Abstract:
:This is the first systematic study on the pancreatic beta cell function in the heterozygous mouse with targeted disruption of the beta cell glucokinase gene. The heterozygotes' beta cell displayed the following characteristics: (1) impaired glucose sensitivity with normal glucose responsiveness, (2) poor discrimination of alpha and beta glucose anomers, and (3) normal response to glucose in the presence of 25 mM K+ and 150 microM diazoxide. Both the first and the second phases of glucose-stimulated insulin release were depressed. Although the heterozygotes were mildly hyperglycemic, insulin treatment further suppressed beta cell function, implying the beta cell glucose toxicity is not the cause of impaired glucose sensitivity. The data are compatible with the glucokinase glucose sensor concept inasmuch as glucose sensitivity is reduced in the heterozygotes' beta cell. The anomeric malaise and preservation of the ATP-sensitive K+ channel-independent glucose action were considered due to chronic hyperglycemia.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Aizawa T,Asanuma N,Terauchi Y,Suzuki N,Komatsu M,Itoh N,Nakabayashi T,Hidaka H,Ohnota H,Yamauchi K,Yasuda K,Yazaki Y,Kadowaki T,Hashizume Kdoi
10.1006/bbrc.1996.1826subject
Has Abstractpub_date
1996-12-13 00:00:00pages
460-5issue
2eissn
0006-291Xissn
1090-2104pii
S0006-291X(96)91826-4journal_volume
229pub_type
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