From:
"Sukie Crandall"
Date: 2007-02-12 00:29:51 UTC
Subject: [ferrethealth] Re: Comatose Ferret
To: ferrethealth@yahoogroups.com
If the DMG caused a large enough release of insulin that could explain what your ferret
went through, I'm afraid, but I do not know if it can cause that high a release of insulin.
More on DMG for diabetes (not insulinoma):
BEGIN QUOTES
Endocrine. 2001 Nov;16(2):113-6.
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.
Cancelas J, Villanueva-Penacarrillo ML, Valverde I, Malaisse WJ.
Fundacion Jimenez Diaz, Madrid, Spain.
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.
PMID: 11887931 [PubMed - indexed for MEDLINE]
Pharmacol Res. 1996 Mar;33(3):191-4.
Effects of the methyl esters of pyruvate, succinate and glutamate on the secretory
response to meglitinide analogues in rat pancreatic islets.
Bakkali Nadi A, Zhang TM, Malaisse WJ.
Laboratory of Experimental Medicine, Brussels Free University, Belgium.
The insulinotropic action of the meglitinide analogues KAD-1229, A-4166 and repaglinide
was examined in rat pancreatic islets deprived of exogenous nutrient or incubated in the
presence of nutrient secretagogues such as D-glucose and the methyl esters of pyruvic
acid, succinic acid and glutamic acid. The meglitinide analogues exerted little effect on
insulin release in the absence of exogenous nutrient or in the presence of methyl
pyruvate. They caused obvious stimulation of insulin output in the presence of D-glucose,
dimethyl succinate or dimethyl glutamate. It is proposed, therefore, that suitable esters of
dicarboxylic nutrients could be used to potentiate the secretory response to meglitinide
analogues in non-insulin-dependent diabetes mellitus.
PMID: 8880890 [PubMed - indexed for MEDLINE]
Am J Physiol. 1994 Oct;267(4 Pt 1):E573-84.
Insulinotropic action of glutamic acid dimethyl ester.
Sener A, Conget I, Rasschaert J, Leclercq-Meyer V, Villanueva-Penacarrillo ML, Valverde I,
Malaisse WJ.
Laboratory of Experimental Medicine, Brussels Free University, Belgium.
Glutamic acid dimethyl ester (GME; 3.0-10.0 mM) enhanced insulin release evoked by
6.0-8.3 mM D-glucose, 1.0-10.0 mM L-leucine, or 5.0-10.0 mM 2-amino-bicyclo(2,2,1)
heptane-2-carboxylic acid, causing a shift to the left of the sigmoidal relationship
between insulin output and D-glucose concentration. In the absence of D-glucose, GME
also unmasked the insulinotropic potential of glibenclamide. In islets exposed to L-
leucine, the insulinotropic action of GME coincided with an early fall and later increase in
86Rb outflow and augmentation of 45Ca outflow from prelabeled islets. The measurement
of O2 uptake, NH4+ output, production of 14CO2 from islets prelabeled with [U-14C]
palmitate, generation of 14C-labeled amino acids and 14CO2 from the dimethyl ester of
either L-[1-14C]glutamic acid or L-[U-14C]glutamic acid, and D-[2-14C]glucose as well
as D-[6-14C]glucose oxidation in the presence or absence of GME indicated that the latter
ester was efficiently converted to L-glutamate and its further metabolites. The overall gain
in O2 uptake represented the balance between GME oxidation and its sparing action on
the catabolism of endogenous fatty acids and exogenous D-glucose. It is proposed that
GME might represent a new tool to bypass beta-cell defects in D-glucose transport,
phosphorylation, and further metabolism and, hence, to stimulate insulin release in
experiments conducted in animal models of non-insulin-dependent diabetes mellitus.
PMID: 7943307 [PubMed - indexed for MEDLINE]
END QUOTES
and there are more in Pub Med.
If that is all that caused things to go wrong then thank goodness it is something which can
be so easily changed.
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