• 四川大學(xué)華西醫(yī)院（成都，610041）1 西藏成辦分院內(nèi)分泌代謝科，2 內(nèi)分泌代謝科，3 內(nèi)分泌代謝實(shí)驗(yàn)室;

【摘要】　目的　 了解不同糖代謝狀態(tài)的人群空腹及口服葡萄糖耐量實(shí)驗(yàn)（oral glucose tolerance test，OGTT）餐后胰高血糖素樣態(tài)-1（GLP-1）和葡萄糖依賴的促胰島素多態(tài)（GIP）水平。　方法　 將受試者根據(jù)OGTT結(jié)果分為3組:正常糖耐量組（NGT，n=61例），糖耐量受損組（IGT，n=53）和2型糖尿病組（T2DM， n=66）。采空腹及糖餐后2 h靜脈血檢測(cè)GLP-1和GIP水平。　結(jié)果　 T2DM組空腹GLP-1水平低于NGT和IGT組（P lt;0.05）。NGT和IGT的空腹GLP-1水平差異無(wú)統(tǒng)計(jì)學(xué)意義（P gt;0.05）。餐后GLP-1水平三組差異無(wú)統(tǒng)計(jì)學(xué)意義（P gt;0.05）?？崭辜安秃驡IP水平在NGT、IGT和T2DM均呈逐漸增加的趨勢(shì)，而且同OGTT-0 h和OGTT-2 h血糖水平呈正相關(guān)（r=0.384，0.426；P lt;0.05）。　結(jié)論　 不同的GLP-1和GIP水平也許是IGT和T2DM胰島素分泌能力不同的原因之一。
【Abstract】　Objective　 To investigate the fasting, and after oral glucose tolerance test (OGTT), the postprandial levels of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) in Chinese people with different degrees of glucose tolerance.　Methods　 Based on the results of OGTT, 180 subjects were divided into three groups: normal glucose tolerance group (NGT group, n=61), impaired glucose tolerance group (IGT group, n=53) and type-2 diabetes mellitus group (T2DM group, n=66). Fasting venous blood and the venous blood 2 hours after OGTT was sampled to detect GLP-1 and GIP levels.　Results　 The fasting GLP-1 level in the T2DM group was significantly lower than that in the NGT and IGT groups (P lt;0.05). There was no significant difference in fasting GLP-1 level between NGT and IGT groups (P gt;0.05). There was no significant difference in GLP-1 level 2 hours after OGTT among all the three groups (P gt;0.05). GIP level gradually increased in the order of NGT, IGT and T2DM both before and after glucose load, and it was positively correlated with glucose levels just after OGTT and 2 hours after OGTT (r=0.384,0.426;P lt;0.05).　Conclusion　 Different GLP-1 and GIP levels may be one of the reasons for different insulin secretion ability between IGT and T2DM

引用本文： 鄔云紅,田浩明,張祥訊,陳香. 不同糖耐量水平人群血漿胰高血糖素樣肽-1和葡萄糖依賴的促胰島素樣多肽水平比較. 華西醫(yī)學(xué), 2011, 26(7): 1018-1021. doi: 復(fù)制

版權(quán)信息： ?四川大學(xué)華西醫(yī)院華西期刊社《華西醫(yī)學(xué)》版權(quán)所有，未經(jīng)授權(quán)不得轉(zhuǎn)載、改編

1. 　Freeman JS. Role of the incretin pathway in the pathogenesis of type 2 diabetes mellitus[J]. Cleve Clin J Med, 2009,76(Suppl 5): 12-19.
2. 　World Health Orgnization. Definition, diagnosis, and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus[S]. WHO/NCD/NCS/99.2ed. Geneva, World Health Orgnization, 1999.
3. 　Henkel E, Menschikowski M, Koehler C, et al. Impact of glucagon response on postprandial hyperglycemia in men with impaired glucose tolerance and type 2 diabetes mellitus[J]. Metabolism, 2005, 54(9): 1168-1173.
4. 　Vollmer K, Holst JJ, Baller B, et al. Predictors of incretin concentrations in subjects with normal, impaired, and diabetic glucose tolerance[J]. Diabetes, 2008, 57(3): 678-687.
5. 　Nauck MA, Heimesaat MM, Orskov C, et al. Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus[J]. J Clin Invest, 1993, 91(1): 301-307.
6. 　Vilsboll T, Krarup T, Deacon CF, et al. Reduced postprandial concentrations of intact biologically active glucagon-like peptide 1 in type 2 diabetic patients[J]. Diabetes, 1993, 50(3): 609-613.
7. 　Muscelli E, Mari A, Casolaro A, et al. Separate impact of obesity and glucose tolerance on the incretin effect in normal subjects and type 2 diabetic patients[J]. Diabetes, 2008, 57(5): 1340-1348.
8. 　Ryskjaer J, Deacon CF, Carr RD, et al. Plasma dipeptidyl peptidase-IV activity in patients with type-2 diabetes mellitus correlates positively with HbAlc levels, but is not acutely affected by food intake[J]. Eur J Endocrinol, 2006, 155(3): 485-493.
9. 　Nauck MA, El-Ouaghlidi A, Gabrys B, et al. Secretion of incretin hormones (GIP and GLP-1) and incretin effect after oral glucose in first-degree relatives of patients with type 2 diabetes[J]. Regul Pept, 2004, 122(3): 209-217.
10. 　Vaag AA, Holst JJ, V?lund A, et al. Gut incretin hormones in identical twins discordant for non-insulin-dependent diabetes mellitus (NIDDM)-evidence for decreased glucagon-like peptide 1 secretion during oral glucose ingestion in NIDDM twins[J]. Eur. J. Endocrinol, 1996, 135(4): 425-432.
11. 　Kozawa J, Okita K, Imagawa A, et al. Similar incretin secretion in obese and non-obese Japanese subjects with type 2 diabetes[J]. Biochem Biophys Res Commun, 2010, 393(3): 410-413.
12. 　Irwin N, Flatt PR. Therapeutic potential for GIP receptor agonists and antagonists[J]. Best Pract Res Clin Endocrinol Metab, 2009, 23(4): 499-512.
13. 　Meier JJ, Gallwitz B, Siepmann N, et al. Gastric inhibitory polypeptide (GIP) dose-dependently stimulates glucagon secretion in healthy human subjects at euglycaemia[J]. Diabetologia, 2003, 46(6): 798-801.
  1. 1. 　Freeman JS. Role of the incretin pathway in the pathogenesis of type 2 diabetes mellitus[J]. Cleve Clin J Med, 2009,76(Suppl 5): 12-19.
  2. 2. 　World Health Orgnization. Definition, diagnosis, and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus[S]. WHO/NCD/NCS/99.2ed. Geneva, World Health Orgnization, 1999.
  3. 3. 　Henkel E, Menschikowski M, Koehler C, et al. Impact of glucagon response on postprandial hyperglycemia in men with impaired glucose tolerance and type 2 diabetes mellitus[J]. Metabolism, 2005, 54(9): 1168-1173.
  4. 4. 　Vollmer K, Holst JJ, Baller B, et al. Predictors of incretin concentrations in subjects with normal, impaired, and diabetic glucose tolerance[J]. Diabetes, 2008, 57(3): 678-687.
  5. 5. 　Nauck MA, Heimesaat MM, Orskov C, et al. Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus[J]. J Clin Invest, 1993, 91(1): 301-307.
  6. 6. 　Vilsboll T, Krarup T, Deacon CF, et al. Reduced postprandial concentrations of intact biologically active glucagon-like peptide 1 in type 2 diabetic patients[J]. Diabetes, 1993, 50(3): 609-613.
  7. 7. 　Muscelli E, Mari A, Casolaro A, et al. Separate impact of obesity and glucose tolerance on the incretin effect in normal subjects and type 2 diabetic patients[J]. Diabetes, 2008, 57(5): 1340-1348.
  8. 8. 　Ryskjaer J, Deacon CF, Carr RD, et al. Plasma dipeptidyl peptidase-IV activity in patients with type-2 diabetes mellitus correlates positively with HbAlc levels, but is not acutely affected by food intake[J]. Eur J Endocrinol, 2006, 155(3): 485-493.
  9. 9. 　Nauck MA, El-Ouaghlidi A, Gabrys B, et al. Secretion of incretin hormones (GIP and GLP-1) and incretin effect after oral glucose in first-degree relatives of patients with type 2 diabetes[J]. Regul Pept, 2004, 122(3): 209-217.
  10. 10. 　Vaag AA, Holst JJ, V?lund A, et al. Gut incretin hormones in identical twins discordant for non-insulin-dependent diabetes mellitus (NIDDM)-evidence for decreased glucagon-like peptide 1 secretion during oral glucose ingestion in NIDDM twins[J]. Eur. J. Endocrinol, 1996, 135(4): 425-432.
  11. 11. 　Kozawa J, Okita K, Imagawa A, et al. Similar incretin secretion in obese and non-obese Japanese subjects with type 2 diabetes[J]. Biochem Biophys Res Commun, 2010, 393(3): 410-413.
  12. 12. 　Irwin N, Flatt PR. Therapeutic potential for GIP receptor agonists and antagonists[J]. Best Pract Res Clin Endocrinol Metab, 2009, 23(4): 499-512.
  13. 13. 　Meier JJ, Gallwitz B, Siepmann N, et al. Gastric inhibitory polypeptide (GIP) dose-dependently stimulates glucagon secretion in healthy human subjects at euglycaemia[J]. Diabetologia, 2003, 46(6): 798-801.