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  • 1
    ISSN: 1432-0428
    Keywords: Magnesium ; insulin receptors ; tyrosine kinase ; skeletal muscle ; insulin secretion ; glucose disposal ; GLUT 4
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The 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/l, p〈0.001), 2) higher basal serum glucose (6.8±0.2 vs 5.5±0.2 mmol/l, 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 5×10−10 mol/l (3.0±0.9 vs 5.4±0.6, p〈0.05) and 5×10−9mol/l (6.3±0.5 vs 8.0±0.5, p〈0.05), 3) normal glucose uptake at a maximal insulin concentration of 1×10−7 mol/l, and 4) 50% reduction in the insulin sensitivity (ED50: 1.3±0.3 vs 0.55±0.1 mol/l, 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 Β-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.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Gliclazide ; skeletal muscle ; glucose uptake ; hindquarter perfusion ; insulin ; ATP-sensitive ; K+ channels ; diazoxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We studied the effect of gliclazide, a second-generation sulphonylurea, on rat skeletal muscle glucose uptake using perfused hindquarter muscle preparations. Gliclazide at concentrations of 10 to 1000 Μg/ml increased (p〈0.05) the basal glucose uptake. The effect of gliclazide on glucose uptake was immediate and dose-dependent, reaching a plateau at a concentration of 300 Μg/ml; the half-maximal effect was obtained between 25 and 50 Μg/ml. The glucose uptake stimulated by gliclazide (300–1000 Μg/ ml) did not differ from that achieved by 10−9 mol/l insulin, and was lower (p〈0.05) than that obtained with 10−7 mol/l insulin. The combination of gliclazide (300 Μg/ml) and 10−9 mol/l insulin produced an increase in glucose uptake (7.7±0.6 Μmol · g−1 · h−1, n=8, mean±SEM) which was higher (p〈0.05) than that achieved with 10−9 mol/l insulin (5.6±0.7 Μmol · g−1 · h−1, n=11) and not different from that obtained with 10−7 mol/l insulin (9.8±1.0 Μmol · g−1 · h−1, n=11). Diazoxide (100 Μmol/l), an ATP-sensitive K+ channel opener, reversed the stimulatory effect of gliclazide (100 Μg/ml) on muscle glucose uptake from 3.1±0.4 to 0.5±0.2 Μmol · g−1 · h−1, (n=7, p〈0.001). The addition of diazoxide prior to gliclazide into the perfusion medium blocked the gliclazide-induced glucose uptake by the hindquarter muscle preparations. In conclusion, gliclazide alone has an immediate stimulatory effect on glucose uptake by skeletal muscle and together with insulin has an additive effect on muscle glucose uptake. The effect of gliclazide on muscle glucose uptake seems to be due to the inhibition of ATP-sensitive K+ channels.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Key words Magnesium ; insulin receptors ; tyrosine kinase ; skeletal muscle ; insulin secretion ; glucose disposal ; GLUT 4.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The 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/l, p 〈 0.001), 2) higher basal serum glucose (6.8 ± 0.2 vs 5.5 ± 0.2 mmol/l, 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 × 10−10 mol/l (3.0 ± 0.9 vs 5.4 ± 0.6, p 〈 0.05) and 5 × 10−9 mol/l (6.3 ± 0.5 vs 8.0 ± 0.5, p 〈 0.05), 3) normal glucose uptake at a maximal insulin concentration of 1 × 10−7 mol/l, and 4) 50 % reduction in the insulin sensitivity (ED50: 1.3 ± 0.3 vs 0.55 ± 0.1 mol/l, 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 β -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. [Diabetologia (1995) 38: 1262–1270]
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 171 (1990), S. 182-188 
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 0090-6980
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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