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Article

A Dipeptidyl Peptidase-4 Inhibitor Inhibits Foam Cell Formation of Macrophages in Type 1 Diabetes via Suppression of CD36 and ACAT-1 Expression

1
Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Tokyo 142-8666, Japan
2
Department of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume 830-0011, Japan
3
Diabetes Center, Ebina General Hospital, Ebina 243-0433, Japan
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2020, 21(13), 4811; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21134811
Received: 11 May 2020 / Revised: 27 June 2020 / Accepted: 6 July 2020 / Published: 7 July 2020
Dipeptidyl peptidase-4 (DPP-4) inhibitors have been reported to play a protective role against atherosclerosis in both animal models and patients with type 2 diabetes (T2D). However, since T2D is associated with dyslipidemia, hypertension and insulin resistance, part of which are ameliorated by DPP-4 inhibitors, it remains unclear whether DPP-4 inhibitors could have anti-atherosclerotic properties directly by attenuating the harmful effects of hyperglycemia. Therefore, we examined whether a DPP-4 inhibitor, teneligliptin, could suppress oxidized low-density lipoprotein (ox-LDL) uptake, foam cell formation, CD36 and acyl-coenzyme A: cholesterol acyltransferase-1 (ACAT-1) gene expression of macrophages isolated from streptozotocin-induced type 1 diabetes (T1D) mice and T1D patients as well as advanced glycation end product (AGE)-exposed mouse peritoneal macrophages and THP-1 cells. Foam cell formation, CD36 and ACAT-1 gene expression of macrophages derived from T1D mice or patients increased compared with those from non-diabetic controls, all of which were inhibited by 10 nmol/L teneligliptin. AGEs mimicked the effects of T1D; teneligliptin attenuated all the deleterious effects of AGEs in mouse macrophages and THP-1 cells. Our present findings suggest that teneligliptin may inhibit foam cell formation of macrophages in T1D via suppression of CD36 and ACAT-1 gene expression partly by attenuating the harmful effects of AGEs. View Full-Text
Keywords: DPP-4 inhibitors; macrophage foam cell formation; CD36; ACAT-1; AGEs; type 1 diabetes DPP-4 inhibitors; macrophage foam cell formation; CD36; ACAT-1; AGEs; type 1 diabetes
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MDPI and ACS Style

Terasaki, M.; Yashima, H.; Mori, Y.; Saito, T.; Matsui, T.; Hiromura, M.; Kushima, H.; Osaka, N.; Ohara, M.; Fukui, T.; Hirano, T.; Yamagishi, S.-i. A Dipeptidyl Peptidase-4 Inhibitor Inhibits Foam Cell Formation of Macrophages in Type 1 Diabetes via Suppression of CD36 and ACAT-1 Expression. Int. J. Mol. Sci. 2020, 21, 4811. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21134811

AMA Style

Terasaki M, Yashima H, Mori Y, Saito T, Matsui T, Hiromura M, Kushima H, Osaka N, Ohara M, Fukui T, Hirano T, Yamagishi S-i. A Dipeptidyl Peptidase-4 Inhibitor Inhibits Foam Cell Formation of Macrophages in Type 1 Diabetes via Suppression of CD36 and ACAT-1 Expression. International Journal of Molecular Sciences. 2020; 21(13):4811. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21134811

Chicago/Turabian Style

Terasaki, Michishige, Hironori Yashima, Yusaku Mori, Tomomi Saito, Takanori Matsui, Munenori Hiromura, Hideki Kushima, Naoya Osaka, Makoto Ohara, Tomoyasu Fukui, Tsutomu Hirano, and Sho-ichi Yamagishi. 2020. "A Dipeptidyl Peptidase-4 Inhibitor Inhibits Foam Cell Formation of Macrophages in Type 1 Diabetes via Suppression of CD36 and ACAT-1 Expression" International Journal of Molecular Sciences 21, no. 13: 4811. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21134811

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