RGD Reference Report - N-methyl-1-deoxynojirimycin (MOR-14), an alpha-glucosidase inhibitor, markedly improves postischemic left ventricular dysfunction. - Rat Genome Database

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N-methyl-1-deoxynojirimycin (MOR-14), an alpha-glucosidase inhibitor, markedly improves postischemic left ventricular dysfunction.

Authors: Nishida, Y  Minatoguchi, S  Arai, M  Takemura, G  Uno, Y  Hashimoto, K  Wang, N  Chen, XH  Fujiwara, T  Fujiwara, H 
Citation: Nishida Y, etal., Heart Vessels. 2000;15(6):268-73.
RGD ID: 2304191
Pubmed: PMID:11766064   (View Abstract at PubMed)

We examined whether pharmacological inhibition of glycogenolysis by N-methyl-1-deoxynojirimycin (MOR-14), a new compound which reduces the glycogenolytic rate by inhibiting the alpha-1,6-glucosidase activity of the glycogen-debranching enzyme, can protect the heart against postischemic left ventricular dysfunction. The hearts of male Sprague-Dawley rats were excised, and perfused on a Langendorff apparatus with Krebs-Henseleit solution with a gas mixture of 95% O2 and 5% CO2. The hearts were paced at 320 beats/min except during the ischemia. Left ventricular developed pressure (LVDP, mmHg), +/-dP/dt (mmHg/s), and coronary flow (ml/min) were continuously monitored. All hearts were perfused for a total of 120 min including a 30-min preischemic period followed by a 30-min episode of global ischemia and 60 min reperfusion. with or without 0.5 or 2 mM of MOR-14 during the 30-min preischemic period or the first 30 min of reperfusion. In another series of experiments, the myocardial content of glycogen and lactate was measured during the 30-min episode of ischemia in groups treated with and without 2mM of MOR-14. Preischemic but not postischemic treatment with MOR-14 significantly improved LVDP and +/-dP/dt without altering coronary flow during reperfusion in a dose-dependent manner. MOR-14 significantly preserved the glycogen content and significantly attenuated the lactate accumulation during the 30-min episode of ischemia. Preischemic treatment with MOR-14 is protective against postischemic left ventricular dysfunction through the inhibition of glycogenolysis in the isolated rat heart.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
AglRatglycogen catabolic process  IMP  RGD 

Molecular Pathway Annotations    Click to see Annotation Detail View

RGD Manual Annotations

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
AGLHumanglycogen degradation pathway   ISOAgl (Rattus norvegicus) RGD 
AglRatglycogen degradation pathway   IMP  RGD 
AglMouseglycogen degradation pathway   ISOAgl (Rattus norvegicus) RGD 
Objects Annotated

Genes (Rattus norvegicus)
Agl  (amylo-alpha-1, 6-glucosidase, 4-alpha-glucanotransferase)

Genes (Mus musculus)
Agl  (amylo-1,6-glucosidase, 4-alpha-glucanotransferase)

Genes (Homo sapiens)
AGL  (amylo-alpha-1, 6-glucosidase, 4-alpha-glucanotransferase)

Additional Information