Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute exogenous hypermagnesaemia in healthy subjects retards glucose assimilation (Kg) and inhibits B cell function. The glycoregulatory effect of hypermagnesaemia was investigated in the course of the intravenous glucose tolerance test (IVGTT) in 16 subjects, incl. eight with impaired glucose tolerance (IGT) and eight with non-insulin dependent diabetes mellitus (NIDDM). Hypermagnesaemia was induced by intravenous infusion of 6 g MgSO4. The secretory response of insulin (IRI) and C-peptide were expressed as the incremental area (IA of S-IRI and IA of S-C-peptide). The results were compared with control IVGTT following infusion of saline. Hypermagnesaemia did not affect glucose assimilation in subjects with IGT as compared with control values nor in subjects with NIDDM. Hypermagnesaemia did not change IA of S-IRI nor of S-C-peptide in IGT as compared with control values (IA of S-IRI were 4308 +/- 1126 vs 3309 +/- 610 microU/ml x min and IA of S-C-peptide 191 +/- 43 vs 177 +/- 46 ng/ml x min) (means +/- SEM). In NIDDM there was no significant difference between the response of C-peptide during hypermagnesaemia and the response during control IVGTT (IA were 72 +/- 20 ng/ml x min vs 73.5 +/- 22.4 ng/ml x min). As no significant insulin response to glucose was obtained after saline or magnesium in NIDDM, the effect of hypermagnesaemia was not possible to evaluate. In conclusion, no significant decline of glucose assimilation and B-cell function in IGT and NIDDM can be proved in the course of exogenous hypermagnesaemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does exogenous hypermagnesaemia inhibit insulin secretion in patients with impaired glucose tolerance or non-insulin-dependent diabetes mellitus? 800 65

Magnesium (Mg) , one of the fundamental minerals acting the co-factor of about 300 kinds of enzymes and natural Ca channel blocker, plays an important role of cardiovascular, neurological, and metabolic functions in physiological, and pathophysiological conditions. Common abnormal Mg metabolism is an absolute or relative deficiency of Mg due to an attenuated Mg intake and an enhanced urinary Mg excretion, particularly in the metabolic syndrome (MetS) , type 2 diabetes (DM) , chronic heart failure (CHF) and hemodialysis (HD) patients with diabetes. It has been reported the Mg deficiency relating to enhanced risk of MetS and type 2 DM, and to fatal cardiac events in CHF and an atherosclerotic, vascular calcification in HD patients. On the otherhand, severe and fatal hypermagnesemia is very rare, except for the condition associated with high dose administration of Mg, renal failure and an abnormally enhanced Mg absorption from damaged intestine in the mesenteric ischemia/infarction, severe constipation or ileus. In this paper, we conduct to review and discuss the pathophysiological and pathogenetical role of the abnormal Mg metabolism focused on Mg deficiency, and the protective and therapeutic significance of Mg administration in the MetS, type 2 DM, CHF and diabetic HD patients.
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PMID:[Abnormalities of magnesium (Mg) metabolism and therapeutic significance of Mg administration in patients with metabolic syndrome, type 2 diabetes, heart failure and chronic hemodialysis]. 2284 58