上海宝山地区糖尿病与非糖尿病人群中血清醛固酮水平差异及其与糖代谢相关性研究
|
摘要
目的:探讨上海宝山地区正常人群以及2型糖尿病患者血清醛固酮水平差异,进一步评价该地区2型糖尿病患者血清醛固酮水平与糖代谢、胰岛素抵抗等的相关性。方法:收集2018年1月至2018年12月于我院住院的2型糖尿病患者(2-DM组,n=684),并收集同时期的健康体检者(NC组,n=180),比较2组间体质量指数、血压、血脂、空腹血糖(fasting plasma glucose,FPG)、糖化血红蛋白(glycated hemoglobin,HbA1c)、稳态模型评估的胰岛素抵抗指数(homeostasis model assessment of insulin resistance,HOMA-IR)及血清醛固酮水平的差异。根据体质量指数、血压、血脂等将684例2型糖尿病患者分为不合并代谢综合征组(非MS组,n=450)与合并代谢综合征组(MS组,n=234),进一步评价2型糖尿病患者中醛固酮水平与FPG、HbA1c、HOMA-IR等的相关性。结果:与NC组[(98.41±33.02) ng/L]相比,2-DM组[(116.19±109.65) ng/L]醛固酮水平明显增高,差异有统计学意义(P<0.05);进一步根据醛固酮水平将非MS组及MS组患者分为高(T3)、中(T2)、低(T1)醛固酮亚组,非MS组中不同亚组间HbA1c、FPG、HOMA-IR差异无统计学意义(P值分别为0.56、0.61和0.64),而在MS组中,与低醛固酮水平组(T1)、中醛固酮水平组(T2)相比,高醛固酮水平组(T3)HbA1c明显升高(8.81%±1.86%,8.79%±1.86%比9.71%±2.24%,P<0.05)。未见醛固酮水平与2-DM组患者HbA1c、FPG、HOMA-IR等糖代谢及胰岛素抵抗指标间存在显著相关性(r分别为0.023、0.013和0.037,P分别为0.58、0.74和0.33)。结论:与健康人群相比,2型糖尿病患者醛固酮水平明显升高,且在2型糖尿病合并代谢综合征患者中,不同醛固酮水平HbA1c存在差异,但未发现2型糖尿病患者醛固酮水平与糖代谢指标间的相关性。
Objective To investigate the serum aldosterone levels between healthy population and type 2 diabetes patients in Baoshan area of Shanghai and explore the correlation between serum aldosterone levels and fasting blood glucose(FPG), glycosylated hemoglobin(HbA1c), homeostasis model assessment of insulin resistance(HOMA-IR) in patients with type 2 diabetes. Methods A total of 684 patients with type 2 diabetes mellitus admitted to our hospital from January 2018 through December 2018 were enrolled and divided into non-metabolic syndrome group(2-DM group, n=450) and metabolic syndrome group(MS group, n=234). A total of 180 healthy subjects were recruited at the same time to constitute normal control group. The indicators of body mass index(BMI), blood pressure, FPG, HbA1c, lipids, HOMA-IR and plasma aldosterone concerntration were determined and the correlation among the indexes were statistically analyzed. Results Compared with normal controls(98.41 ±33.02) ng/L, the aldosterone level was significantly increased in 2-DM group(117.87±118.86) ng/L and MS group(112.96±97.25) ng/L(P<0.05). Patients of MS group were subdivided according to the aldosterone level as group T1, T2 and T3(aldosterone from low to high). The FPG [(10.07±3.37) mmol/L vs(8.92±2.48)mmol/L, P<0.05)] and HbA1c(8.81%±1.86% vs 9.71%±2.24%, P<0.05) was significantly higher in T3 group than in T1 group. No significant correlation between aldosterone and HbA1c、FPG、HOMA-IR was found in patients with type 2 diabetes(r: 0.023, 0.013, and 0.037, and P values: 0.58, 0.74, and 0.33). Conclusions Compared with healthy poplutation,the aldosterone level increased significantly in patients with type 2 diabetes mellitus, however, there was no correlation between parameters of glucose metabolism and aldosterone level. Neither did the HbA1 ccorrelate with aldosterone level in patients complicated with metabolism syndrom.
Objective To investigate the serum aldosterone levels between healthy population and type 2 diabetes patients in Baoshan area of Shanghai and explore the correlation between serum aldosterone levels and fasting blood glucose(FPG), glycosylated hemoglobin(HbA1c), homeostasis model assessment of insulin resistance(HOMA-IR) in patients with type 2 diabetes. Methods A total of 684 patients with type 2 diabetes mellitus admitted to our hospital from January 2018 through December 2018 were enrolled and divided into non-metabolic syndrome group(2-DM group, n=450) and metabolic syndrome group(MS group, n=234). A total of 180 healthy subjects were recruited at the same time to constitute normal control group. The indicators of body mass index(BMI), blood pressure, FPG, HbA1c, lipids, HOMA-IR and plasma aldosterone concerntration were determined and the correlation among the indexes were statistically analyzed. Results Compared with normal controls(98.41 ±33.02) ng/L, the aldosterone level was significantly increased in 2-DM group(117.87±118.86) ng/L and MS group(112.96±97.25) ng/L(P<0.05). Patients of MS group were subdivided according to the aldosterone level as group T1, T2 and T3(aldosterone from low to high). The FPG [(10.07±3.37) mmol/L vs(8.92±2.48)mmol/L, P<0.05)] and HbA1c(8.81%±1.86% vs 9.71%±2.24%, P<0.05) was significantly higher in T3 group than in T1 group. No significant correlation between aldosterone and HbA1c、FPG、HOMA-IR was found in patients with type 2 diabetes(r: 0.023, 0.013, and 0.037, and P values: 0.58, 0.74, and 0.33). Conclusions Compared with healthy poplutation,the aldosterone level increased significantly in patients with type 2 diabetes mellitus, however, there was no correlation between parameters of glucose metabolism and aldosterone level. Neither did the HbA1 ccorrelate with aldosterone level in patients complicated with metabolism syndrom.
引文
[1]Joseph JJ,Echouffo Tcheugui JB,Effoe VS,et al.Reninangiotensin-aldosterone system,glucose metabolism and incident type 2 diabetes mellitus:MESA[J].J Am Heart Assoc,2018,7(17):e9890.
[2]Bothou C,Beuschlein F,Spyroglou A.Links between aldosterone excess and metabolic complications:a comprehensive review[J].Diabetes Metab,2019.[Epub ahead of print].
[3]中华医学会糖尿病学分会.中国2型糖尿病防治指南(2017年版)[J].中华糖尿病杂志,2018,10(1):4-67.
[4]中华医学会糖尿病学分会代谢综合征研究协作组.中华医学会糖尿病学分会关于代谢综合征的建议[J].中华糖尿病杂志,2004,12(5):156-161.
[5]安芳,崔明亮,程晨.代谢综合征患者血浆醛固酮水平变化及其与代谢综合征组分相关性研究[J].中国糖尿病杂志,2014,22(4):317-319.
[6]吴沐,黄桂生,苏广瑞,等.不同糖代谢状态下患者血浆醛固酮水平的差异[J].广东医学,2017,38(8):1214-1215.
[7]Underwood PC,Adler GK.The renin angiotensin aldosterone system and insulin resistance in humans[J].Curr Hypertens Rep,2013,15(1):59-70.
[8]Hofmann A,Brunssen C,Peitzsch M,et al.Aldosterone synthase inhibition improves glucose tolerance in zucker diabetic fatty(ZDF)rats[J].Endocrinology,2016,157(10):3844-3855.
[9]Luther JM.Effects of aldosterone on insulin sensitivity and secretion[J].Steroids,2014,91:54-60.
[10]Guo C,Ricchiuti V,Lian BQ,et al.Mineralocorticoid receptor blockade reverses obesity-related changes in expression of adiponectin,peroxisome proliferator-activated receptor-gamma,and proinflammatory adipokines[J].Circulation,2008,117(17):2253-2261.
[11]Kumagai E,Adachi H,Jacobs DR Jr,et al.Plasma aldosterone levels and development of insulin resistance:prospective study in a general population[J].Hypertension,2011,58(6):1043-1048.
[12]Joseph JJ,Echouffo-Tcheugui JB,Kalyani RR,et al.Aldosterone,renin,and diabetes mellitus in African Americans:The Jackson Heart Study[J].J Clin Endocrinol Metab,2016,101(4):1770-1778.
[13]McMurray JJ,Holman RR,Haffner SM,et al.Effect of valsartan on the incidence of diabetes and cardiovascular events[J].N Engl J Med,2010,362(16):1477-1490.
[2]Bothou C,Beuschlein F,Spyroglou A.Links between aldosterone excess and metabolic complications:a comprehensive review[J].Diabetes Metab,2019.[Epub ahead of print].
[3]中华医学会糖尿病学分会.中国2型糖尿病防治指南(2017年版)[J].中华糖尿病杂志,2018,10(1):4-67.
[4]中华医学会糖尿病学分会代谢综合征研究协作组.中华医学会糖尿病学分会关于代谢综合征的建议[J].中华糖尿病杂志,2004,12(5):156-161.
[5]安芳,崔明亮,程晨.代谢综合征患者血浆醛固酮水平变化及其与代谢综合征组分相关性研究[J].中国糖尿病杂志,2014,22(4):317-319.
[6]吴沐,黄桂生,苏广瑞,等.不同糖代谢状态下患者血浆醛固酮水平的差异[J].广东医学,2017,38(8):1214-1215.
[7]Underwood PC,Adler GK.The renin angiotensin aldosterone system and insulin resistance in humans[J].Curr Hypertens Rep,2013,15(1):59-70.
[8]Hofmann A,Brunssen C,Peitzsch M,et al.Aldosterone synthase inhibition improves glucose tolerance in zucker diabetic fatty(ZDF)rats[J].Endocrinology,2016,157(10):3844-3855.
[9]Luther JM.Effects of aldosterone on insulin sensitivity and secretion[J].Steroids,2014,91:54-60.
[10]Guo C,Ricchiuti V,Lian BQ,et al.Mineralocorticoid receptor blockade reverses obesity-related changes in expression of adiponectin,peroxisome proliferator-activated receptor-gamma,and proinflammatory adipokines[J].Circulation,2008,117(17):2253-2261.
[11]Kumagai E,Adachi H,Jacobs DR Jr,et al.Plasma aldosterone levels and development of insulin resistance:prospective study in a general population[J].Hypertension,2011,58(6):1043-1048.
[12]Joseph JJ,Echouffo-Tcheugui JB,Kalyani RR,et al.Aldosterone,renin,and diabetes mellitus in African Americans:The Jackson Heart Study[J].J Clin Endocrinol Metab,2016,101(4):1770-1778.
[13]McMurray JJ,Holman RR,Haffner SM,et al.Effect of valsartan on the incidence of diabetes and cardiovascular events[J].N Engl J Med,2010,362(16):1477-1490.