While some antiarrhythmic agents have potential hypoglycemic effects and indeed some reports of hypoglycemic adverse effect of those drugs, no systematic reports have been issued. We studied the hypoglycemic effects of cibenzoline, a class I antiarrhythmic agent. Cibenzoline succinate (150–300 mg/day) was given orally for 12 weeks to 10 patients who had ventricular premature complexes (VPCs) of <1000 per 24 hours and abnormal glucose tolerance before treatment with cibenzoline. Abnormal glucose tolerance, judged by a 75-g oral glucose tolerance test (OGTT), was defined as the response designated as “diabetic” or “borderline” type according to the criteria specified by the Japan Diabetes Society. In OGTT, the insulinogenic index (defined as the ratio of the increment of IRI [immunoreactive insulin] to that of plasma glucose at 30 minutes after a glucose load) and the sum of IRI (ΣIRI) were also determined. Holter ECG recordings, OGTT, and measurements of fasting plasma glucose IRI, and HbA1 c were performed before and during cibenzoline treatment. Cibenzoline caused VPC reduction of < 70% in 6 of the 10 patients. The drug significantly decreased fasting plasma glucose and HbA1 c (mean ± SD) 12 weeks after treatment, from 6.18 ± 0.92 mM/L to 5.54 ± 1.08 mM/L and from 6.17 ± 1.03% to 5.83 ± 0.96%, respectively (P < 0.05). While it significantly increased fasting IRI from 4.99 ± 1.50 to 6.51 ± 1.47 μU/mL (P < 0.01), the insulinogenic index from 0.33 ± 0.26 to 0.65 ± 0.38 (P < 0.05), and ∑ IRI from 168 ± 67 μU/mL to 199 ± 46 (P < 0.05). Cibenzoline exerted a hypoglycemic effect, facilitating insulin secretion in patients with abnormal glucose tolerance and ventricular arrhythmias.