(Na++K+)-ATPase activity in kidney basolateral membranes of non insulin dependent diabetic rats

Levy, Joseph; Avioli, Louis V.; Roberts, Marilyn L.; Gavin, James R.

doi:10.1016/s0006-291x(86)80321-7

Cited by 19 publications

(7 citation statements)

References 24 publications

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“…Note how insulin, which was reported to decrease 5'-nucleotidase activity of erythrocyte membrane (14), whereas it.retained this property in control cells, stimulates to nearly control levels the same activity in IDDM patients, a feature that, even though it appears to be shared by the Na + -pumping system, suggests some mediation exerted by the membrane microenvironment (40). The absence of insulin sensitivity observed in NIDDM (41) has also been reported for the Na + -K + -ATPase of rat kidney (42). Our results concerning Na + -K + -ATPase activity mea- Data are reported as relative molar percentages.…”

Section: Discussionmentioning

confidence: 61%

Membrane Lipid Alterations and Na+-Pumping Activity in Erythrocytes From IDDM and NIDDM Subjects

et al. 1989

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The Na+-pumping activity of the erythrocyte plasma membrane in diabetic subjects was studied together with the lipid composition. Insulin-dependent diabetes mellitus (IDDM) patients (n = 25) were divided into young (28.1 +/- 7.4 yr old, mean +/- SD; n = 16) and old (7.17 +/- 9.8 yr old; n = 10) subjects; the age of non-insulin-dependent (NIDDM) patients was 70.7 +/- 11.5 yr (n = 10). The Na+-pumping activity, estimated from both Na+-K+-ATPase and ouabain binding, was significantly decreased in IDDM and NIDDM subjects, but its insulin sensitivity was retained only in young IDDM subjects. The total cholesterol and phospholipid content of the erythrocyte plasma membrane was lowered in IDDM subjects, and cholesterol-to-phospholipid molar ratio was significantly decreased. In NIDDM subjects the significant decreased of the two lipid components did not alter their ratio. The analysis of major phospholipid components of erythrocyte membranes revealed that only phosphatidylcholine is significantly increased in young diabetic subjects. The fatty acid composition of major phospholipid classes was significantly altered in all cases: the unsaturation index appeared to be increased in phosphatidylserine and sphingomyelin for both IDDM and NIDDM subjects and was also increased in phosphatidylcholine in the latter group.

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Section: Discussionmentioning

confidence: 61%

Membrane Lipid Alterations and Na+-Pumping Activity in Erythrocytes From IDDM and NIDDM Subjects

et al. 1989

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“…Concerning data in experimental diabetes, Cohen and co‐workers (178), in STZ‐diabetic rats , reported a decreased kidney glomerular Na,K‐ATPase in animals with acute (<18 days) diabetes, but a significantly increased enzyme activity in rats with more chronic (>32 days) disease, which suggested that the time of the examination after the induction of diabetes is critical for the influence on Na,K‐ATPase activity. Other investigators, however, found an increased kidney Na,K‐ATPase in animal diabetes (179–183). In a recent study (22, Iannello et al ., unpublished), we observed an increased enzyme activity in the kidney of STZ‐diabetic Swiss mice and ob/ob mice .…”

Section: Literature Review and Discussionmentioning

confidence: 92%

Animal and human tissue Na,K‐ATPase in normal and insulin‐resistant states: regulation, behaviour and interpretative hypothesis on NEFA effects

2007

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The sodium(Na)- and potassium(K)-activated adenosine-triphosphatase (Na,K-ATPase) is a membrane enzyme that energizes the Na-pump by hydrolysing adenosine triphosphate and wasting energy as heat, so playing a role in thermogenesis and energy balance. Na,K-ATPase regulation by insulin is controversial; in tissue of hyperglycemic-hyperinsulinemic ob/ob mice, we reported a reduction, whereas in streptozotocin-treated hypoinsulinemic-diabetic Swiss and ob/ob mice we found an increased activity, which is against a genetic defect and suggests a regulation by hyperinsulinemia. In human adipose tissue from obese patients, Na,K-ATPase activity was reduced and negatively correlated with body mass index, oral glucose tolerance test-insulinemic area and blood pressure. We hypothesized that obesity is associated with tissue Na,K-ATPase reduction, apparently linked to hyperinsulinemia, which may repress or inactivate the enzyme, thus opposing thyroid hormones and influencing thermogenesis and obesity development. Insulin action on Na,K-ATPase, in vivo, might be mediated by the high level of non-esterified fatty acids, which are circulating enzyme inhibitors and increase in obesity, diabetes and hypertension. In this paper, we analyse animal and human tissue Na,K-ATPase, its level, and its regulation and behaviour in some hyperinsulinemic and insulin-resistant states; moreover, we discuss the link of the enzyme with non-esterified fatty acids and attempt to interpret and organize in a coherent view the whole body of the exhaustive literature on this complicated topic.

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“…However, several lines of evidence argue against it. These include: 1) In the diabetic animals kidney function and histology were shown to be normal [18] and the activity of another ATPase, (Na++K+)-ATPase, in their kidney BLM is not altered [44]; 2) The previously described loss of ability of insulin to regulate the (Ca 2+ + Mg2+)-ATPase activity in kidney BLM of diabetic rats could be reversed by physiologic perturbation (submitting the animals to an 18-h food restriction) [45]; 3) Abnormalities in (Ca2+ + Mg2 § -Pase were recently observed by us in erythrocyte membranes of diabetic animals (unpublished data) and by others [46], in erythrocytes of diabetic patients [46] revealing that the defect in this enzyme activity in diabetes is not restricted to kidney tissue and can occur in the absence of STZ; 4) Similar to our observations, alterations in membrane phospholipids content and behaviour (specifically PE) were described also in erythrocytes and platelets of diabetic patients [36,40]. Taken together, it appears that the possibility that our observations in the diabetic animals are due to toxic effects of STZ is unlikely.…”

Section: Discussionmentioning

confidence: 99%

Plasma membrane phospholipid content in non-insulin-dependent streptozotocin-diabetic rats — effect of insulin

et al. 1988

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The activity of (Ca 2-+ Mg 2 +)-ATPase is impaired in kidney basolateral membranes from non-insulin-dependent streptozotocin-diabetic rats. To study the possible role of changes in membrane phospholipid content in the malfunction of this enzyme in kidney membranes of the diabetic animals, phospholipid (phosphatidic acid, phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine, and sphingomyelin) content was measured in kidney and liver membranes obtained from non-insulin-dependent diabetic rats. Total phospholipid content was similar in liver and kidney membranes of diabetic and control rats (595+47 versus 624+29 in liver and 469+22 versus 458__+ 17 nmol Pi/mg protein in kidney respectively). Phosphatidylethanolamine content in kidney and liver membranes of diabetic rats was lower than in control rats (87.7___ 1.8 versus 96.4 + 2.2 nmol Pi/mg protein, p < 0.01 and 87.1 + 3.7 versus 101.8 + 3.5, p < 0.02 respectively). Phosphatidylinositol content was higher in kidney (28.0+0.6 versus 23.9+2.1, p< 0.02) but not liver membranes from diabetic rats.The in vitro direct effect of insulin on the phospholipid content in kidney membranes was also measured. Physiologic concentrations of insulin (718 pmol/l for 30 min) increased the phosphatidic acid content in membranes from control but not from diabetic rats by 34.2% (p <0.02). This rise was readily measurable after 3 min of exposure to insulin. Insulin did not induce a significant change in the content of any other phospholipid in membranes from control or diabetic rats.These differences in phospholipid content demonstrated in isolated membranes obtained from non-insulin-dependent diabetic and control rats, before and after exposure to insulin, may explain, in part, the impaired function of the (Ca2+ + Mf+)-ATPase observed previously in kidney membranes of the diabetic rats.

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(Na++K+)-ATPase activity in kidney basolateral membranes of non insulin dependent diabetic rats

Cited by 19 publications

References 24 publications

Membrane Lipid Alterations and Na+-Pumping Activity in Erythrocytes From IDDM and NIDDM Subjects

Membrane Lipid Alterations and Na+-Pumping Activity in Erythrocytes From IDDM and NIDDM Subjects

Animal and human tissue Na,K‐ATPase in normal and insulin‐resistant states: regulation, behaviour and interpretative hypothesis on NEFA effects

Plasma membrane phospholipid content in non-insulin-dependent streptozotocin-diabetic rats — effect of insulin

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