住院2型糖尿病患者血钾稳态与糖代谢的关系

Association of serum potassium homeostasis with glucose metabolism in hospitalized patients withtype 2 diabetes

目的探讨住院2型糖尿病患者血钾稳态与糖代谢的关系。方法连续收集2016年1至12月在我院内分泌科住院的362例2型糖尿病患者的空腹及标准餐后血糖、血钾、胰岛素、C肽及其糖化血红蛋白（HbA1c）、血压等代谢指标。根据患者空腹血钾分为≥4.0 mmol/L组（n=183）和〈4.0 mmol/L组（n=179），根据餐后血钾是否升高分为餐后血钾升高组（Δ血钾〉0组，n=205）和餐后血钾未升高组（Δ血钾≤0组，n=157），比较各组间糖代谢相关指标的差异，采用t检验、秩和检验和偏相关分析进行统计学分析。结果血钾≥4.0 mmol/L较〈4.0 mmol/L组空腹胰岛素更高[14.1（7.8，27.1）比10.8（5.8，23.3）mU/L，Z=-2.317，P=0.020]，空腹C肽更高[473（280，681）比330.6（229，535）pmol/L，Z=-3.575，P〈0.001]，餐后2 h胰岛素更高[44.9（24.2，75.5）比31.7（18.5，54.1）mU/L，Z=-3.390，P=0.001]，餐后2 h C肽更高[1 088（538，1 646）比846（443，1 316）pmol/L，Z=-2.698，P=0.007]，餐后血钾升高更少[（-0.02±0.30）比（0.21±0.25）mmol/L，t=-7.778，P〈0.001]。但两组间空腹、餐后2 h血糖、HbA1c、病程和预估肾小球滤过率差异均无统计学意义（均P〉0.05）。Δ血钾〉0组较Δ血钾≤0组餐后2 h胰岛素更低[32.2（20.2，54.3）比45.7（4.7，74.1）mU/L，Z=-3.143，P=0.002]，餐后2 h血糖更高[（11.9±4.0）比（10.8±3.9）mmol/L，t=2.487，P=0.013]。结论在2型糖尿病住院患者中空腹血钾在正常范围内高值者较低值者有更好的胰岛素分泌功能，而空腹血钾正常低值者空腹及餐后2 h胰岛素水平较低，餐后2 h血糖更易升高。

ObjectiveTo investigate the association between serum potassium homeostasis and glucose metabolism in hospitalized patients with type 2 diabetes.MethodsA total of 362 patients with type 2 diabetes who were admitted to our hospital from January 2016 to December 2016 were enrolled. Glycated hemoglobin A1c （HbA1c）, blood pressure and fasting, 2 hour postprandial glucose after a standard meal, potassium, insulin and C-peptide were measured. The participants were grouped into 2 groups： ≥4.0 mmol/L （n=183） and 〈4.0 mmol/L （n=179） group based on fasting potassium level and another 2 groups [Δ potassium〉0 （n=205） and Δ potassium≤0 （n=157） group] based on the change of serum potassium concentration after a standard diet. The data were compared between the groups with t test or rank sum test and associations between potassium and glucose metabolism characteristics were examined with partial relative analysis.ResultsCompared with the group with fasting serum potassium〈4.0 mmol/L, the other group had higher fasting serum insulin, C-peptide and 2 h postprandial serum insulin, C-peptide and lower 2 h postprandial potassium increase [14.1 （7.8, 27.1） vs 10.8 （5.8, 23.3） mU/L, Z=-2.317, P=0.020; 473 （280, 681） vs 331 （229, 535） pmol/L, Z=-3.575, P〈0.001; 44.9 （24.2, 75.5） vs 31.7 （18.5, 54.1） mU/L, Z=-3.390, P=0.001; 1 088 （538, 1 646） vs 846 （443, 1 316） pmol/L, Z=-2.698, P=0.007; （-0.02±0.30） vs （0.21±0.25） mmol/L, t=-7.778, P〈0.001]. No difference was found in fasting and postprandial glucose, HbA1c, disease duration and estimated glomerular filtration rate （all P〉0.05）. Compared with Δ potassium≤0 group, the group with Δ potassium〉0 has lower 2 h postprandial serum insulin concentration [32.2 （20.2, 54.3） vs 45.7 （24.7, 74.1） mU/L, Z=-3.143, P=0.002] and higher 2 h postprandial glucose level [（11.9±4.0） vs （10.8±3.9） mmol/L, t=2.487, P=0.013].ConclusionIn-ward type 2 diabetic patients with lower normal fasting serum potassium level （3.5-4.0 mmol/L） have a worse fasting and postprandial insulin secretion function, higher postprandial glucose excursion.