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Anti-hypertensive azelnidipine preserves insulin signaling and glucose uptake against oxidative stress in 3T3-L1 adipocytes.

Abstract
It is known that reactive oxygen species (ROS) are involved in the development of insulin resistance as well as pancreatic β-cell dysfunction both of which are often observed in type 2 diabetes. In this study, we evaluated the effects of azelnidipine, a calcium channel blocker, on ROS-mediated insulin resistance in adipocytes. When 3T3-L1 adipocytes were exposed to ROS, insulin-mediated glucose uptake was suppressed, but such phenomena were not observed in the presence of azelnidipine. Phosphorylation of insulin receptor and phosphorylation of Akt were suppressed by ROS, which was mitigated by azelnidipine treatment. Activation of the JNK pathway induced by ROS was also reduced by azelnidipine. Various inflammatory cytokine levels were increased by ROS, which was also suppressed by azelnidipine treatment. In contrast, adiponectin mRNA and secreted adiponectin levels were reduced by ROS, which was refilled by azelnidipine treatment. In conclusion, azelnidipine preserves insulin signaling and glucose uptake against oxidative stress in 3T3-L1 adipocytes.
AuthorsFuminori Tatsumi, Hideaki Kaneto, Mitsuru Hashiramoto, Kazuhito Tawaramoto, Atsushi Obata, Tomohiko Kimura, Masashi Shimoda, Sumiko Hamamoto, Yukiko Kanda-Kimura, Shinji Kamei, Tomoatsu Mune, Masafumi Matsuda, Kohei Kaku
JournalEndocrine journal (Endocr J) Vol. 62 Issue 8 Pg. 741-7 ( 2015) ISSN: 1348-4540 [Electronic] Japan
PMID26073866 (Publication Type: Journal Article)
Chemical References
  • Antihypertensive Agents
  • Dihydropyridines
  • Insulin
  • Reactive Oxygen Species
  • Azetidinecarboxylic Acid
  • Receptor, Insulin
  • Proto-Oncogene Proteins c-akt
  • Glucose
  • azelnidipine
Topics
  • 3T3-L1 Cells
  • Adipocytes (metabolism)
  • Animals
  • Antihypertensive Agents (pharmacology)
  • Azetidinecarboxylic Acid (analogs & derivatives, pharmacology)
  • Dihydropyridines (pharmacology)
  • Glucose (metabolism)
  • Insulin (metabolism)
  • Mice
  • Oxidative Stress (drug effects)
  • Phosphorylation (drug effects)
  • Proto-Oncogene Proteins c-akt (metabolism)
  • Reactive Oxygen Species (metabolism)
  • Receptor, Insulin (metabolism)
  • Signal Transduction (drug effects)

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