RT Journal Article
SR Electronic
T1 Recognition of Insulin-Releasing Fuels by Pancreatic B-Cells
JF Molecular Pharmacology
JO Mol Pharmacol
FD American Society for Pharmacology and Experimental Therapeutics
SP 76
OP 82
VO 20
IS 1
A1 UWE PANTEN
A1 JÜRGEN BIERMANN
A1 WERNER GRAEN
YR 1981
UL http://molpharm.aspetjournals.org/content/20/1/76.abstract
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.