Yulia Khodneva1, Anath Shalev2, Stuart J Frank2, April P Carson3, Monika M Safford2. 1. Department of Medicine and Comprehensive Diabetes Center, School of Medicine, University of Alabama at Birmingham, Birmingham AL, United States. Electronic address: khodneva@uab.edu. 2. Department of Medicine and Comprehensive Diabetes Center, School of Medicine, University of Alabama at Birmingham, Birmingham AL, United States. 3. Department of Epidemiology, School of Public Health, University of Alabama at Birmingham, Birmingham AL, United States.
Abstract
BACKGROUND: Ca(2+) channel blockers (CCB) and verapamil in particular prevented β-cell apoptosis and enhanced endogenous insulin levels in recent studies of mouse models of diabetes. Verapamil's effect on serum glucose levels in humans with diabetes is not described. METHODS: We used data from the REasons for Geographic and Racial Differences in Stroke (REGARDS), a national cohort study of community-dwelling middle-aged and older adults, enrolled between 2003 and 2007 from the continental United States. We examined associations of CCB and verapamil use with fasting serum glucose among 4978 adults with diabetes, controlling for covariates in generalized linear models (GLM). FINDINGS: The sample included 1484 (29.6%) CCB users, of which 174 (3.4%) were verapamil users. In fully adjusted GLMs, CCB users had 5mg/dL lower serum glucose compared to non-users. Verapamil users had on average 10mg/dL lower serum glucose compared to CCB non-users with substantially greater differences among insulin users: 24mg/dL lower serum glucose among users of insulin in combination with oral agents and 37mg/dL lower among users of insulin alone. INTERPRETATION: CCB and in particular verapamil use was associated with lower fasting blood glucose levels among REGARDS participants with diabetes. FUNDING: UO1NS041588 from the National Institute of Neurological Disorders and Stroke, NIH; K24HL111154 and R01HL080477 from the National Heart, Lung, and Blood Institute.
BACKGROUND: Ca(2+) channel blockers (CCB) and verapamil in particular prevented β-cell apoptosis and enhanced endogenous insulin levels in recent studies of mouse models of diabetes. Verapamil's effect on serum glucose levels in humans with diabetes is not described. METHODS: We used data from the REasons for Geographic and Racial Differences in Stroke (REGARDS), a national cohort study of community-dwelling middle-aged and older adults, enrolled between 2003 and 2007 from the continental United States. We examined associations of CCB and verapamil use with fasting serum glucose among 4978 adults with diabetes, controlling for covariates in generalized linear models (GLM). FINDINGS: The sample included 1484 (29.6%) CCB users, of which 174 (3.4%) were verapamil users. In fully adjusted GLMs, CCB users had 5mg/dL lower serum glucose compared to non-users. Verapamil users had on average 10mg/dL lower serum glucose compared to CCB non-users with substantially greater differences among insulin users: 24mg/dL lower serum glucose among users of insulin in combination with oral agents and 37mg/dL lower among users of insulin alone. INTERPRETATION:CCB and in particular verapamil use was associated with lower fasting blood glucose levels among REGARDS participants with diabetes. FUNDING: UO1NS041588 from the National Institute of Neurological Disorders and Stroke, NIH; K24HL111154 and R01HL080477 from the National Heart, Lung, and Blood Institute.
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