Establishment of a Pancreatic β Cell Line That Retains Glucose-Inducible Insulin Secretion: Special Reference to Expression of Glucose Transporter Isoforms*

TLDR

The MIN6 cell line is intended to facilitate studies of β‑cell mechanisms regulating insulin secretion in response to extracellular glucose and to explore the role of glucose transporter isoforms in glucose sensing. The study established MIN6 and MIN7 insulinoma‑derived β‑cell lines; MIN6 secretes insulin in a glucose‑dependent manner like normal islets, expresses high liver‑type glucose transporter mRNA, lacks MHC antigens unless induced, and thus preserves physiological β‑cell traits, whereas MIN7 lacks glucose‑inducible secretion and expresses both liver‑ and brain‑type transporters. Published in Endocrinology 127:126–132 (1990).

Abstract

Two cell lines have been established from insulinomas obtained by targeted expression of the simian virus 40 T antigen gene in transgenic mice. These cell lines, designated MIN6 and MIN7, produce insulin and T antigen and have morphological characteristics of pancreatic β cells. MIN6 cells exhibit glucose-inducible insulin secretion comparable with cultured normal mouse islet cells, whereas MIN7 cells do not. Both cell lines produce liver-type glucose transporter (GT) mRNA at high level. Brain-type GT mRNA is also present at considerable level in MIN7 cells, but is barely detectable in MIN6 cells, suggesting that exclusive expression of the liver-type GT is related to glucose-inducible insulin secretion. MIN6 cells do not express either major histocompatibility (MHC) class I or class II antigens on the cell surface. However, treatment with interferon-γ induces high levels of MHC class I antigens, and a combination of interferon-γ and tumor necrosis factor-β induces a MHC class II antigen on the cell surface. These results emphasize that the MIN6 cell line retains physiological characteristics of normal β cells. The MIN6 cell line will be especially useful to analyze the molecular mechanisms by which β cells regulate insulin secretion in response to extracellular glucose concentrations. We discuss a possible role of GT isoforms in glucose sensing by β cells. (Endocrinology127: 126–132,1990)