| Literature DB >> 30900372 |
Dong Zhao1, Yu Cao2, Cai-Guo Yu1, Sha-Sha Yuan1, Ning Zhang1, Yuan-Yuan Zhang1, Jan A Staessen3,4, Ying-Mei Feng1,2.
Abstract
Type 2 diabetes mellitus (T2DM) patients are often accompanied with hypertension. However, the association of antihypertensive drugs with β-cell function has not been well studied. To investigate this question, the authors performed a cross-sectional study involving 882 hypertensive T2DM patients. To assess β-cell function, patients were given 75g glucose orally and C-peptide levels before and 1, 2, and 3 hours after glucose intake were measured. Homa-β was computed by Homeostasis Model Assessment model to evaluate β-cell function using fasting C-peptide and glucose levels in the plasma. Multivariable-adjusted analysis was performed to evaluate the association of antihypertensive drugs with C-peptide levels, HbA1c, and Homa-β. Among 882 hypertensive patients, 547 (62.0%) received antihypertensive treatment. Multivariate-adjusted analysis demonstrated that use of calcium channel blockers (CCBs) was negatively associated with HbA1c levels (CCBs: 0.95 [95% CI: 0.92-0.98], P = 0.002). Our data further illustrated that the C-peptide levels before and 1, 2, and 3 hours of OGTT were 1.10-, 1.18-, 1.19-, and 1.15-fold increase in T2DM patients taking CCBs (P = 0.084 for fasting C-peptide levels; P ≤ 0.024 for C-peptide levels at 1, 2, and 3 hours after OGTT) in comparison with non-CCB users. Nevertheless, usage of any other antihypertensive drugs did neither associated with HbA1c nor associated with C-peptide levels (P ≥ 0.11). In conclusion, CCB treatment was negatively associated with HbA1c levels but positively associated with β-cell function in hypertensive T2DM patients, implying that CCBs could be considered to treat hypertensive T2DM patients with reduced β-cell function. ©2019 Wiley Periodicals, Inc.Entities:
Keywords: calcium channel blocker; hypertension; inhibitor of renin-angiotensin-aldosterone system; type 2 diabetes mellitus; β-cell function
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Year: 2019 PMID: 30900372 PMCID: PMC8030459 DOI: 10.1111/jch.13517
Source DB: PubMed Journal: J Clin Hypertens (Greenwich) ISSN: 1524-6175 Impact factor: 3.738