The effect of anagliptin treatment on glucose metabolism and lipid metabolism, and oxidative stress in fasting and postprandial states using a test meal in Japanese men with type 2 diabetes
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It has been generally recognized that postprandial hyperglycemia and hyperlipidemia are highly related to the development of atherosclerosis [1, 2]. Hyperglycemia is known to damage vascular endothelial cells, increase oxidative stress, promote the expression of adhesion molecule and inhibit nitric oxide (NO) production . Remnant lipoprotein, an important component of postprandial hyperlipidemia, promotes foam cell formation of macrophages and proliferation of smooth muscle cells . Dipeptidyl peptidase 4 (DPP-4) inhibitors have attracted attention as a new class of anti-diabetic agents for the treatment of type 2 diabetes . Anagliptin, a member of the medication class of DPP-4 inhibitors, has been recently available in the market in Japan. Animal studies suggest that anagliptin treatment is associated with improvement of glucose tolerance either by amelioration of insulin resistance or enhancing insulin secretion  and the decrease in the development of atherosclerosis ....
KeywordsAnagliptin Test meal Adiponectin Remnant Renal function 8-OHdG
Conflict of interest
There is no conflict of interest for all of the authors regarding this work.
- 6.K. Nakaya, N. Kubota, I. Takamoto, T. Kubota, H. Katsuyama, H. Sato, K. Tokuyama, S. Hashimoto, M. Goto, T. Jomori, K. Ueki, T. Kadowaki, Dipeptidyl peptidase-4 inhibitor anagliptin ameliorates diabetes in mice with haploinsufficiency of glucokinase on a high-fat diet. Metabolism 62, 939–951 (2013)CrossRefPubMedGoogle Scholar
- 7.N. Ervinna, T. Mita, E. Yasunari, K. Azuma, R. Tanaka, S. Fujimura, D. Sukmawati, T. Nomiyama, A. Kanazawa, R. Kawamori, Y. Fujitani, H. Watada, A DPP-4 inhibitor, suppresses proliferation of vascular smooth muscles and monocyte inflammatory reaction and attenuates atherosclerosis in male apo E-deficient mice. Endocrinology 154, 1260–1270 (2013)CrossRefPubMedGoogle Scholar