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Year : 2018  |  Volume : 22  |  Issue : 2  |  Page : 185-190

Characterization of metabolic parameters in responders and nonresponders treated with canagliflozin monotherapy in drug-naive subjects with Type 2 diabetes

1 Division of Clinical Research, Biomedical Center, Tokyo; Department of Internal Medicine, Division of Endocrinology and Metabolism, Gyoda General Hospital, Saitama; Department of Internal Medicine, Division of Diabetes and Metabolism, Higashitotsuka Memorial Hospital, Yokohama, Japan
2 Department of Internal Medicine, Division of Endocrinology and Metabolism, Gyoda General Hospital, Saitama, Japan
3 Division of Clinical Research, Biomedical Center, Tokyo, Japan

Correspondence Address:
Eiji Kutoh
Division of Clinical Research, Biomedical Center, Tokyo
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2230-8210.232379

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Objectives: The aim of this project is to compare the effect of canagliflozin monotherapy on metabolic parameters between responders and nonresponders with this drug. This study is a prospective, unblinded, observational study. Subjects and Methods: Drug-naïve patients with type 2 diabetes mellitus received only 50–100 mg/day canagliflozin for 3 months (n = 39). They were divided into two groups according to the novel “A1c index” to assess glycemic efficacies; responders (n = 24) and nonresponders (n = 15). Results: At baseline, glycated hemoglobin (HbA1c) and fasting blood glucose (FBG) were significantly higher and homeostatic model assessment (HOMA)-B and body mass index (BMI) were significantly lower in responders. In both groups, similar, significant reductions of BMI (−1.9% with responder and −1.8% with nonresponder) and HOMA-R (−35.8% for responder and –31.5% for nonresponder) were observed. However, differences were seen with other parameters as follows: 1) responders: significant reductions of HbA1c (10.95%–8.44%), FBG (−29.6%) or free fatty acid (FFA) (−16.2%), and significant increases of HOMA-B (79.7%) were observed. 2) Nonresponders: significant reductions of serum uric acid (UA) (−8.6%) levels were seen. Significant correlations were observed between the baseline levels of serum UA and those of HOMA-B (R = 0.7259). However, this link became uncorrelated with the treatment with canagliflozin. Conclusions: These results suggest that (1) responders with canagliflozin have lower BMI and beta-cell function. Reductions of body weight with canagliflozin were not associated with its glycemic efficacy, (2) reduced FFA levels and enhanced insulin sensitivity/beta-cell function could be a potential mechanism of good glycemic efficacy of canagliflozin, and (3) serum UA might be involved in modulating beta-cell function during canagliflozin treatment.

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