Magnesium, a second messenger for insulin: Ion translocation coupled to transport activity

Lostroh, Ardis J.; Krahl, M. E.

doi:10.1016/0065-2571(74)90007-7

Cited by 51 publications

(20 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…(311,322,503). Most recently in a study on T-cell activation, MagT1 channels were shown to mediate Mg 2ϩ influx upon T-cell receptor activation and EGF stimulation (311).…”

Section: Othersmentioning

confidence: 99%

Magnesium in Man: Implications for Health and Disease

Baaij

Hoenderop

Bindels

2015

Physiological Reviews

1,245

1,363

View full text Add to dashboard Cite

show abstract

“…(311,322,503). Most recently in a study on T-cell activation, MagT1 channels were shown to mediate Mg 2ϩ influx upon T-cell receptor activation and EGF stimulation (311).…”

Section: Othersmentioning

confidence: 99%

Magnesium in Man: Implications for Health and Disease

Baaij

Hoenderop

Bindels

2015

Physiological Reviews

1,245

1,363

View full text Add to dashboard Cite

show abstract

“…On the other hand, magnesium is a cofactor of many enzymes involved in glucose metabolism, especially those using high energy phosphate bonds [6]. In vitro studies have shown that this cation has an important role in insulin action [1,7]. A relation-ship between hypomagnesaemia and insulin resistance has been reported among diabetic patients [8,9], and furthermore, chronic administration of magnesium has been found to improve the insulin sensitivity in non-insulin-dependent diabetic subjects [10] and in patients with severe hypomagnesaemia [11].…”

mentioning

confidence: 99%

Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats

Su�rez¹,

Pulido

Casla

et al. 1995

Diabetologia

View full text Add to dashboard Cite

SummaryThe effect of magnesium deficiency on glucose disposal, glucose-stimulated insulin secretion and insulin action on skeletal muscle was investigated in rats which were fed a low magnesium-containing diet for 4 days. Control rats were fed a standard diet. Compared to the control rats, the rats fed with low magnesium diet presented: 1) lower serum magnesium levels (0.45 + 0.02 vs 0.78 + 0.01 mmol/1, p < 0.001), 2) higher basal serum glucose (6.8 +__ 0.2 vs 5.5 + 0.2 mmol/1, p < 0.05) and similar basal serum insulin, 3) 40 % reduction (p < 0.001) in the glucose disappearance rate after its i.v. administration, and 4) 45 % reduction (p < 0.05) in the glucose-stimulated insulin secretion. The insulin action upon the glucose uptake by skeletal muscle was determined by means of hindquarter perfusions. Compared with control rats, magnesium-deficient rats presented: 1) normal basal glucose uptake, 2) lower stimulatory effect on the glucose uptake by insulin at the concentrations of 5 x 10 -l~ mol/1 (3.0 + 0.9 vs 5.4 + 0.6, p < 0.05) and 5 x 10 -9 tool/1 (6.3 + 0.5 vs 8.0 + 0.5, p < 0.05), 3) normal glucose uptake at a maximal insulin concentration of i x 10 .7 mol/1, and 4) 50 % reduction in the insulin sensitivity (ED50:1.3 +_ 0.3 vs 0.55 + 0.1 mol/1, p < 0.05). In partially purified insulin receptors prepared from gastrocnemius muscle, 125I-insulin binding was similar in both groups of rats. However, the autophosphorylation of the fi-subunit of the insulin receptor was significantly reduced by 50 % in magnesium-deficient rats and the tyrosine kinase activity of insulin receptors toward the exogenous substrate Poly Glu4: Tyr 1 was also reduced (p < 0.05) by hypomagnesaemia. The abundance of the insulin-sensitive glucose transporter protein (muscle/fat GLUT4), measured by Western blot analysis using polyclonal antisera, was similar in muscles of control and hypomagnesaemic rats. These findings indicate that hypomagnesaemia has a deleterious effect on glucose metabolism due to an impairment of both insulin secretion and action. The insulin resistance observed in skeletal muscle of magnesium-deficient rats may be attributed, at least in part, to a defective tyrosine kinase activity of insulin receptors.

show abstract

“…A insulina, entre outros hormônios, tem sido reconhecida como uma substância regulatória importante para o balanço do Mg. Lostroh & Krahl (1974) demonstraram que a insulina adicionada in vitro promove aumento no acúmulo de magnésio e potássio nas células do músculo liso do útero de ratas. Segundo sugerem os autores, a insulina, após se ligar ao seu receptor da membrana plasmática, pode afetar uma bomba ATPase, aumentando a entrada de magnésio e potássio na célula.…”

Section: A Deficiência De Magnésio Como Resultado Da Resistência à Inunclassified

“…Sanui & Rubin (1978), ratificaram o conceito anterior (Lostroh & Krahl, 1974) sobre o magnésio como segundo mensageiro na ação da insulina. Através de estudos in vitro utilizando fibroblastos embrionários de galinha, Sanui & Rubin (1978) descreveram que os efeitos metabólicos da insulina dependeram de mudanças no transporte e conteúdo catiônico celular.…”

Section: A Deficiência De Magnésio Levando Ao Desenvolvimento Da Resiunclassified

Alterações do metabolismo da glicose na deficiência de magnésio

2002

View full text Add to dashboard Cite

O magnésio é um cátion essencial o qual age como co-fator para adenosina trifosfatases em inúmeras reações enzimáticas. Vários estudos mostram seu envolvimento na ação e secreção de insulina e os efeitos deste hormônio sobre o metabolismo e transporte do magnésio. Entretanto, os resultados são conflitantes. Sugerem que a deficiência de magnésio está implicada direta ou indiretamente com a resistência à insulina no diabetes mellitus, enquanto outros descrevem uma relação inversa ou, ainda, um aumento da captação de glicose decorrente da falta de magnésio. A interação deste cátion com outros íons, os mecanismos hormonais e neuro-hormonais compensadores e possivelmente a duração da deficiência são alguns dos fatores descritos como responsáveis pelas variações na regulação glicêmica observadas durante a deficiência de magnésio.

show abstract

Magnesium, a second messenger for insulin: Ion translocation coupled to transport activity

Cited by 51 publications

References 22 publications

Magnesium in Man: Implications for Health and Disease

Magnesium in Man: Implications for Health and Disease

Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats

Alterações do metabolismo da glicose na deficiência de magnésio

Contact Info

Product

Resources

About