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首页> 外文期刊>Endocrine journal >Fasting serum total bile acid levels are associated with insulin sensitivity, islet β -cell function and glucagon levels in response to glucose challenge in patients with type 2 diabetes
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Fasting serum total bile acid levels are associated with insulin sensitivity, islet β -cell function and glucagon levels in response to glucose challenge in patients with type 2 diabetes

机译：禁食血清总胆汁酸水平与胰岛素敏感性，胰岛素β-细胞功能和胰高血糖素水平相关，响应2型糖尿病患者的葡萄糖攻击

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Type 2 diabetes (T2D) is characterized by islet β -cell dysfunction and impaired suppression of glucagon secretion of α -cells in response to oral hyperglycaemia. Bile acid (BA) metabolism plays a dominant role in maintaining glucose homeostasis. So we evaluated the association of fasting serum total bile acids (S-TBAs) with insulin sensitivity, islet β -cell function and glucagon levels in T2D. Total 2,952 T2D patients with fasting S-TBAs in the normal range were recruited and received oral glucose tolerance tests for determination of fasting and postchallenge glucose, C-peptide and glucagon. Fasting and systemic insulin sensitivity were assessed by homeostasis model assessment (HOMA) and Matsuda index using C-peptide, i.e. , IS HOMA-cp and ISI M -cp , respectively. Islet β -cell function was assessed by the insulin-secretion-sensitivity-index-2 using C-peptide (ISSI2 cp ). The area under the glucagon curve (AUC gla ) was used to assess postchallenge glucagon. The results showed IS HOMA-cp , ISI M -cp and ISSI2 cp decreased, while AUC gl a notably increased, across ascending quartiles of S-TBAs but not fasting glucagon. Moreover, S-TBAs were inversely correlated with IS HOMA-cp , ISI M -cp and ISSI2 cp ( r = –0.21, –0.15 and –0.25, respectively, p 0.001) and positively correlated with AUC gl a ( r = 0.32, p 0.001) but not with fasting glucagon ( r = 0.033, p = 0.070). Furthermore, after adjusting for other clinical covariates by multiple linear regression analyses, the S-TBAs were independently associated with IS HOMA-cp ( β = –0.04, t = –2.82, p = 0.005), ISI M -cp ( β = –0.11, t = –7.05, p 0.001), ISSI2 cp ( β = –0.15, t = –10.26, p 0.001) and AUC gla ( β = 0.29, t = 19.08, p 0.001). Increased fasting S-TBAs are associated with blunted fasting and systemic insulin sensitivity, impaired islet β -cell function and increased glucagon levels in response to glucose challenge in T2D.
机译：2型糖尿病（T2D）的特征在于胰岛β - 细胞功能障碍和抑制α-Cells的胰高血糖素分泌的抑制，响应口腔高血糖血症。胆汁酸（BA）代谢在维持葡萄糖稳态中起着显着作用。因此，我们评估了T2D中的胰岛素敏感性，胰岛素敏感性，胰岛β-Cel功能和胰高血糖素水平的禁食血清总胆汁酸（S-TBA）的关联。招募了2,952例T2D T2D患者在正常范围内的禁食S-TBA患者，并接受了口服葡萄糖耐量试验，用于测定禁食和后打良葡萄糖，C-肽和胰高血糖素。通过C-肽的稳态模型评估（HOMA）和Matsuda指数评估禁食和全身胰岛素敏感性，即分别是HOMA-CP和ISI M -CP。使用C-肽（ISSI2 CP）通过胰岛素分泌敏感性-ING-2评估胰岛β-Cel功能。胰高血糖素曲线（AUCGLA）下的区域用于评估后打良血糖素。结果显示为HOMA-CP，ISI M -CP和ISSI2 CP减少，而AUCGL A显着增加，横跨S-TBA的升序但不是空腹胰高血糖素。此外，S-TBA与IS-CP，ISI M -CP和ISSI2 CP（r = -0.21，-0.15和-0.25分别，P <0.001）与AUC GL A正相关（R = 0.32，P <0.001），但不具有空腹胰高血糖素（R = 0.033，P = 0.070）。此外，通过多元线性回归分析调节其他临床协变量，S-TBA与HOMA-CP（β= -0.04，T = -2.82，P = 0.005）独立相关，ISI M -CP（β= - 0.11，t = -7.05，p <0.001），ISSI2 CP（β= -0.15，T = -10.26，P <0.001）和AUC GLA（β= 0.29，T = 19.08，P <0.001）。增加的禁食S-TBA与钝化速度和全身胰岛素敏感性相关，胰岛受损的β-细胞功能和增加的胰高血糖素水平响应于T2D中的葡萄糖攻击。

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