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Ricci, Renato Pietro; Santini, Massimo; Puglisi, Andrea; Azzolini, Paolo; Capucci, Alessandro; Pignalberi, Carlo; Boriani, Giuseppe; Botto, G; Spampinato, A.; Bellocci, Fulvio; Proclemer, Alessandro; Grammatico, Andrea; Seta, Francesco De

doi:10.1023/a:1009801706928

Cited by 68 publications

(1 citation statement)

References 27 publications

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“…While pacing of atria under anesthesia is considered a standard technique when examining propensity toward AF in both animal models and human patients (36,41), a study in free-running mice fitted with telemetric monitoring would be an interesting future study. Although not all the animals were inducible, our results indicated that untreated T1Dx animals had overall significantly greater frequency and longer duration of atrial tachy-arrhythmias, including AF, atrial tachycardia and brady-tachy syndrome (which has been reported to precede AF) (42). Specifically, the frequency and duration of AF episodes were greater in T1Dx animals vs. controls.…”

Section: Discussionmentioning

confidence: 56%

Insulin Treatment Reduces Susceptibility to Atrial Fibrillation in Type 1 Diabetic Mice

Maria

Campolo

Scherlag

et al. 2020

Front. Cardiovasc. Med.

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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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Section: Discussionmentioning

confidence: 56%