Anagliptin decreases serum lathosterol level in patients with type 2 diabetes: a pilot study

Abstract

Objective: The mechanism responsible for the lipid-lowering effect of dipeptidyl peptidase-4 (DPP-4) inhibitors remains unknown in humans. We evaluated the effect of anagliptin on serum lipid profiles, including cholesterol synthesis and absorption markers, in Japanese patients with type 2 diabetes.

Methods: Thirty patients with type 2 diabetes (20 – 70 years old, low-density lipoprotein cholesterol (LDL-C) level over 120 mg/dl, and no history of treatment with antidiabetic or antihyperlipidemic drugs) were enrolled. One hundred milligrams of anagliptin were administered twice a day for a month.

Results: After treatment of anagliptin, the LDL-C and total cholesterol (TC) levels did not decrease overall, but the TC level decreased significantly in 28 patients whose HbA1c levels decreased. Lathosterol decreased significantly, whereas no changes in campesterol, sitosterol or cholestanol were observed.

Conclusion: These results of our study show no significant change in LDL-C, a tendency of decrease in TC and non-high-density lipoprotein cholesterol (non-HDL-C) after treatment of anagliptin for 1 month. Anagliptin therapy decreased the cholesterol synthesis marker lathosterol without changing cholesterol absorption markers.

Keywords:

• anagliptin
• campesterol
• cholestanol
• lathosterol
• sitosterol
• type 2 diabetes

Acknowledgments

Trial Registration: UMIN000013878.

Declaration of interest

This study was funded by Sanwa Kagaku Kenkyusho Co., Ltd. This work was supported in part by Grants-in-Aid for Scientific Research (B) 21390282 and (B) 24390235 from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan, and a Medical Award from the Japan Medical Association. Yasuo Terauchi has received honoraria for lectures from MSD K.K.; Ono Pharmaceutical Co., Ltd.; Nippon Boehringer Ingelheim Co., Ltd.; Novartis Pharma K.K.; Takeda Pharmaceutical Co., Ltd.; Mitsubishi Tanabe Pharma Corp.; Daiichi Sankyo Co., Ltd.; Sanwa Kagaku Kenkyusho Co., Ltd.; Kowa Pharmaceutical Co., Ltd.; Novo Nordisk Pharma Ltd.; Eli Lilly Japan K.K.; Sanofi K.K.; Shionogi & Co., Ltd.; Bayer Yakuhin, Ltd.; and AstraZeneca K.K. and has obtained research support from MSD K.K.; Ono Pharmaceutical Co., Ltd.; Nippon Boehringer Ingelheim Co., Ltd.; Novartis Pharma K.K.; Takeda Pharmaceutical Co., Ltd.; Mitsubishi Tanabe Pharma Corp.; Daiichi Sankyo Co., Ltd.; Sanwa Kagaku Kenkyusho Co., Ltd.; Novo Nordisk Pharma Ltd.; Eli Lilly Japan K.K.; Sanofi K.K.; Dainippon Sumitomo Pharma Co., Ltd.; Shionogi & Co., Ltd.; Bayer Yakuhin, Ltd.; Astellas Pharma, Inc.; Pfizer Japan, Inc.; and AstraZeneca K.K. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Notes