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Propionate inhibits glucose‐induced insulin secretion in isolated rat pancreatic islets
Author(s) -
Ximenes Helena M. A.,
Hirata Aparecida E.,
Rocha Marlene S.,
Curi Rui,
Carpinelli Angelo R.
Publication year - 2006
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1297
Subject(s) - propionate , medicine , endocrinology , insulin , pancreatic islets , chemistry , butyrate , pyruvate dehydrogenase complex , decarboxylation , sodium propionate , biochemistry , biology , islet , fermentation , enzyme , catalysis
Dietary fibers, probably by generating short chain fatty acids (SCFA) through enterobacterial fermentation, have a beneficial effect on the control of glycemia in patients with peripheral insulin resistance. We studied the effect of propionate on glucose‐induced insulin secretion in isolated rat pancreatic islets. Evidence is presented that propionate, one of the major SCFA produced in the gut, inhibits insulin secretion induced by high glucose concentrations (11.1 and 16.7 mM) in incubated and perfused pancreatic islets. This short chain fatty acid reduces [U‐ 14 C]‐glucose decarboxylation and raises the conversion of glucose to lactate. Propionate causes a significant decrease of both [1‐ 14 C]‐ (84%) and [2‐ 14 C]‐pyruvate (49%) decarboxylation. These findings indicate pyruvate dehydrogenase as the major site for the propionate effect. These observations led us to postulate that the reduction in glucose oxidation and the consequent decrease in the ATP/ADP ratio may be the major mechanism for the lower insulin secretion to glucose stimulus induced by propionate. Copyright © 2006 John Wiley & Sons, Ltd.