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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
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