Open AccessEstablishment of new clonal pancreatic β‐cell lines (MIN6‐K) useful for study of incretin/cyclic adenosine monophosphate signaling
Author(s) -
Iwasaki Masahiro,
Minami Kohtaro,
Shibasaki Tadao,
Miki Takashi,
Miyazaki Junichi,
Seino Susumu
Publication year - 2010
Publication title -
journal of diabetes investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.089
H-Index - 50
eISSN - 2040-1124
pISSN - 2040-1116
DOI - 10.1111/j.2040-1124.2010.00026.x
Subject(s) - incretin , medicine , cyclic adenosine monophosphate , endocrinology , adenosine , glucagon like peptide 1 , enteroendocrine cell , insulin , pancreatic islets , secretion , microbiology and biotechnology , cell culture , signal transduction , islet , type 2 diabetes , diabetes mellitus , receptor , biology , hormone , endocrine system , genetics
Incretin/cyclic adenosine monophosphate (cAMP) signaling is critical for potentiation of insulin secretion. Although several cell lines of pancreatic β‐cells are currently available, there are no cell lines suitable for investigation of incretin/cAMP signaling. In the present study, we have newly established pancreatic β‐cell lines (named MIN6‐K) from the IT6 mouse, which develops insulinoma. MIN6‐K8 cells respond to both glucose and incretins, such as glucagon‐like peptide‐1 (GLP‐1) and glucose‐dependent insulinotropic polypeptide (GIP), as is the case in pancreatic islets, whereas MIN6‐K20 cells respond to glucose, but not to incretins. Despite the difference in incretin‐potentiated insulin secretion between these two cell lines, the accumulation of cAMP after stimulation of GLP‐1 is comparable in these cells. Interestingly, we also found that incretin responsiveness is drastically induced by the formation of pseudoislets from MIN6‐K20 cells to a level comparable to that of pancreatic islets. Thus, these cell lines are useful for studying incretin/cAMP signaling in β‐cells. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.00026.x, 2010)