Normal islet vascularization is dispensable for expansion of beta-cell mass in response to high-fat diet induced insulin resistance |
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Authors: | Yukiko Toyofuku Shiho Nakayama Ryuzo Kawamori Yoshio Fujitani Masahiro Inoue |
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Institution: | a Department of Medicine, Metabolism and Endocrinology, Juntendo University, School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan b Sportology Center, Graduate School of Medicine, Juntendo University, Tokyo, Japan c Center for Therapeutic Innovations in Diabetes, Graduate School of Medicine, Juntendo University, Tokyo, Japan d Center for Beta Cell Biology and Regeneration, Graduate School of Medicine, Juntendo University, Tokyo, Japan e Department of Biochemistry, Osaka Medical Center for Cancer and Cardiovascular Disease, Osaka 537-8511, Japan |
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Abstract: | The inability to increase of islet mass adequately to compensate for the demand of insulin due to insulin resistance is an important pathophysiological feature of type 2 diabetes. Previous studies suggested a relationship between pancreatic beta-cell mass and islet vascularization, although no evidence has confirmed this association in response to insulin resistance. Vascular endothelial growth factor-A (VEGF-A) in islets is essential for maintaining normal islet blood vessels. Here, insulin resistance was induced in mice carrying a beta-cell-specific VEGF-A gene mutation (RIP-Cre:Vegffl/fl) by 20-week feeding of high-fat diet as a model of impaired islet vascularization. These mice showed only a modest decrease in glucose tolerance, compared with control mice. In addition, although the endothelial cell area in the islets of high-fat-fed RIP-Cre:Vegffl/fl mice remained diminished, the pancreatic beta-cell area was modestly more than in high-fat-fed control mice. Thus, normal islet vascularization does not seem to be essential for expansion of beta cell mass in response to insulin resistance. |
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Keywords: | IPGTT intraperitoneal glucose tolerance test KRBB Krebs-Ringer bicarbonate buffer |
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