Insulin secretion and differential gene expression in glucose-responsive and -unresponsive MIN6 sublines

1  Department of Molecular Medicine, Chiba University Graduate School of Medicine, Chiba 260 - 8670; and 2  Department of Nutrition and Physiological Chemistry, Graduate School of Medicine, Osaka University, Suita 565 - 0871, Japan We have established two sublines derived from the insulin-secreting...

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Published in:American journal of physiology: endocrinology and metabolism 2000-10, Vol.279 (4), p.E773-E781
Main Authors: Minami, Kohtaro, Yano, Hideki, Miki, Takashi, Nagashima, Kazuaki, Wang, Chang-Zheng, Tanaka, Hiroko, Miyazaki, Jun-Ichi, Seino, Susumu
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - metabolism
Amino Acid Transport System X-AG
Animals
ATP-Binding Cassette Transporters - genetics
ATP-Binding Cassette Transporters - metabolism
Biological Transport - genetics
Calcium - metabolism
Calcium Channels - metabolism
Cell Line
Electron Transport Complex IV - genetics
Electron Transport Complex IV - metabolism
Gene Expression Regulation - drug effects
Glucose - metabolism
Glucose - pharmacology
Glucose Transporter Type 2
Insulin - genetics
Insulin - metabolism
Insulin Secretion
Islets of Langerhans - metabolism
L-Lactate Dehydrogenase - metabolism
Mice
Models, Biological
Monosaccharide Transport Proteins - genetics
Monosaccharide Transport Proteins - metabolism
NADH Dehydrogenase - genetics
NADH Dehydrogenase - metabolism
Organ Specificity
Patch-Clamp Techniques
Potassium Channels - metabolism
RNA, Messenger - metabolism
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Summary:1  Department of Molecular Medicine, Chiba University Graduate School of Medicine, Chiba 260 - 8670; and 2  Department of Nutrition and Physiological Chemistry, Graduate School of Medicine, Osaka University, Suita 565 - 0871, Japan We have established two sublines derived from the insulin-secreting mouse pancreatic -cell line MIN6, designated m9 and m14. m9 Cells exhibit glucose-induced insulin secretion in a concentration-dependent manner, whereas m14 cells respond poorly to glucose. In m14 cells, glucose consumption and lactate production are enhanced, and ATP production is largely through nonoxidative pathways. Moreover, lactate dehydrogenase activity is increased, and hexokinase replaces glucokinase as a glucose-phosphorylating enzyme. The ATP-sensitive K + channel activity and voltage-dependent calcium channel activity in m14 cells are reduced, and the resting membrane potential is significantly higher than in m9 cells. Thus, in contrast to m9, a model for -cells with normal insulin response, m14 is a model for -cells with impaired glucose-induced insulin secretion. By mRNA differential display of these sublines, we found 10 genes to be expressed at markedly different levels. These newly established MIN6 cell sublines should be useful tools in the analysis of the genetic and molecular basis of impaired glucose-induced insulin secretion. pancreatic -cells; mRNA differential display; MIN6-m9; MIN6-m14
ISSN:0193-1849
1522-1555
DOI:10.1152/ajpendo.2000.279.4.e773