Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Succinic acid monomethyl ester (SAM) was recently proposed as an insulinotropic tool in non-insulin-dependent diabetes mellitus. Three models were now used to investigate whether SAM protects the B-cell against the impairment of glucose-stimulated insulin release caused by either glucose deprivation or starvation. In the first model, preincubation of the islets for 180 min at low glucose concentration in the presence of SAM prevented the decrease in the secretory response to D-glucose otherwise observed during a subsequent incubation. In the second model, an impaired secretory response to D-glucose was observed after 3-day culture at low (2.8 or 5.6 mM) as distinct from high (11.1 mM) hexose concentration and the presence of SAM in the culture medium again protected against this anomaly. In the third model, the infusion of SAM for 3 days to starved rats restored the secretory potential of isolated islets to a level comparable to that otherwise found in fed rats. Thus, during glucose deprivation or starvation, SAM is indeed able to maintain B-cell responsiveness to D-glucose.
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PMID:SAM prevents impairment of glucose-stimulated insulin secretion caused by hexose deprivation or starvation. 773 55

Succinic acid monomethyl ester (SAM) was recently proposed as an insulinotropic tool in non-insulin-dependent diabetes mellitus. The present study was designed to define whether SAM has the vascular effect in thoracic aorta of streptozotocin (STZ)-diabetic rats. (1) Body weights of diabetic rats were significantly increased after SAM treatment (P < 0.05). (2) Ten-day SAM treatment did not significantly affect blood glucose levels in SAM-treated control and SAM-treated STZ-diabetic rats. (3) Maximum tension responses to noradrenaline and KCl (80 mmol l-1) were not significantly different among all the experimental groups. (4) pD2 (-log EC50) values for noradrenaline of untreated diabetic rats were significantly less than those of controls, SAM-treated control and SAM-treated diabetic rats (P < 0.01, P < 0.001 and P < 0.05, respectively). SAM treatment normalized the decreased sensitivity of noradrenaline response in diabetic rats. (5) Fast, slow and total components of responses to noradrenaline (10(-5) mol l-1 approximately equal to EC90) were not significantly different among all the experimental groups. (6) There were no significant differences between aorta precontracted with noradrenaline from controls and STZ-diabetic (untreated and SAM-treated) rats in pD2 values and the potency of maximum relaxation to acetylcholine or in pD2 values to sodium nitroprusside. In conclusion, 10-day SAM treatment increases the sensitivity of diabetic-aortic rings to noradrenaline compared to untreated diabetic control rats.
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PMID:The effect of succinic acid monomethyl ester (SAM) on the responses of isolated thoracic aorta in streptozotocin-diabetic rats. 969 58