Animal and Human Tissue Na,K-ATPase in Obesity and Diabetes: A New Proposed Enzyme Regulation

Iannello, Silvia; Milazzo, Paolina; Belfiore, Francesco

doi:10.1097/00000441-200701000-00001

Cited by 39 publications

(24 citation statements)

References 32 publications

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“…There is an agreement in the literature on the diabetes-associated reduction in Na + /K + ATPase activity [10,12]. However, our present study is a first in the demonstration of a positive effect of the selenium treatment on Na + /K + pump activity in diabetic vascular tissue.…”

Section: Discussionsupporting

confidence: 86%

“…Dysfunction of the diabetic vascular tissues involve reduced nitric oxide (NO) production, increased VSMC proliferation, and vessel wall thickening [9]. It is also reported that diabetes causes a reduction in Na + /K + ATPase (NKA) expression and activity [10][11][12]. NKA is possibly the most important membrane protein for cell survival, since its function is necessary for establishing and protecting the ion gradients and voltage across the membrane of all mammalian cells.…”

mentioning

confidence: 99%

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Selenium Inhibits Proliferation Signaling and Restores Sodium/Potassium Pump Function of Diabetic Rat Aorta

Aydemir-Koksoy

Turan

2008

Biol Trace Elem Res

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Diabetes is characterized with increased oxidant stress, vasculopathy, and neuropathy. In diabetic vasculopathy, the observed thickening of the media and intima is not only a result of vascular smooth muscle cell proliferation but also due to modification of the extracellular matrix by these cells. Also, there is hampered membrane function and a reduction in sodium pump expression in the vessels of the diabetic animals. Selenium, being a trace element, has both insulinomimetic and antioxidant effects. Thus, we hypothesized that selenium treatment will reduce proliferation, restore physiology, and correct increased proliferation signaling of diabetic aorta. Diabetes was induced by streptozotocin (50 mg/kg body weight), and rats were then treated with sodium selenate (15 mumol/kg body weight/day) for 4 weeks. Our data from diabetic rats showed an increase in proliferation rate and matrix metalloproteinase activity in aortic cell cultures. We observed marked increases in MAPK phosphorylation and caveolin 1 expression but a decrease in Na(+)/K(+) ATPase activity in diabetic rat aorta homogenates. Selenium treatment resulted in complete normalization of the above parameters to control level, while it increased Na(+)/K(+) pump activity by 40%. Our results suggest that selenium treatment of diabetics can play beneficial role in protecting vascular architecture and function against diabetes-induced pathology.

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Section: Discussionsupporting

confidence: 86%

mentioning

confidence: 99%

Selenium Inhibits Proliferation Signaling and Restores Sodium/Potassium Pump Function of Diabetic Rat Aorta

Aydemir-Koksoy

Turan

2008

Biol Trace Elem Res

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“…Another good candidate in the 1q24 region is the ATP1B1 gene, which encodes for the ␤-1 subunit of the Na ϩ /K ϩ ATPase protein, as the ATPase activity has been correlated with obesity and energy consumption in several studies (37,38). Additional plausible candidate genes include PRDX6, PLA2G4A, and SOAT1 genes, which are all involved in the phospholipids or cholesterol metabolism.…”

Section: Discussionmentioning

confidence: 99%

Identification and Replication of a Novel Obesity Locus on Chromosome 1q24 in Isolated Populations of Cilento

et al. 2008

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OBJECTIVE-Obesity is a complex trait with a variety of genetic susceptibility variants. Several loci linked to obesity and/or obesity-related traits have been identified, and relatively few regions have been replicated. Studying isolated populations can be a useful approach to identify rare variants that will not be detected with whole-genome association studies in large populations.RESEARCH DESIGN AND METHODS-Random individuals were sampled from Campora, an isolated village of the Cilento area in South Italy, phenotyped for BMI, and genotyped using a dense microsatellite marker map. An efficient pedigree-breaking strategy was applied to perform genome-wide linkage analyses of both BMI and obesity. Significance was assessed with ad hoc simulations for the two traits and with an original local false discovery rate approach to quantitative trait linkage analysis for BMI. A genealogy-corrected association test was performed for a single nucleotide polymorphism located in one of the linkage regions. A replication study was conducted in the neighboring village of Gioi.RESULTS-A new locus on chr1q24 significantly linked to BMI was identified in Campora. Linkage at the same locus is suggested with obesity. Three additional loci linked to BMI were also detected, including the locus including the INSIG2 gene region. No evidence of association between the rs7566605 variant and BMI or obesity was found. In Gioi, the linkage on chr1q24 was replicated with both BMI and obesity.CONCLUSIONS-Overall, our results confirm that successful linkage studies can be accomplished in these populations both to replicate known linkages and to identify novel quantitative trait linkages. Diabetes 57: [783][784][785][786][787][788][789][790] 2008

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“…In cardiac muscle, Na + /K + -ATPase plays a crucial role in the regulation of cardiac electrophysiology and cardiomyocytes contractility, while various cardiac disorders including cardiac hypertrophy and hypertension, which commonly occur as a consequence of obesity, are associated with reduction of Na + /K + -ATPase activity and expression [18,19,41,37]. We have previously reported that in the hypertrophic heart of male rats a HF diet reduces the activity and expression of the ɑ1 and ɑ2 subunits of Na + /K + -ATPase, while estradiol treatment reduced heart hypertrophy and increased Na + /K + -ATPase expression/activity [42,39].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, obesity is associated with the reduction of Na + /K + -ATPase activity in heart, skeletal muscle and liver, probably due to the development of IR since it has been shown that INS induces translocation of Na + /K + -ATPase subunits from intracellular stores to plasma membrane by a phosphatidylinositol 3-kinase (PI3K) dependent pathway [16][17][18][19]. In addition, gender-specific regulation of Na + /K + -ATPase exist, and estradiol exerts its cardioprotective effects partially by up-regulating Na + /K + -ATPase activity/expression [20][21][22].…”

Section: Introductionmentioning

confidence: 99%

Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet

et al. 2017

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Animal and Human Tissue Na,K-ATPase in Obesity and Diabetes: A New Proposed Enzyme Regulation

Cited by 39 publications

References 32 publications

Selenium Inhibits Proliferation Signaling and Restores Sodium/Potassium Pump Function of Diabetic Rat Aorta

Selenium Inhibits Proliferation Signaling and Restores Sodium/Potassium Pump Function of Diabetic Rat Aorta

Identification and Replication of a Novel Obesity Locus on Chromosome 1q24 in Isolated Populations of Cilento

Changes in cardiac Na+/K+-ATPase expression and activity in female rats fed a high-fat diet

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