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Alpha2A adrenergic receptor genetic variation contributes to hyperglycemia after myocardial infarction.

ABSTRACT: Acute myocardial infarction (AMI) is frequently associated with transient hyperglycemia even in patients without pre-existing diabetes. Acute stress can lead to increased blood glucose through the effect of catecholamines on alpha2A-adrenergic receptors (?2A-ARs) present in pancreatic islet ?-cells. Variation in the gene (ADRA2A) that encodes the ?2A-AR affects insulin release and glucose control and may play a particularly important role during times of stress.We performed a retrospective cohort study using de-identified electronic medical records linked to a DNA repository in 521 Caucasians and 55 African-American non-diabetic patients with AMI. We examined the association between admission blood glucose concentrations and ten selected ADRA2A SNPs in Caucasians.Three ADRA2A SNPS were associated with stress-induced hyperglycemia in Caucasians. Individuals homozygous for the rs10885122 variant (n=9) had a 23% lower admission glucose (geometric mean [95% CI], 99 [83-118]mg/dl) compared with non-carriers (121 [118-125] mg/dl; n=401; P=0.001). Admission glucose was 14% higher in rs1800544 variant homozygotes (134 [119-150]mg/dl; n=36) compared to non-carriers (118 [115-121]mg/dl; n=290, P=0.046). Furthermore, homozygotes of the rs553668 variant (n=13) had a 13% higher glucose (133 [110-160]mg/dl) compared to non-carriers (118 [115-122]mg/dl; n=366; P=0.056). Haplotypes including these ADRA2A SNPs were associated with higher admission glucose levels.Three ADRA2A genetic variants are associated with blood glucose and stress-induced hyperglycemia after AMI in Caucasians.

SUBMITTER: Adefurin A

PROVIDER: S-EPMC4879094 | biostudies-literature | 2016 Jul

REPOSITORIES: biostudies-literature

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Alpha2A adrenergic receptor genetic variation contributes to hyperglycemia after myocardial infarction.

Adefurin Abiodun A Vanderbilt Charles C Okafor Chimalum C Kawai Vivian V Li Chun C Shah Anushi A Wei Wei-Qi WQ Kurnik Daniel D Stein C Michael CM

International journal of cardiology 20160413

<h4>Background</h4>Acute myocardial infarction (AMI) is frequently associated with transient hyperglycemia even in patients without pre-existing diabetes. Acute stress can lead to increased blood glucose through the effect of catecholamines on alpha2A-adrenergic receptors (α2A-ARs) present in pancreatic islet β-cells. Variation in the gene (ADRA2A) that encodes the α2A-AR affects insulin release and glucose control and may play a particularly important role during times of stress.<h4>Methods</h4 ...[more]

PMID: 27131769

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Project description:BackgroundCardiac sympathetic nerve sprouting and the dysregulation of β-adrenergic receptor (β-AR) play a critical role in the deterioration of cardiac function after myocardial infarction (MI). Growing evidence indicates that exercise provides protection against MI. The aims of this study were to investigate whether aerobic exercise following MI could inhibit sympathetic nerve sprouting and restore the balance of β3-AR/β1-AR.MethodsMale Sprague-Dawley rats were divided into three groups: sham-operated control group (SC), MI group (MI), and MI with aerobic exercise group (ME). The rats in ME group were assigned to 8 weeks of exercise protocol (16 m/min, 50 min/d, 5 d/wk). The expression of nerve growth factor (NGF), the sympathetic nerve marker-tyrosine hydroxylase (TH), the nerve sprouting marker-growth associated protein 43 (GAP43), and β1- and β2-AR expression in the peri-infarct area of the left ventricle (LV) were measured by Western blot and immunohistochemistry, while β3-AR expression was determined by Western blot and immunofluorescence. Endothelial nitric oxide synthase (NOS2), phospho-NOS2 (p-NOS2), and neuronal nitric oxide synthase (NOS1) were measured by Western blot.ResultsMI increased LV end-diastolic pressure (LVEDP), and decreased LV systolic pressure (LVSP). Compared with the MI group, aerobic exercise significantly decreased LVEDP and increased LVSP. The protein expression of TH, GAP43 and NGF was significantly increased after MI, which was normalized by exercise. Compared with the SC group, the ratios of β2-AR/β1-AR and β3-AR/β1-AR were elevated in the MI group, and the protein expression of β3-AR and NOS1 increased after MI. Compared with the MI group, the ratios of β2-AR/β1-AR and β3-AR/β1-AR were normalized in the ME group, while the protein expression of β3-AR and NOS1 significantly increased, and NOS2 was activated by exercise.ConclusionsAerobic exercise inhibits cardiac sympathetic nerve sprouting, restores β3-AR/β1-AR balance and increases β3-AR expression through the activation of NOS2 and NOS1 after myocardial infarction.

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Alpha2A adrenergic receptor genetic variation contributes to hyperglycemia after myocardial infarction.

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Alpha2A adrenergic receptor genetic variation contributes to hyperglycemia after myocardial infarction.

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