史的正常對照1 348例（NGT-C組）。測量兩組血壓、體重、腰圍；檢測口服葡萄糖耐量試驗（OGTT）中0、0.5、2 h血糖、胰島素水平；測定空腹血脂；計算體重指數、HOMA-胰島素抵抗指數（HOMA-IR）、胰島β細胞功能指數（HOMA-β），β細胞早相分泌功能指數（△I30/△G30），并比較兩組間上述指標的差異和代謝綜合征（MS）及其各組分的發病情況。　結果　 ①NGT-FDR組MS發生率高于NGT-C組，發生MS的風險是后者的1.737倍。NGT-FDR組高甘油三酯血癥（hypertriglyceridemia，HTG）、空腹血糖偏高（5.6~6.0 mmol/L）的發生率高于NGT-C組，合并4種及以上代謝異常的幾率亦高于NGT-C組（P lt;0.05）；②年齡 lt;40歲的NGT-FDR中心性肥胖、HTG、空腹血糖偏高和MS均高于同年齡對照；男性NGT-FDR空腹血糖偏高和MS發病率高于男性對照（P lt;0.05）；③腰圍、收縮壓（SBP）、空腹血糖（FBG）、甘油三酯（TG）及糖尿病家族史同HOMA-IR呈正相關。腰圍、SBP、TG及糖尿病家族史同HOMA-β呈正相關，FBG則同HOMA-β呈負相關。　結論　 2型糖尿病糖耐量正常一級親屬比無家族史的對照表現出更多的代謝異常，尤其是在年齡 lt;40歲及男性中。各種代謝異常可加重胰島素抵抗，影響胰島基礎分泌功能。故有必要對糖耐量正常的一級親屬進行各項代謝指標的監測和早期預防性干預。
【Abstract】　Objective　 To investigate the metabolic status of the normal glucose-tolerant first-degree relatives (NGT-FDR) of type-2 diabetic patients and its relationship with insulin resistance (IR) and β-cell function in Chengdu area.　Methods　 From July to September 2007, a total of 312 NGT-FDR of type-2 diabetic patients and 1 348 normal glucose tolerant controls without positive family history of diabetes (NGT-C) were enrolled in this study. Blood pressure, weight, waists, plasma glucose at hour 0, 1/2 and 2 in oral glucose tolerance test (OGTT), insulin levels and fasting blood lipids were measured. Body mass index (BMI), HOMA-IR, HOMA-β and the early insulin secreting index (△I30/△G30) were calculated. Then, we compared the above-mentioned data and the incidence of metabolic syndrome (MS) between the two groups.　Results　 ①The incidence of MS, hypertriglyceridemia (HTG), higher fasting blood glucose (FBG) (5.6-6.0 mmol/L) in the NGT-FDR group were all significantly higher than those in the NGT-C group. The risk of developing MS in the NGT-FDR group was 1.737 times as high as that in the NGT-C group. Furthermore, the incidence of 4 or more than 4 co-existent metabolic disorders in the NGT-FDR group was also significantly higher than that in the NGT-C group (P lt;0.05); ②For subjects less than 40 years old, the incidence of central obesity, HTG, higher FBG and MS in the NGT-FDR group were all higher than those in the NGT-C group. In male subjects, the rates of higher FBG and MS were all significantly higher in the NGT-FDR group than those in the NGT-C group. (P lt;0.05); ③Waists, FBG, systolic blood pressure (SBP), triglycerides (TG) and diabetic family history were positively correlated with HOMA-IR. Waists, SBP, TG and diabetic family history were positively correlated with HOMA-β.　Conclusion　 NGT-FDR present significantly increased metabolic disorders than NGT controls, especially in the less than 40-year-old and the male subjects. The metabolic disorders can aggravate insulin resistance and influence islet β-cell secretion function, so it is necessary to monitor the metabolic status of the NGT-FDR of type-2 diabetic patients and provide early preventive interventions.

引用本文： 劉宋芳,龔媛,劉圓圓,宋潔,田浩明,陳濤,冉興無,喻紅玲,張祥迅,龍洋,任艷. 成都地區2型糖尿病患者糖耐量正常一級親屬代謝紊亂的臨床研究. 華西醫學, 2011, 26(2): 177-180. doi: 復制

1.	Humphriss DB, stewart MW, Berrish TS, et al. Mutiple metabolic abnormalities in normal glucose tolerant relatives of NIDDM families[J]. Diabetologia, 1997, 40(10): 1185-1190.
2.	Anon. A worldwide consensus definition for the metabolic syndrome[J]. Rev Panam salud publica, 2005, 18(6): 451-454.
3.	da Silva RC, Miranda WL, Chacra AR, et al. Metabolic syndrome and insulin resistance in normal glucose tolerant brazilian adolescents with family history of type 2 diabetes[J]. Diabetes Care, 2005, 28(3): 716-718.
4.	陳明衛, 楊明功, 王長江, 等. 2型糖尿病患者的NGT一級親屬代謝綜合征組分與HbA1C有關[J]. 中華內分泌代謝雜志, 2005, 21(6): 540-541.
5.	Martha LC, Marc JW, Terry TK, et al. The metabolic syndrome in overweight hispanic youth and the role of insulin sensitivity[J]. J Clin Endocrinol Metab, 2004, 89(1): 108-113.
6.	Kwame O, Scott R, Trudy G, et al. Impaired insulin sensitivity, insulin, secretion, and glucose effectiveness predict future development of impaired glucose tolerance and type 2 diabetes in prediabetic African Americans[J]. Diabetes Care, 2004, 27(6): 1439-1446.
7.	盧艷慧, 陸菊明, 王淑玉, 等. 糖尿病前期人群的胰島β細胞功能和胰島素抵抗的探討[J]. 中國糖尿病雜志, 2008, 16(9): 518-520.
8.	Weyer C, Bogardus C, Mott DM, et al. The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus[J]. J Clin Invest, 1999, 104(6): 787-794.
9.	Larsson H, Ahren B. Glucose intolerance is predicted by low insulin secretion and high glucagon secretion: outcome of a prospective study in postmenopausal Caucasian women[J]. Diabetologia, 2000, 43(2): 194-202.
10.	Miriam C, Josep V, Rebeccal H, et al. Progressive loss of β-cell function leads to worsening glucose tolerance in first-degree relatives of subjects with type 2 diabetes[J]. Diabetes Care, 2007, 30(3): 677-682.
11.	高洪偉, 王海寧, 洪天配, 等. 2型糖尿病家族史是糖耐量正常的個體發生代謝綜合征的獨立危險因素[J]. 中國糖尿病雜志, 2008, 16(2): 83-86.
12.	Austin MA, Edwards KL, McNeely MJ, et al. Heritability of multivariate factors of the metabolic syndrome in nondiabetic Japanese Americans[J]. Diabetes, 2004, 53(4): 1166-1169.
13.	Lin HF, Boden-Albala B, Juo SH, et al. Heritabilities of the metabolic syndrome and its components in the Northern Manhattan Family Study[J]. Diabetologia, 2005, 48(10): 2006-2012.

1. 　Humphriss DB, stewart MW, Berrish TS, et al. Mutiple metabolic abnormalities in normal glucose tolerant relatives of NIDDM families[J]. Diabetologia, 1997, 40(10): 1185-1190.
2. 　Anon. A worldwide consensus definition for the metabolic syndrome[J]. Rev Panam salud publica, 2005, 18(6): 451-454.
3. 　da Silva RC, Miranda WL, Chacra AR, et al. Metabolic syndrome and insulin resistance in normal glucose tolerant brazilian adolescents with family history of type 2 diabetes[J]. Diabetes Care, 2005, 28(3): 716-718.
4. 　陳明衛, 楊明功, 王長江, 等. 2型糖尿病患者的NGT一級親屬代謝綜合征組分與HbA1C有關[J]. 中華內分泌代謝雜志, 2005, 21(6): 540-541.
5. 　Martha LC, Marc JW, Terry TK, et al. The metabolic syndrome in overweight hispanic youth and the role of insulin sensitivity[J]. J Clin Endocrinol Metab, 2004, 89(1): 108-113.
6. 　Kwame O, Scott R, Trudy G, et al. Impaired insulin sensitivity, insulin, secretion, and glucose effectiveness predict future development of impaired glucose tolerance and type 2 diabetes in prediabetic African Americans[J]. Diabetes Care, 2004, 27(6): 1439-1446.
7. 　盧艷慧, 陸菊明, 王淑玉, 等. 糖尿病前期人群的胰島β細胞功能和胰島素抵抗的探討[J]. 中國糖尿病雜志, 2008, 16(9): 518-520.
8. 　Weyer C, Bogardus C, Mott DM, et al. The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus[J]. J Clin Invest, 1999, 104(6): 787-794.
9. 　Larsson H, Ahren B. Glucose intolerance is predicted by low insulin secretion and high glucagon secretion: outcome of a prospective study in postmenopausal Caucasian women[J]. Diabetologia, 2000, 43(2): 194-202.
10. 　Miriam C, Josep V, Rebeccal H, et al. Progressive loss of β-cell function leads to worsening glucose tolerance in first-degree relatives of subjects with type 2 diabetes[J]. Diabetes Care, 2007, 30(3): 677-682.
11. 　高洪偉, 王海寧, 洪天配, 等. 2型糖尿病家族史是糖耐量正常的個體發生代謝綜合征的獨立危險因素[J]. 中國糖尿病雜志, 2008, 16(2): 83-86.
12. 　Austin MA, Edwards KL, McNeely MJ, et al. Heritability of multivariate factors of the metabolic syndrome in nondiabetic Japanese Americans[J]. Diabetes, 2004, 53(4): 1166-1169.
13. 　Lin HF, Boden-Albala B, Juo SH, et al. Heritabilities of the metabolic syndrome and its components in the Northern Manhattan Family Study[J]. Diabetologia, 2005, 48(10): 2006-2012.

《華西醫學》

成都地區2型糖尿病患者糖耐量正常一級親屬代謝紊亂的臨床研究

摘要 全文 圖表 視頻 參考文獻 施引文獻 補充材料

Format

Content

《華西醫學》

成都地區2型糖尿病患者糖耐量正常一級親屬代謝紊亂的臨床研究

摘要 全文 圖表 視頻 參考文獻 施引文獻 補充材料

Format

Content

摘要全文圖表視頻參考文獻施引文獻補充材料