Key result
In vivo insulin treatment significantly reduced the duration of induced atrial fibrillation episodes from 19.6 seconds to 1.9 seconds in type 1 diabetic mice.
Why the study?
Whether glucose and insulin disturbances observed during diabetes enhance atrial arrhythmogenicity, potentially leading to AF, was not well known.
Does insulin treatment reduce susceptibility to atrial fibrillation in type 1 diabetic mice?
Does insulin treatment reduce susceptibility to atrial fibrillation in type 1 diabetic mice?
Absolute Event Rate: 1.9% vs 19.6%
p-value: p=<0.05
In a mouse model of type 1 diabetes, insulin treatment restored atrial glucose transporter expression and reduced vulnerability to induced atrial fibrillation.
Insulin may attenuate AF vulnerability in diabetic models; hypothesis-generating and requires human trials before clinical consideration.
Diabetes has been identified as an independent risk factor for atrial fibrillation (AF), the most common chronic cardiac arrhythmia. Whether or not glucose and insulin disturbances observed during diabetes enhance arrhythmogenicity of the atria, potentially leading to AF, is not well known. We hypothesized that insulin deficiency and impaired glucose transport provide a metabolic substrate for the development and maintenance of AF during diabetes. Transesophageal atrial pacing was used to induce AF in healthy, streptozotocin-induced insulin-deficient type 1 diabetic and insulin-treated diabetic mice. Translocation of insulin-sensitive glucose transporters (GLUTs) to the atrial cell surface was measured using a biotinylated photolabeling assay in the perfused heart. Fibrosis and glycogen accumulation in the atrium were measured using histological analysis. Diabetic mice displayed mild hyperglycemia, increased duration and frequency of AF episodes vs. age-matched controls (e.g., AF duration: 19.7 ± 6.8 s vs. 1.8 ± 1.1 s, respectively, p=0.032), whereas insulin-treated diabetic animals did not. The translocation of insulin-sensitive GLUT-4 and -8 to the atrial cell surface was significantly downregulated in the diabetic mice (by 67% and 79%, respectively; p ≤0.001), and rescued by insulin treatment. We did not observe fibrosis or glycogen accumulation in the atria of diabetic mice. Therefore, these data suggest that insulin and glucose disturbances were sufficient to induce AF susceptibility during mild diabetes.
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Maria et al. (2020) studied Type 1 Diabetes and Atrial Fibrillation (n=33). Insulin vs. Untreated type 1 diabetic mice was evaluated on Duration of induced atrial fibrillation episodes (seconds) (p=<0.05). In vivo insulin treatment significantly reduced the duration of induced atrial fibrillation episodes from 19.6 seconds to 1.9 seconds in type 1 diabetic mice.
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