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  • 1
    ISSN: 1520-5835
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 88 (1966), S. 1786-1792 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 36 (1964), S. 2188-2189 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 80 (1958), S. 3607-3609 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 32 (1989), S. 329-329 
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Key words Insulin ; C-peptide ; fructosamine ; triglyceride ; birthweight ; fatty acid ; non-insulin-dependent diabetes mellitus.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Many ethnic groups at high risk of non-insulin-dependent diabetes mellitus are hyperinsulinaemic by early adult life. This study assessed whether such hyperinsulinaemia is present at birth. Cross sectional comparisons of maternal biochemistry, umbilical cord biochemistry and neonatal anthropometry were made between one ’low risk' and three ’high risk' ethnic groups, without diabetes in pregnancy in Auckland, New Zealand. The study comprised 123 European, Polynesian (Maori and Pacific Islands) and Indian normal pregnancies. Indian mothers were the smallest, with the highest insulin and non-esterified fatty acid concentrations. Polynesian mothers were the most obese with a higher fructosamine concentration. From these pregnancies, Indian neonates were smaller, slimmer, with the highest cord triglyceride (0.6 mmol/l vs 0.4 mmol/l, p 〈 0.01), and lowest cord insulin concentrations (7.1 mU/l vs 8.6 mU/l (European), 9.2 mU/l (Polynesian), p 〈 0.05). Polynesian babies had a high cord insulin: C-peptide ratio (52.5 mU/nmol vs 44.4 mU/nmol (European), 44.1 mU/nmol (Indian), p = 0.05). Although reduced intrauterine growth may contribute to the excess of diabetes and heart disease in Indians, it cannot explain the excess of diabetes in Polynesians. Exposure to minor relative maternal hyperglycaemia in the mother and abnormal neonatal insulin handling (as demonstrated by the higher insulin: C-peptide ratio) may be of long-term significance in Polynesians. [Diabetologia (1994) 37: 930–936]
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0428
    Keywords: (Na+, K+)-ATPase ; adenosine ; glucose ; myo-inositol ; aorta
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mechanism by which hyperglycaemia causes decreased (Na+, K+)-ATPase activity preventable by aldose reductase inhibitors and by raising plasma myo-inositol in specific tissues can be activated in vitro in normal rabbit aortic wall; it selectively inhibits a component of resting (Na+, K+)-ATPase activity maintained by a novel regulatory system through rapid basal phosphatidylinositol turnover (hydrolysis) in a discrete pool, which is replenished by a fraction of phosphatidylinositol synthesis that selectively requires myoinositol transport. A role for endogenously released adenosine in this regulatory system was examined. Adding adenosine deaminase or 8-phenyltheophylline, an adenosine receptor antagonist, selectively inhibited the component of (Na+, K+)-ATPase activity maintained by the regulatory system; when inhibited with adenosine deaminase this component was restored by 2-chloroadenosine, 5′-N-ethylcarboxamidoadenosine, and 1-oleoyl-2-acetylglycerol, but not by forskolin (which also did not inhibit this component). Adenosine deaminase inhibited the rapid basal turnover of the discrete phosphatidylinositol pool, and 2-chloroadenosine then stimulated its turnover. Raising medium glucose from 5 to 10–30 mmol/l inhibits the regulatory system by making myo-inositol transport at a normal plasma level inadequate to maintain the replenishment of the discrete phosphatidylinositol pool. 2-Chloroadenosine stimulation of the “adenosine-sensitive” component of (Na+, K+)-ATPase activity was inhibited in tissue incubated with 30 mmol/l glucose and myoinositol in a normal plasma level, but this effect was demonstrable when the medium myo-inositol was raised seven-fold. Hyperglycaemia-induced decreased (Na+, K+)-ATPase activity that is preventable by aldose reductase inhibitors and by raising plasma myo-inositol results from the inhibition of a novel adenosine-(Na+, K+)-ATPase regulatory system.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 36 (1993), S. 212-217 
    ISSN: 1432-0428
    Keywords: Na+-K+-ATPase ; insulin ; vascular smooth muscle ; vasodilation ; vasoconstriction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To determine whether insulin regulates vascular smooth muscle Na+, K+-ATPase activity and if impaired insulin stimulation of vascular smooth muscle Na+, K+-ATPase activity could be a cause of increased vascular reactivity to norepinephrine and angiotensin II in diabetic states, the effects of insulin on Na+, K+-ATPase activity were examined in normal rabbit aortic intima-media incubated with normal plasma glucose and myo-inositol levels for 30 min. Insulin at 100 μU/ml (600 pmol/l) had no effect on Na+, K+-ATPase activity. At 250 μU/ml it caused a 4.2±0.8% increase, and at 500 μU/ml insulin caused a 17.7±1.4% increase in Na+, K+-ATPase activity that was completely inhibited by amiloride (1 mmol/l). Human insulin-like growth factor I (600 pmol/l) caused an 18.0±1.0% increase in Na+, K+-ATPase activity that was inhibited by amiloride. Insulin does not regulate (stimulate) aortic vascular smooth muscle Na+, K+-ATPase activity. Supraphysiological insulin concentrations, probably acting through an insulin-like growth factor I receptor, stimulate Na+/H+ exchange in aortic vascular smooth muscle and cause small secondary increases in Na+, K+-ATPase activity. In aortic intima-media incubated with normal plasma glucose and myo-inositol levels, endogenously released adenosine stimulates and maintains a component of resting Na+, K+-ATPase activity and stimulates acute increases in activity when norepinephrine (1 μmol/l) or angiotensin II (100 nmol/l) is added. These adenosine-stimulated components of Na+, K+-ATPase activity are selectively inhibited when the medium glucose is raised to 30 mmol/l during a 30-min equilibration and 30-min incubation. Insulin (100 μU/ml) added during the incubation had no effect on the alterations in Na+, K+-ATPase activity induced by glucose at an elevated plasma level. Impaired insulin stimulation of vascular smooth muscle Na+, K+-ATPase activity is not a possible cause for alterations in vascular reactivity in diabetes.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0428
    Keywords: Aorta ; (Na+, K+)-ATPase ; adenosine ; angiotensin II ; norepinephrine ; hyperglycaemia ; vasodilation ; vasoconstriction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The (Na+, K+)-ATPase activity operative in rabbit aortic intima-media incubated with normal plasma levels of glucose and myo-inositol (70 μmol/l) is decreased when the glucose content of the medium is raised from 5 to 10 mmol/l or higher; this effect is prevented by aldose reductase inhibitors and by raising the myo-inositol content of the medium to 500 μmol/l. The decrease in (Na+, K+)-ATPase activity results from the loss of a component normally regulated (stimulated) by endogenously released adenosine through a receptor that stimulates phosphatidylinositol turnover in a discrete pool. The replenishment of this phosphatidylinositol pool selectively requires myo-inositol transport and is inhibited when increased polyol pathway activity impairs myo-inositol transport at a normal plasma level. Adenosine is a vasodilator, some endothelium-released vasodilators modulate the responses to vasoconstrictors by stimulating an increase in (Na+, K+)-ATPase activity in vascular smooth muscle. Whether adenosine mediates this effect in angiotensin II or norepinephrine-stimulated aorta was examined. Angiotensin II (100 nmol/l) and norepinephrine (1 μmol/l) evoked marked increases in (Na+, K+)-ATPase activity in aortic intima-media incubated with 5 mmol/l glucose and 70 μmol/l myo-inositol, which were inhibited when adenosine deaminase was added or the medium myo-inositol omitted to inhibit myo-inositol transport. Raising the medium glucose to 30 mmol/l inhibited the angiotensin II and norepinephrine evoked increases in (Na+, K+)-ATPase activity, and this was prevented when tolrestat (10 μmol/l) was added or the myo-inositol content of the medium was raised from 70 to 500 μmol/l. Hyperglycaemia causes decreased (Na+, K+)-ATPase activity prevented by aldose reductase inhibitors and by raising plasma myo-inositol by a mechanism which inhibits an adenosine-(Na+, K+)-ATPase regulatory system, which modulates the responses to angiotensin II and norepinephrine in some blood vessels.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0428
    Keywords: Sodium ; leucocytes ; amiloride ; protein kinase ; Type 1 (insulin-dependent) diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It is uncertain why only one third of Type 1 (insulin-dependent) diabetic patients develop nephropathy. One suggestion is the inheritance of a predisposition to essential hypertension. We have previously found elevated Na+/H+ antiport activity and a raised intracellular pH in leucocytes from hypertensive and Type 1 diabetic subjects with albuminuria using a novel double ionophore fluorimetric technique. These changes are not found in Type 1 diabetic subjects without albuminuria. We wished to test the effect of a protein kinase C inhibitor staurosporine (100 nmol/l) on the elevated antiport activity, and the degree of stimulation achieved by exogenous diacyl glycerol. Raised leucocyte Na+/H+ antiport activity of Type 1 diabetic subjects with albuminuria (73.8±17.2 mmol·l−1·min−1) was restored to normal levels with staurosporine (54.9±17.9 mmol·l−1·min−1, p〈0.001). The leucocyte Na+/H+ antiport activity of diabetic subjects without albuminuria fell significantly also with staurosporine but to a lesser extent (57.3±11.6 to 50.0±12.8 mmol/l, p〈0.003). In contrast, leucocytes from normal control subjects showed no change in antiport activity with staurosporine (54.3±8.5 to 52.6±10.4 mmol ·1−1·min−1). Dioctanoyl glycerol stimulated the leucocyte Na+/H+ antiport in normal subjects and diabetic patients without albuminuria, with significantly less stimulation in diabetic patients with albuminuria. We conclude that reversal by staurosporine of the elevated Na+/H+ antiport activity in Type 1 diabetic subjects with albuminuria could indicate a role for protein kinase C in activating the antiport. This hypothesis is supported by the reduced stimulation of the antiport by dioctanoyl glycerol in this group of patients.
    Type of Medium: Electronic Resource
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