Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methyl pyruvate, when tested at a 10mM concentration, caused a rapid and sustained increase of insulin release evoked by either 7.0 or 16.7 mM D-glucose in the isolated perfused rat pancreas. Under these conditions, methyl pyruvate caused a modest and biphasic stimulation of glucagon release. In anaesthetized fed rats, methyl pyruvate (1.0 to 2.5 mumol/g body wt) given intravenously provoked a short-lived and dose-related increase in plasma insulin concentration, but failed to affect plasma glucagon concentration. D-glucose and methyl pyruvate, when injected together, acted additively upon insulin release. The in vivo secretory response to methyl pyruvate was comparable in fed, overnight fasted and 2-d starved rats, and only slightly decreased in fed animals that were injected with streptozotocin during the neonatal period. These results suggest that methyl pyruvate could be used as an insulinotropic agent to bypass site-specific defects of D-glucose metabolism in the B-cell, such as those found in starvation or non-insulin-dependent diabetes mellitus.
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PMID:In vitro and in vivo insulinotropic action of methyl pyruvate. 877 Jun 21

Methyl pyruvate (MP) stimulates insulin release both in vivo and in vitro. The present study aims at investigating whether MP is also able to enhance the B-cell secretory response to glucagon-like peptide 1 (GLP-1). In anaesthetized rats receiving a primed constant infusion of MP, the ester augmented plasma insulin concentration before GLP-1 injection and potentiated the insulinotropic action of the intestinal hormone. MP infusion also augmented plasma D-glucose concentration, whether in the absence or presence of GLP-1. A further rise in plasma D-glucose concentration was observed when the infusion of MP was halted, this coinciding with a fall in plasma insulin concentration. Whilst documenting that MP indeed enhances the B-cell secretory response to GLP-1, these findings do not suggest that MP is an appropriate tool for optimizing the hypoglycaemic action of the enteric hormone in the treatment of type-2 diabetes mellitus.
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PMID:Potentiation by methyl pyruvate of GLP-1 insulinotropic action in normal rats. 1135 Dec 75

Methyl pyruvate and the dimethyl ester of L-glutamic acid were administered intravenously, as a primed constant infusion (1.0-2.0 micromol followed by 0.5-1.0 micromol/min, both expressed per gram of body wt), in adult rats that had been injected with streptozotocin during the neonatal period. Each ester augmented plasma insulin concentration and potentiated and/or prolonged the insulinotropic action of glucagon-like peptide 1 (GLP-1) injected intravenously (5 pmol/g of body wt) at min 5 of the test. It is proposed, therefore, that suitable nonglucidic nutrients, susceptible to bypassing the site-specific defects of D-glucose transport and metabolism responsible for the preferential impairment of the B-cell secretory response to D-glucose in non-insulin-dependent diabetes, could be used to optimize the insulinotropic action of GLP-1.
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PMID:Potentiation and prolongation of the insulinotropic action of glucagon-like peptide 1 by methyl pyruvate or dimethyl ester of L-glutamic acid in a type 2 diabetes animal model. 1188 31