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

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.
 ...
PMID:Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms. 129 67

A large body of evidence demonstrates the prevalence and adverse clinical consequences of magnesium deficiency in patients with diabetes mellitus. It would be prudent for physicians who treat these patients to consider magnesium deficiency as a contributing factor in many diabetic complications and in exacerbation of the disease itself. Repletion of the deficiency or prophylactic supplementation with oral magnesium may help avoid or ameliorate such complications as arrhythmias, hypertension, and sudden cardiac death and may even improve the course of the diabetic condition.
 ...
PMID:Magnesium deficiency and diabetes mellitus. Causes and effects. 140 73

Magnesium deficiency is common but difficult to diagnose and to assess in clinical practice. The use of a magnesium loading test was therefore evaluated to diagnose magnesium deficiency in 661 hospitalized patients with medical conditions assumed to interfere with magnesium uptake and excretion. Thirty millimoles of magnesium sulphate were administered intravenously during 8 h as a loading test and related to the urinary excretion in the following 24 h. A group of 30 patients without any known predisposition for magnesium deficiency and a group of 27 healthy volunteers served as controls. The mean (with 95% confidence interval) magnesium retention was 4 (-2-10)% in the control group of patients and 3 (-2-8)% in healthy subjects. A significantly higher retention was observed in all the groups of the patients: atrial fibrillation 18 (11-25)%, other arrhythmias 18 (11-24)%, hypertension 27 (20-33)%, coronary artery disease 25 (20-30)%, congestive heart failure 31 (26-37)%, cerebrovascular events 38 (24-51)%, gastrointestinal disorders 22 (14-29)%, diabetes mellitus 16 (9-22)%, and alcoholics 33 (29-36)%. The percentage of patients with a retention greater than mean + 2 SD of the two control groups varied between 22% and 54% among the different patient groups. The mean serum magnesium among the patient groups was similar to the control group of patients, except for the alcoholics, hypertensives and young healthy controls, who had significantly reduced levels. Magnesium retention was significantly correlated to age and renal function, and among the alcoholics negatively correlated to serum magnesium.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Magnesium deficiency diagnosed by an intravenous loading test. 143 10

Diabetes mellitus is the most frequent chronic disease associated with secondary magnesium deficit. Hypomagnesaemia is a central feature of the deficit, which is often reported in experimental and clinical forms of the disease. In diabetic rats as in man, plasma magnesium concentrations may correlate inversely with the degree of hyperglycaemia. The duration of the disease also appears to be relevant. The hypomagnesaemia of diabetes might be expected to affect intracellular concentrations of the ion. However, although some animal and clinical studies have reported subnormal magnesium concentrations in blood cells, bone, and soft tissues of diabetics, the relationship between plasma magnesium concentration and intracellular level of the ion is inconsistent. Clinical studies have speculated on a potential link between the magnesium deficit of diabetes and several diabetic complications, including cardiovascular problems and retinopathy. Recent experimental studies are largely supportive of such a link; myocardial disorders associated with magnesium deficiency have been reported in diabetic mice and rabbits. It is possible that a common mechanism involving magnesium may be responsible for some of the diverse complications of diabetes. The aetiology of hypomagnesaemia in diabetes is complex. Nevertheless, plasma magnesium concentrations are ultimately determined by four processes: intake, gastrointestinal absorption, redistribution within body pools, and urinary excretion. This review considers in turn the potential role of each of these processes in the development of diabetic hypomagnesaemia. Both experimental and clinical studies suggest that hypermagnesiuria may be the major factor involved. Recent animal studies have described a specific renal tubular magnesium defect in diabetes, which, together with the osmotic diuresis, is responsible for large magnesium losses. The precise cause of the defect is unknown, but it may relate to the prolonged hyperglycaemia, insulinopenia, disturbance of phosphate metabolism, or other hormonal changes which characterize the disease.
 ...
PMID:New experimental data on the relationship between diabetes mellitus and magnesium. 146 58

In order to determine the effects of hypoinsulinaemia or hyperinsulinaemia on nephrocalcinosis induced by the interaction between fructose and magnesium (Mg) deficiency, we compared kidney calcification in obese versus lean, and non-diabetic versus diabetic female Zucker rats fed a magnesium-deficient fructose diet. One half of the obese and lean animals, respectively, was injected with streptozotocin to produce diabetes, and the other half was injected with citrate buffer alone. Diabetic, non-diabetic, obese, and lean animals were divided into two dietary groups, consisting of high starch or high fructose without added Mg. After a four week period, 24 hour urine was collected for urinary output, protein, oxalate, citrate, MG, and calcium (Ca) measurements. The animals were then decapitated, and blood was collected for glucose, Mg, and Ca determinations, and kidneys were removed to determine their Mg and Ca contents. All fructose-fed animals exhibited significantly more kidney Ca then the starch-fed animals. Lean non-diabetic rats fed fructose showed the greatest kidney Ca along with the greatest urinary protein excretion among all experimental groups. The significant finding in the present study is that diabetes or obesity reduced nephrocalcinosis regardless of the insulin status of the rats. Diuresis and hypercitraturia in diabetic and/or obese animals may cause a reduction in nephrocalcinosis induced by the interaction between fructose and magnesium deficiency. Hyperproteinuria (uromucoid) in combination with hypercalciuria and hypomagnesuria may be responsible for greater nephrocalcinosis in the fructose than the starch group. The possible mechanisms for this interaction on nephrocalcinosis have been discussed.
 ...
PMID:Comparison of renal calcium concentration in obese, lean, diabetic, and non-diabetic Zucker rats fed a magnesium-deficient fructose diet. 183 14

Because insulin-dependent diabetes mellitus is associated with altered electrolyte metabolism and a derangement of the parathyroid hormone (PTH)-vitamin D endocrine system, we studied 23 children with diabetes (age 9.4 +/- 2.5 years) and found lower serum values for total and ionized calcium, magnesium, intact PTH, calcitriol, and osteocalcin than in age- and sex-matched control subjects. All patients were given magnesium orally (6 mg/kg daily of elemental magnesium) for up to 60 days. During treatment, serum magnesium, total and ionized calcium, intact PTH, calcitriol, and osteocalcin concentrations significantly increased, reaching control values. After a 3-day low-calcium diet, the patients had a significantly reduced delta-increment of PTH and calcitriol in comparison with values obtained during hypomagnesemia. After magnesium repletion, the delta-increments of both PTH and calcitriol, in response to the low-calcium diet, were not significantly different from control values. These data suggest that magnesium deficiency plays a pivotal role in altering mineral homeostasis in insulin-dependent diabetes mellitus.
 ...
PMID:Hypomagnesemia and the parathyroid hormone-vitamin D endocrine system in children with insulin-dependent diabetes mellitus: effects of magnesium administration. 191 9

There is accumulating evidence that the changes which occur in the metabolism of some micronutrients in diabetes mellitus might have a specific role in the pathogenesis and complications of this disease. Magnesium deficiency is the most evident disturbance of metal metabolism in insulin-dependent diabetes mellitus. Hypomagnesemia has been linked both to the acute metabolic and late chronic complication of diabetes. Of particular concern, is the association between hypomagnesemia and ischemic heart disease and severe retinopathy in humans with diabetes mellitus. Appropriate magnesium supplementation might prove beneficial in normalizing the low plasma and tissue magnesium levels and prevent or retard the development of vascular complications in diabetic patients. However, well designed and documented experiments need to be performed before the rationales for such therapy are well established.
Diabetes Res Clin Pract
PMID:Magnesium and insulin-dependent diabetes mellitus. 207 66

Careful consideration of all relevant scientific evidence and a critical assessment of data quality show that thiazide diuretics are not cardiotoxic. Of 12 reported trials only two recorded more coronary heart disease events in thiazide-treated patients than in controls. One of these two was a subgroup of a larger study (Heart Attack Prevention in Primary Hypertension, HAPPHY) which found no difference between thiazide-treated and beta-blocker-treated patients. The other, the Oslo study, was too small to allow valid conclusions. Results from a subgroup in the Multiple Risk Factor Intervention Trial (MRFIT) that appeared to supply evidence for thiazide-related cardiotoxicity are suspect when examined critically. Further evidence from 24- to 28-h ECG monitoring does not support the hypothesis that thiazide diuretics, either in the presence or absence of hypokalemia, increase the frequency or severity of ventricular arrhythmias. Reports of a thiazide-induced intracellular magnesium deficiency as a cause of ventricular arrhythmias have also not been confirmed; the development of arrhythmias in acute myocardial infarction appears to be due to an increase in catecholamine levels rather than hypokalemia. There appears to be little evidence to support the assumption that long-term use of thiazide diuretics aggravates or accelerates atherosclerosis of the coronary arteries; any fall in serum cholesterol appears to be transient. For the great majority of patients with uncomplicated hypertension, without a previous myocardial infarction, congestive heart failure, diabetes mellitus or gout, thiazide diuretics appear to be both safe and effective antihypertensive agents.
 ...
PMID:The cardiotoxicity of thiazide diuretics: review of the evidence. 221 84

A common complication of critically ill patients is cardiac tachyarrhythmia. The role played by magnesium is not well appreciated. Well-documented cases indicated that magnesium may be effective in controlling the rhythm when conventional methods fail. The following tachyarrhythmias respond favorably to magnesium: (1) intractable ventricular tachycardia and fibrillation, whether hypo- or normomagnesemic, (2) torsades de pointes, (3) digitalis-toxic ventricular tachyarrhythmia, (4) multifocal atrial tachycardia and (5) hypomagnesemic atrial tachyarrhythmia. It is recommended that 10-15 ml of 20% MgSO4 be infused over 1 min, followed by 500 ml of 2% MgSO4 over 5 h. A second 500 ml over 10 h may be necessary. Renal failure, disappearance of deep tendon reflex, rise in serum Mg above 5 mEq/l, drop in systolic blood pressure below 80 or drop in pulse below 60 contraindicate the continued use of magnesium. If serum potassium is at or falls below 4.0 mEq/l, 20-40 mEq/l KCl should be added. Magnesium deficiency can be confirmed by a low serum level or by a greater than 50% retention of administered magnesium. The causes of magnesium deficiency can be remembered under 10 DS: (1) Diarrhea and gastrointestinal losses, (2) Diuretics and renal losses, (3) Diabetes and endocrine causes, (4) Dietary lack, (5) Diverted to free fatty acids, (6) Drugs such as cisplatin, (7) Drinking alcohol to excess, (8) Delivery with toxemia, (9) Decompensated heart, lungs or liver and (10) Denuded skin, such as burns.
 ...
PMID:Magnesium therapy of cardiac arrhythmias in critical-care medicine. 269 48

Magnesium has been a controversial issue in cardiology for a long time. The following facts are now known: Magnesium plays a decisive role in the treatment of malign ventricular rhythm disturbances; this is especially true for Torsade pointes, which is connected with post-depolarisation and frequently causes sudden cardiac death. In the critical infarction phase intravenous magnesium therapy results in a reduction of malign rhythm disturbances and of the mortality rate. Magnesium plays a role in glycoside intolerance in patients with congestive heart failure. Magnesium deficiency is an important but rather neglected intermediary factor for the occurrence of (avoidable) side effects of renal, ototoxic and cardiac nature, emerge when using cytostatics, immunosuppressives and antibiotics. In several types of poisoning, but also in many other emergency situations with high levels of catecholamine (tetanus, phaeochromocytoma) magnesium can be used as an antidote. Clinically significant situations in which the role of magnesium has been either demonstrated or is still to be determined include diabetes (frequent deficiency demonstrated, significance for late complications under review), alcohol abuse (frequent deficiency of magnesium and its significance for rhythm disturbances demonstrated, correlations with other complications under review), tetanic syndrome, numerous psychiatric-neuromuscular disturbances, including generalized convulsive attacks, transitional syndromes, thromboembolic complications, lipometabolism disturbances, TIAS, PRINDS and loss of hearing.
 ...
PMID:[Magnesium in cardiology. A challenge for new studies]. 305 94


1 2 3 4 5 6 7 8 Next >>