PT  - JOURNAL ARTICLE
AU  - UWE PANTEN
AU  - JÜRGEN BIERMANN
AU  - WERNER GRAEN
TI  - Recognition of Insulin-Releasing Fuels by Pancreatic B-Cells
DP  - 1981 Jul 01
TA  - Molecular Pharmacology
PG  - 76--82
VI  - 20
IP  - 1
4099  - http://molpharm.aspetjournals.org/content/20/1/76.short
4100  - http://molpharm.aspetjournals.org/content/20/1/76.full
SO  - Mol Pharmacol1981 Jul 01; 20
AB  - α-Ketoisocaproic acid released insulin from isolated mouse islets with a threshold concentration at 2-3 mM and a maximal effect at 15-20 mM. Stimulation of insulin secretion was accompanied by small increases of cyclic AMP accumulation by islets which could be prevented by omission of Ca2+ from the incubation media. Extramitochondrial metabolites that could arise from α-ketoisocaproic acid released much less insulin than their mother substance. Accumulation of intramitochondrial CoA compounds typical for degradation of α-ketoisocaproic acid probably did not cause the specific B-cell response to this keto acid. It is concluded that metabolites do not represent primary signals during α-ketoisocaproic acid-induced insulin secretion. The experimental data are compatible with the view that increase of intramitochondrial production of reducing equivalents is necessary for recognizing insulin-releasing fuels by B-cells. ACKNOWLEDGMENTS We thank Professor E. Brunner and his colleagues for help with the statistical testing.