Okita Kenji, Mizuguchi Toru, Shigenori Ota, Ishii Masayuki, Nishidate Toshihiko, Ueki Tomomi, Meguro Makoto, Kimura Yasutoshi, Tanimizu Naoki, Ichinohe Norihisa, Torigoe Toshihiko, Kojima Takashi, Mitaka Toshihiro, Sato Noriyuki, Sawada Norimasa, Hirata Koichi
Department of Surgery, Surgical Oncology, Sapporo Medical University, Sapporo, Hokkaido, 060-8543, Japan.
Department of Tissue Development and Regeneration, Research Institute for Frontier Medicine, Sapporo Medical University, Sapporo, Hokkaido, 060-8556, Japan.
Surg Today. 2016 Jun;46(6):633-40. doi: 10.1007/s00595-015-1215-2. Epub 2015 Jul 7.
Pancreatic regeneration (PR) is an interesting phenomenon that could provide clues as to how the control of diabetes mellitus might be achieved. Due to the different regenerative abilities of the pancreas and liver, the molecular mechanism responsible for PR is largely unknown. In this review, we describe five representative murine models of PR and thirteen humoral mitogens that stimulate β-cell proliferation. We also describe pancreatic ontogenesis, including the molecular transcriptional differences between α-cells and β-cells. Furthermore, we review 14 murine models which carry defects in genes related to key transcription factors for pancreatic ontogenesis to gain further insight into pancreatic development.
胰腺再生（PR）是一种有趣的现象，它可能为实现糖尿病控制提供线索。由于胰腺和肝脏的再生能力不同，负责PR的分子机制在很大程度上尚不清楚。在这篇综述中，我们描述了五种代表性的PR小鼠模型和13种刺激β细胞增殖的体液有丝分裂原。我们还描述了胰腺的个体发生，包括α细胞和β细胞之间的分子转录差异。此外，我们回顾了14种在与胰腺个体发生关键转录因子相关的基因中存在缺陷的小鼠模型，以进一步深入了解胰腺发育。
