Document Detail


Oxo-4-methylpentanoic acid directs the metabolism of GABA into the Krebs cycle in rat pancreatic islets.
MedLine Citation:
PMID:  16819942     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OMP (oxo-4-methylpentanoic acid) stimulates by itself a biphasic secretion of insulin whereas L-leucine requires the presence of L-glutamine. L-Glutamine is predominantly converted into GABA (gamma-aminobutyric acid) in rat islets and L-leucine seems to promote its metabolism in the 'GABA shunt' [Fernández-Pascual, Mukala-Nsengu-Tshibangu, Martín del Río and Tamarit-Rodríguez (2004) Biochem. J. 379, 721-729]. In the present study, we have investigated how 10 mM OMP affects L-glutamine metabolism to uncover possible differences with L-leucine that might help to elucidate whether they share a common mechanism of stimulation of insulin secretion. In contrast with L-leucine, OMP alone stimulated a biphasic insulin secretion in rat perifused islets and decreased the islet content of GABA without modifying its extracellular release irrespective of the concentration of L-glutamine in the medium. GABA was transaminated to L-leucine whose intracellular concentration did not change because it was efficiently transported out of the islet cells. The L-[U-14C]-Glutamine (at 0.5 and 10.0 mM) conversion to 14CO2 was enhanced by 10 mM OMP within 30% and 70% respectively. Gabaculine (250 microM), a GABA transaminase inhibitor, suppressed OMP-induced oxygen consumption but not L-leucine- or glucose-stimulated respiration. It also suppressed the OMP-induced decrease in islet GABA content and the OMP-induced increase in insulin release. These results support the view that OMP promotes islet metabolism in the 'GABA shunt' generating 2-oxo-glutarate, in the branched-chain alpha-amino acid transaminase reaction, which would in turn trigger GABA deamination by GABA transaminase. OMP, but not L-leucine, suppressed islet semialdehyde succinic acid reductase activity and this might shift the metabolic flux of the 'GABA shunt' from gamma-hydroxybutyrate to succinic acid production.
Authors:
Inés Hernández-Fisac; Sergio Fernández-Pascual; Henrik Ortsäter; Javier Pizarro-Delgado; Rafael Martín del Río; Peter Bergsten; Jorge Tamarit-Rodriguez
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Biochemical journal     Volume:  400     ISSN:  1470-8728     ISO Abbreviation:  Biochem. J.     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-10-25     Completed Date:  2006-11-27     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  2984726R     Medline TA:  Biochem J     Country:  England    
Other Details:
Languages:  eng     Pagination:  81-9     Citation Subset:  IM    
Affiliation:
Biochemistry Department, Medical School, Complutense University, Madrid-28040, Spain.
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MeSH Terms
Descriptor/Qualifier:
Aldehyde Oxidoreductases / antagonists & inhibitors,  metabolism
Amino Acids / metabolism
Animals
Cerebellum / drug effects,  enzymology,  metabolism
Citric Acid Cycle / drug effects*
Cyclohexanecarboxylic Acids / pharmacology
Glucose / pharmacology
Glutamine / metabolism,  pharmacology
Insulin / secretion
Islets of Langerhans / drug effects*,  metabolism
Keto Acids / pharmacology*
Leucine / pharmacology
Male
Oxidation-Reduction / drug effects
Oxygen / metabolism
Rats
Rats, Wistar
Succinate-Semialdehyde Dehydrogenase / antagonists & inhibitors,  metabolism
Time Factors
Transaminases / antagonists & inhibitors,  metabolism
gamma-Aminobutyric Acid / metabolism*
Chemical
Reg. No./Substance:
0/Amino Acids; 0/Cyclohexanecarboxylic Acids; 0/Keto Acids; 11061-68-0/Insulin; 50-99-7/Glucose; 56-12-2/gamma-Aminobutyric Acid; 56-85-9/Glutamine; 61-90-5/Leucine; 7782-44-7/Oxygen; 816-66-0/alpha-ketoisocaproic acid; 87980-11-8/gabaculine; EC 1.2.-/Aldehyde Oxidoreductases; EC 1.2.1.24/Succinate-Semialdehyde Dehydrogenase; EC 2.6.1.-/Transaminases
Comments/Corrections

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