Deterioration of HbA1c-Lowering Effects in Dipeptidyl-Peptidase Inhibitor and Dietary Habits in Japanese Type 2 Diabetes—Comparison with That of Metformin

Abstract

Aims: This study was designed to assess the possible relationship between deterioration of HbA1c-lowering effects with dipeptidyl peptidase-4 inhibitor (DPP-4i) or metformin (MET) treatment and macronutrient intake among patients with type 2 diabetes. Methods: Medical records of individuals visiting Kansai Electric Power Hospital during the period between September 20and June 2017 were retrospectively analyzed, based on predefined criteria, for initiation and continuation of DPP-4i or MET without any prescription change as well as HbA1c, bodyweight and macro-nutrient intake. Identified patients were stratified into two groups based on changes in HbA1c from 0.5 to 1 year (δHbA1c [1-0.5 year]) as previously described: Group A, patients whose HbA1c was maintained 1 year after initiation of DPP-4i or MET (δHbA1c [1-0.5 year] <0.4%), and group B, patients whose HbA1c was increased (δHbA1c [1-0.5 year] ≥0.4%). Results: Screening of 65,323 individuals’ medical records identified 63 DPP-4i patients (Groups A and B: n=53 and 10; age 65.2±1.6 and 58.2±4.2 years; BMI 24.6±1.6 and 25.3±1.2 kg/m2) and 35 MET patients (Groups A and B: n=27 and 8; age 52.6±11.7 and 53.9±2.4 years; BMI 30.7±7.4 and 30.2±2.7 kg/m2). In the DPP-4i patients, group B had significantly higher total energy intake and fat intake while the two groups had similar carbohydrate and protein intake. Group B also had significantly higher intake of saturated and monounsaturated fats but not polyunsaturated fats. A stepwise multiple regression analysis showed that δHbA1c (1-0.5 year) was independently correlated with saturated fat intake (B=0.032, SE=0.010, p< 0.01). In the MET patients, the two groups had similar intake of total energy, carbohydrate, protein and fat. Conclusion: The current findings show a novel association between deterioration of the HbA1c-lowering effects in DPP-4i-treated, but not in MET-treated patients, and dietary saturated fat intake. Disclosure S. Okamoto: None. H. Kuwata: None. D. Yabe: Speaker's Bureau; Self; MSD K.K., Novo Nordisk Pharma Ltd., Takeda Pharmaceutical Co., Ltd., Taisho Toyama Pharmaceutical Co., Ltd.. Research Support; Self; Nippon Boehringer Ingelheim Co. Ltd., Eli Lilly and Company, MSD K.K., Ono Pharmaceutical Co., Ltd., Arkray, Inc., Taisho Toyama Pharmaceutical Co., Ltd., Novo Vordisk Pharma Ltd., Takeda Pharamaceutical Co., Ltd.. K. Murotani: None. Y. Seino: None. R. Usui: None. H. Tatsuoka: None. Y. Hamamoto: None. T. Kurose: Consultant; Self; Sanofi, Ono Pharmaceutical Co., Ltd.. Other Relationship; Self; Abbott. Consultant; Self; Taisho Pharmaceutical Co., Ltd.. Other Relationship; Self; Takeda Pharmaceutical Co., Ltd., Merck Sharp & Dohme Corp., Novo Nordisk Inc., Novartis Pharma K.K. Y. Seino: Speaker's Bureau; Self; MSD K.K., Kao Corporation, Taisho Pharmaceutical Co., Ltd., Nippon Boehringer Ingelheim Co. Ltd., Taisho Toyama Pharamceutical Co., Ltd., Takeda Pharmaceutical Co., Ltd., Nippon Becton Dickinson Co., Ltd., Novo Nordisk Pharma Ltd.. Research Support; Self; Terumo Medical Corporation, Bayer Yakuhin, Ltd., Boehringer Ingelheim GmbH, Arkray, Inc., Ono Pharmaceutical Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd., Taisho Toyama Pharmaceutical Co., Ltd., Novo Nordisk Pharma Ltd..