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原发性醛固酮增多症患者胰岛素抵抗和胰岛β细胞功能分析

Analysis of insulin resistance and pancreatic β cell function in patients with primary aldosteronism

  • 摘要:
    目的 探讨原发性醛固酮增多症(primary aldosteronism,PA)患者胰岛素敏感性和胰岛β细胞功能变化情况。
    方法 选取2014年1月至2015年12月复旦大学附属上海市第五人民医院收治的PA患者95例和原发性高血压(essential hypertension,EH)患者210例。根据有无糖尿病病史分层分析PA患者和EH患者中胰岛素抵抗和胰岛β细胞功能的情况。根据醛固酮/肾素活性(aldosterone to active renin ratio,ARR)是否大于50,将PA患者分为PA高值组(45例)及PA低值组(50例)。采用QUICK指数、HOMA指数评估胰岛素敏感性,HOMA-β、早时相胰岛功能(ΔI30/ΔG30)评估胰岛β细胞功能。
    结果 单因素分析中,无糖尿病病史人群,PA高值组HOMA-β低于EH组(P < 0.05),PA高值组及低值组ΔI30/ΔG30均低于EH组(P < 0.05);而在有糖尿病病史患者中,仅PA高值组HOMA-β低于EH组(P < 0.05)。多元线性回归显示,无糖尿病病史人群中,立位醛固酮水平对LnΔI30/ΔG30有显著负性影响(β=-0.375,P < 0.05);有糖尿病病史人群,立位醛固酮对LnHOMA-β有显著负性影响(β=-0.367,P < 0.01)。无论有无糖尿病病史,醛固酮水平对胰岛素抵抗指标无影响。
    结论 PA引起的糖代谢异常可能与醛固酮增高致胰岛功能分泌障碍有关。

     

    Abstract:
    Objective To explore the insulin sensitivity and pancreatic β cell function in patients with primary aldosteronism (PA).
    Methods 95 PA patients and 210 essential hypertension (EH) patients were admitted in Shanghai Fifth People's Hospital, Fudan University from January 2014 to December 2015. The insulin resistance and β cell function in PA and EH patients were analyzed according to the history of diabetes. According to whether the activity of aldosterone to active renin ration (ARR) was greater than 50, PA patients were divided into high PA group (45 cases) and low PA group (50 cases). QUICK index and HOMA-IR were used to evaluate the insulin sensitivity, the HOMA-β cell index and first phase insulin secretion (ΔI30/ΔG30) were used to assess the pancreatic β cell function.
    Results Univariate analysis showed that, for patients without history of diabetes, HOMA-β in the high PA group was lower than that in the EH group (P < 0.05), and ΔI30/ΔG30 in the high PA and low PA groups was lower than that in the EH group (P < 0.05). While for patients with history of diabetes, only HOMA-β in the high PA group was lower than that in the EH group (P < 0.05). The results of multiple linear regression showed that, the level of upright plasma aldosterone had a significant negative effect on LnΔI30/ΔG30 in non-diabetic patients (β=-0.375, P < 0.05). And the level of upright plasma had significant negative effect on LnHOMA-β in patients with history of diabetes (β=-0.367, P < 0.01). Aldosterone level had no significant effect on insulin resistance regardless of diabetes history.
    Conclusions The abnormality of glucose metabolism caused by primary hyperaldosteronism may be related to the dysfunction of islet function induced by elevated aldosterone.

     

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