scholarly journals Preadipocyte factor 1 induces pancreatic ductal cell differentiation into insulin-producing cells

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Marie Rhee ◽  
Seung-Hwan Lee ◽  
Ji-Won Kim ◽  
Dong-Sik Ham ◽  
Heon-Seok Park ◽  
...  
2019 ◽  
Vol 14 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Aravinth P. Jawahar ◽  
Siddharth Narayanan ◽  
Gopalakrishnan Loganathan ◽  
Jithu Pradeep ◽  
Gary C. Vitale ◽  
...  

Islet cell auto-transplantation is a novel strategy for maintaining blood glucose levels and improving the quality of life in patients with chronic pancreatitis (CP). Despite the many recent advances associated with this therapy, obtaining a good yield of islet infusate still remains a pressing challenge. Reprogramming technology, by making use of the pancreatic exocrine compartment, can open the possibility of generating novel insulin-producing cells. Several lineage-tracing studies present evidence that exocrine cells undergo dedifferentiation into a progenitor-like state from which they can be manipulated to form insulin-producing cells. This review will present an overview of recent reports that demonstrate the potential of utilizing pancreatic ductal cells (PDCs) for reprogramming into insulin- producing cells, focusing on the recent advances and the conflicting views. A large pool of ductal cells is released along with islets during the human islet isolation process, but these cells are separated from the pure islets during the purification process. By identifying and improving existing ductal cell culture methods and developing a better understanding of mechanisms by which these cells can be manipulated to form hormone-producing islet-like cells, PDCs could prove to be a strong clinical tool in providing an alternative beta cell source, thus helping CP patients maintain their long-term glucose levels.


2021 ◽  
Author(s):  
Yosuke Miyachi ◽  
Miki Nishio ◽  
Junji Otani ◽  
Shinji Matsumoto ◽  
Akira Kikuchi ◽  
...  

2006 ◽  
Vol 281 (50) ◽  
pp. 38385-38395 ◽  
Author(s):  
Therese B. Deramaudt ◽  
Mira M. Sachdeva ◽  
Melanie P. Wescott ◽  
Yuting Chen ◽  
Doris A. Stoffers ◽  
...  

1993 ◽  
Vol 54 (3) ◽  
pp. 199-202 ◽  
Author(s):  
Kazuhiro Iwase ◽  
Masahiko Miyata ◽  
Tokio Yamaguchi ◽  
Takanobu Kawaguchi ◽  
Yasuhiro Tanaka ◽  
...  

2016 ◽  
Vol 113 (3) ◽  
pp. 650-655 ◽  
Author(s):  
Mingfeng Zhang ◽  
Qing Lin ◽  
Tong Qi ◽  
Tiankun Wang ◽  
Ching-Cheng Chen ◽  
...  

We previously reported that long-term administration of a low dose of gastrin and epidermal growth factor (GE) augments β-cell neogenesis in late-stage diabetic autoimmune mice after eliminating insulitis by induction of mixed chimerism. However, the source of β-cell neogenesis is still unknown. SRY (sex-determining region Y)-box 9+ (Sox9+) ductal cells in the adult pancreas are clonogenic and can give rise to insulin-producing β cells in an in vitro culture. Whether Sox9+ ductal cells in the adult pancreas can give rise to β cells in vivo remains controversial. Here, using lineage-tracing with genetic labeling of Insulin- or Sox9-expressing cells, we show that hyperglycemia (>300 mg/dL) is required for inducing Sox9+ ductal cell differentiation into insulin-producing β cells, and medium hyperglycemia (300–450 mg/dL) in combination with long-term administration of low-dose GE synergistically augments differentiation and is associated with normalization of blood glucose in nonautoimmune diabetic C57BL/6 mice. Short-term administration of high-dose GE cannot augment differentiation, although it can augment preexisting β-cell replication. These results indicate that medium hyperglycemia combined with long-term administration of low-dose GE represents one way to induce Sox9+ ductal cell differentiation into β cells in adult mice.


2013 ◽  
Vol 21 (1) ◽  
pp. 228-239 ◽  
Author(s):  
Tayaramma Thatava ◽  
Yogish C Kudva ◽  
Ramakrishna Edukulla ◽  
Karen Squillace ◽  
Josep Genebriera De Lamo ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document