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Effects of a 33 residue interleukin-1 beta peptide and the antioxidant PQQ on interleukin-1 beta-mediated inhibition of glucose-stimulated insulin release from cultured mouse pancreatic islets.
Res Commun Mol Pathol Pharmacol. 1996 Nov; 94(2):115-28.RC

Abstract

Interleukin-1 beta (IL-1 beta) significantly inhibits insulin secretion from glucose stimulated islet cells. The mechanism for this inhibition has been hypothesized to be due to stimulation of the inducible form of nitric oxide synthase and a resulting increase in nitric oxide (NO) concentration. Ways to block the effect of IL-1 beta have focused on blocking the binding of IL-1 beta to the IL-1 receptor and the use of antioxidants to neutralize increases in NO. This report focuses on a 33 residue peptide synthesized based on the C-terminal region of the IL-1 beta molecule, a reported binding site of the IL-1 beta molecule, and the redoxcycling antioxidant pyrroloquinoline quinone (PQQ). The 33 residue peptide did not function as an antagonist, but as a weak agonist. High concentrations of PQQ itself inhibited glucose-dependent insulin release while low concentrations did not. PQQ had no effect on the actions of IL-1 beta. Three isosteric and isomeric analogues of PQQ were also investigated. One of the PQQ isomers had an inhibitory effect on insulin secretion at low concentrations where PQQ had no effect. These results reflect the sensitivity of islets to oxidative stress.

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Authors+Show Affiliations

McInerney MF
Department of Medicinal & Biological Chemistry, College of Pharmacy, University of Toledo, OH 43606, USA.
Seidel MJ
No affiliation info available
Nguyen JM
No affiliation info available
Flynn JC
No affiliation info available
Sturm N
No affiliation info available
Lee H
No affiliation info available
Zhang Z
No affiliation info available
Tillekeratne LM
No affiliation info available
Hudson RA
No affiliation info available

MeSH

Amino Acid SequenceAnimalsCells, CulturedGlucoseInsulinInsulin AntagonistsInsulin SecretionInterleukin-1Islets of LangerhansMiceMice, Inbred CBAMice, Inbred NODMolecular Sequence DataPeptide Fragments

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8987109

Citation

McInerney, M F., et al. "Effects of a 33 Residue Interleukin-1 Beta Peptide and the Antioxidant PQQ On Interleukin-1 Beta-mediated Inhibition of Glucose-stimulated Insulin Release From Cultured Mouse Pancreatic Islets." Research Communications in Molecular Pathology and Pharmacology, vol. 94, no. 2, 1996, pp. 115-28.
McInerney MF, Seidel MJ, Nguyen JM, et al. Effects of a 33 residue interleukin-1 beta peptide and the antioxidant PQQ on interleukin-1 beta-mediated inhibition of glucose-stimulated insulin release from cultured mouse pancreatic islets. Res Commun Mol Pathol Pharmacol. 1996;94(2):115-28.
McInerney, M. F., Seidel, M. J., Nguyen, J. M., Flynn, J. C., Sturm, N., Lee, H., Zhang, Z., Tillekeratne, L. M., & Hudson, R. A. (1996). Effects of a 33 residue interleukin-1 beta peptide and the antioxidant PQQ on interleukin-1 beta-mediated inhibition of glucose-stimulated insulin release from cultured mouse pancreatic islets. Research Communications in Molecular Pathology and Pharmacology, 94(2), 115-28.
McInerney MF, et al. Effects of a 33 Residue Interleukin-1 Beta Peptide and the Antioxidant PQQ On Interleukin-1 Beta-mediated Inhibition of Glucose-stimulated Insulin Release From Cultured Mouse Pancreatic Islets. Res Commun Mol Pathol Pharmacol. 1996;94(2):115-28. PubMed PMID: 8987109.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of a 33 residue interleukin-1 beta peptide and the antioxidant PQQ on interleukin-1 beta-mediated inhibition of glucose-stimulated insulin release from cultured mouse pancreatic islets. AU - McInerney,M F, AU - Seidel,M J, AU - Nguyen,J M, AU - Flynn,J C, AU - Sturm,N, AU - Lee,H, AU - Zhang,Z, AU - Tillekeratne,L M, AU - Hudson,R A, PY - 1996/11/1/pubmed PY - 1996/11/1/medline PY - 1996/11/1/entrez SP - 115 EP - 28 JF - Research communications in molecular pathology and pharmacology JO - Res Commun Mol Pathol Pharmacol VL - 94 IS - 2 N2 - Interleukin-1 beta (IL-1 beta) significantly inhibits insulin secretion from glucose stimulated islet cells. The mechanism for this inhibition has been hypothesized to be due to stimulation of the inducible form of nitric oxide synthase and a resulting increase in nitric oxide (NO) concentration. Ways to block the effect of IL-1 beta have focused on blocking the binding of IL-1 beta to the IL-1 receptor and the use of antioxidants to neutralize increases in NO. This report focuses on a 33 residue peptide synthesized based on the C-terminal region of the IL-1 beta molecule, a reported binding site of the IL-1 beta molecule, and the redoxcycling antioxidant pyrroloquinoline quinone (PQQ). The 33 residue peptide did not function as an antagonist, but as a weak agonist. High concentrations of PQQ itself inhibited glucose-dependent insulin release while low concentrations did not. PQQ had no effect on the actions of IL-1 beta. Three isosteric and isomeric analogues of PQQ were also investigated. One of the PQQ isomers had an inhibitory effect on insulin secretion at low concentrations where PQQ had no effect. These results reflect the sensitivity of islets to oxidative stress. SN - 1078-0297 UR - https://www.unboundmedicine.com/medline/citation/8987109/Effects_of_a_33_residue_interleukin_1_beta_peptide_and_the_antioxidant_PQQ_on_interleukin_1_beta_mediated_inhibition_of_glucose_stimulated_insulin_release_from_cultured_mouse_pancreatic_islets_ L2 - https://medlineplus.gov/diabetesmedicines.html DB - PRIME DP - Unbound Medicine ER -