Correction of metabolic acidosis improves insulin resistance in chronic kidney disease.

Correction of metabolic acidosis improves insulin resistance in chronic kidney disease.
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DOI:
10.1186/s12882-016-0372-x
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发表时间:
2016-10-22
期刊:
影响因子:
2.3
通讯作者:
UBI study investigators
UBI study investigators
中科院分区:
医学4区
文献类型:
--
作者:
Bellasi A;Di Micco L;Santoro D;Marzocco S;De Simone E;Cozzolino M;Di Lullo L;Guastaferro P;Di Iorio B;UBI study investigators

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通过营养治疗或碳酸氢盐给药纠正代谢性酸中毒(MA)广泛用于慢性肾脏病(CKD)患者。然而,目前尚不清楚这些干预措施是否能降低糖尿病肾病患者的胰岛素抵抗(IR)。我们试图评估MA校正对2型糖尿病(DM 2)CKD患者内源性胰岛素作用的影响。共145例接受口服降糖药治疗的2型糖尿病CKD受试者(83例男性和62例女性)纳入研究,并随访1年。所有患者均以1:1的比例随机分配至开放标签(A)口服碳酸氢盐以达到24-28 mmol/L的血清碳酸氢盐水平(治疗组)或(B)无治疗(对照组)。稳态模型评估(HOMA)指数用于评估研究开始和结束时的IR。使用参数和非参数检验以及线性回归。基线时,两组之间的人口统计学和临床特征无差异。治疗组中碳酸氢盐的平均剂量为0.7 ± 0.2 mmol/kg。经治疗的患者表现出更好的代谢控制,这通过较低的胰岛素水平(13.4 ± 5.2 vs 19.9 ± 6.3;治疗组和对照组受试者分别为; p < 0.001)、Homa-IR(5.9[5.0-7.0] vs 6.3[5.3-8.2]; p = 0.01)和口服降糖药物的需求得到证实。血清碳酸氢盐与HOMA-IR的关系为非线性,血清碳酸氢盐水平在24 - 28 mmol/l之间时HOMA-IR降低幅度最大。调整混杂因素后,提示血清碳酸氢盐而非治疗对HOMA-IR的影响。血清碳酸氢盐与IR相关,最大的HOMA-IR降低见于血清碳酸氢盐在24 - 28 mmol/l之间。碳酸氢盐治疗影响IR,而血清碳酸氢盐的变化解释了治疗对HOMA指数的影响。需要进一步努力在糖尿病和非糖尿病CKD患者中验证这些结果。该试验在www.clinicaltrial.gov上注册(慢性肾功能不全(UBI)研究中使用Bicycline-NCT 01640119)
Correction of metabolic acidosis (MA) with nutritional therapy or bicarbonate administration is widely used in chronic kidney disease (CKD) patients. However, it is unknown whether these interventions reduce insulin resistance (IR) in diabetic patients with CKD. We sought to evaluate the effect of MA correction on endogenous insulin action in diabetic type 2 (DM2) CKD patients. A total of 145 CKD subjects (83 men e 62 women) with DM2 treated with oral antidiabetic drugs were included in the study and followed up to 1 year. All patients were randomly assigned 1:1 to either open-label (A) oral bicarbonate to achieve serum bicarbonate levels of 24–28 mmol/L (treatment group) or (B) no treatment (control group). The Homeostatic model assessment (HOMA) index was used to evaluate IR at study inception and conclusion. Parametric and non-parametric tests as well as linear regression were used. At baseline no differences in demographic and clinical characteristics between the two groups was observed. Average dose of bicarbonate in the treatment group was 0.7 ± 0.2 mmol/kg. Treated patients showed a better metabolic control as confirmed by lower insulin levels (13.4 ± 5.2 vs 19.9 ± 6.3; for treated and control subjects respectively; p < 0.001), Homa-IR (5.9[5.0-7.0] vs 6.3[5.3–8.2]; p = 0.01) and need for oral antidiabetic drugs. The serum bicarbonate and HOMA-IR relationship was non-linear and the largest HOMA-IR reduction was noted for serum bicarbonate levels between 24 and 28 mmol/l. Adjustment for confounders, suggests that serum bicarbonate rather than treatment drives the effect on HOMA-IR. Serum bicarbonate is related to IR and the largest HOMA-IR reduction is noted for serum bicarbonate between 24 and 28 mmol/l. Treatment with bicarbonate influences IR. However, changes in serum bicarbonate explains the effect of treatment on HOMA index. Future efforts are required to validate these results in diabetic and non-diabetic CKD patients. The trial was registered at www.clinicaltrial.gov (Use of Bicarbonate in Chronic Renal Insufficiency (UBI) study - NCT01640119)
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发表时间: 2016-03-01
影响因子: 3.2
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发表时间: 2014-08-24
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