title: Ameliorated pancreatic β cell dysfunction in type 2 diabetic patients treated with a sodium-glucose cotransporter 2 inhibitor ipragliflozin.
abstract: It remains to be seen whether pancreatic β cell dysfunction in type 2 diabetic patients can be ameliorated just by correcting hyperglycemia. The current pilot study investigated β cell function after a four-week treatment with a sodium-glucose cotransporter 2 (SGLT2) inhibitor ipragliflozin in Japanese patients with type 2 diabetes mellitus. Ten participants (age, 51±13 years; hemoglobin A1c levels, 9.4±1.0%) took 50 mg of ipragliflozin L-proline for four weeks and thereafter discontinued the agent for one week. A 75-g oral glucose tolerance test (OGTT) was performed at 0 (baseline), 4 (end of medication), and 5 weeks (end of washout). The β cell function was evaluated using the disposition index, which was calculated as the product of the ΔIns₀₋₁₂₀/ΔGlu₀₋₁₂₀ and the Matsuda index, where ΔIns₀₋₁₂₀/ΔGlu₀₋₁₂₀ represents the ratio of the incremental concentrations of insulin to those of glucose during the 0- to 120-min time period of the OGTT. The fasting glucose level was 182±34 mg/dL at 0 week, 137±20 mg/dL at 4 weeks (p<0.001), and 154±31 mg/dL at 5 weeks (p=0.001). Compared to baseline, the disposition index was significantly elevated not only at 4 weeks (p<0.001) but also at 5 weeks (p=0.008). In conclusion, the current pilot study showed that the β cell function assessed by the OGTT-derived disposition index was significantly improved after a four-week treatment with ipragliflozin in Japanese patients with type 2 diabetes mellitus.
authors.affiliation: Department of Metabolic Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
authors.forename: Mitsuyoshi
authors.initials: M
authors.lastname: Takahara
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Shiraiwa
authors.forename: Taka-aki
authors.initials: TA
authors.lastname: Matsuoka
authors.forename: Naoto
authors.initials: N
authors.lastname: Katakami
authors.forename: Iichiro
authors.initials: I
authors.lastname: Shimomura
mesh_terms: D000328:Adult; D000465:Algorithms; D001786:Blood Glucose / Q000032:analysis; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy* / Q000208:ethnology / Q000503:physiopathology; D005260:Female; D005951:Glucose Tolerance Test; D005960:Glucosides / Q000627:therapeutic use*; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D006943:Hyperglycemia / Q000517:prevention & control*; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D007333:Insulin Resistance; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000378:metabolism; D007564:Japan; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D000077203:Sodium-Glucose Transporter 2 Inhibitors; D013876:Thiophenes / Q000627:therapeutic use*
chemical_list: D001786:Blood Glucose; D005960:Glucosides; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D007328:Insulin; D000077203:Sodium-Glucose Transporter 2 Inhibitors; D013876:Thiophenes; C517652:hemoglobin A1c protein, human; C572941:ipragliflozin