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Wyszukujesz frazę "leptin" wg kryterium: Temat


Wyświetlanie 1-3 z 3
Tytuł:
Spectrophotometric assay of renal ouabain-resistant Na+-ATPase and its regulation by leptin and dietary-induced obesity.
Autorzy:
Bełtowski, Jerzy
Jamroz-Wiśniewska, Anna
Nazar, Jarosław
Wójcicka, Grażyna
Powiązania:
https://bibliotekanauki.pl/articles/1041514.pdf
Data publikacji:
2004
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
leptin
obesity
Na+,K+-ATPase
Na+-ATPase
Opis:
Apart from Na+,K+-ATPase, a second sodium pump, Na+-stimulated, K+-independent ATPase (Na+-ATPase) is expressed in proximal convoluted tubule of the mammalian kidney. The aim of this study was to develop a method of Na+-ATPase assay based on the method previously used by us to measure Na+,K+-ATPase activity (Acta Biochim Polon.; 2002, 49: 515-27). The ATPase activity was assayed as the amount of inorganic phosphate liberated from ATP by isolated microsomal fraction. Na+-ATPase activity was calculated as the difference between the activities measured in the presence and in the absence of 50 mM NaCl. Na+-ATPase activity was detected in the renal cortex (3.5 ± 0.2 μmol phosphate/h per mg protein), but not in the renal medulla. Na+-ATPase was not inhibited by ouabain or an H+,K+-ATPase inhibitor, Sch 28080, but was almost completely blocked by 2 mM furosemide. Leptin administered intraperitoneally (1 mg/kg) decreased the Na+,K+-ATPase activity in the renal medulla at 0.5 and 1 h by 22.1% and 27.1%, respectively, but had no effect on Na+-ATPase in the renal cortex. Chronic hyperleptinemia induced by repeated subcutaneous leptin injections (0.25 mg/kg twice daily for 7 days) increased cortical Na+,K+-ATPase, medullary Na+,K+-ATPase and cortical Na+-ATPase by 32.4%, 84.2% and 62.9%, respectively. In rats with dietary-induced obesity, the Na+,K+- ATPase activity was higher in the renal cortex and medulla by 19.7% and 34.3%, respectively, but Na+-ATPase was not different from control. These data indicate that both renal Na+-dependent ATPases are separately regulated and that up-regulation of Na+-ATPase may contribute to Na+ retention and arterial hypertension induced by chronic hyperleptinemia.
Źródło:
Acta Biochimica Polonica; 2004, 51, 4; 1003-1014
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Spectrophotometric method for the determination of renal ouabain-sensitive H+,K+ -ATPase activity.
Autorzy:
Bełtowski, Jerzy
Wójcicka, Grażyna
Powiązania:
https://bibliotekanauki.pl/articles/1043791.pdf
Data publikacji:
2002
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
leptin
kidney
H+,K+-ATPase
ouabain
Sch 28080
Na+,K+-ATPase
Opis:
The aim of this work was to develop a method for renal H+,K+-ATPase measurement based on the previously used Na+,K+-ATPase assay (Bełtowski et al.: J Physiol Pharmacol.; 1998, 49: 625-37). ATPase activity was assessed by measuring the amount of inorganic phosphate liberated from ATP by isolated microsomal fraction. Both ouabain-sensitive and ouabain-resistant K+-stimulated and Na+-independent ATPase activity was detected in the renal cortex and medulla. These activities were blocked by 0.2 mM imidazolpyridine derivative, Sch 28080. The method for ouabain- sensitive H+,K+-ATPase assay is characterized by good reproducibility, linearity and recovery. In contrast, the assay for ouabain-resistant H+,K+-ATPase was unsatisfactory, probably due to low activity of this enzyme. Ouabain-sensitive H+,K+-ATPase was stimulated by K+ with Km of 0.26 ± 0.04 mM and 0.69 ± 0.11 mM in cortex and medulla, respectively, and was inhibited by ouabain (Ki of 2.9 ± 0.3 μM in the renal cortex and 1.9 ± 0.4 μM in the renal medulla) and by Sch 28080 (Ki of 1.8 ± 0.5 μM and 2.5 ± 0.9 μM in cortex and medulla, respectively). We found that ouabain-sensitive H+,K+-ATPase accounted for about 12% of total ouabain-sensitive activity in the Na+,K+-ATPase assay. Therefore, we suggest to use Sch 28080 during Na+,K+-ATPase measurement to block H+,K+-ATPase and improve the assay specificity. Leptin administered intraperitoneally (1 mg/kg) decreased renal medullary Na+,K+-ATPase activity by 32.1% at 1 h after injection but had no effect on H+,K+-ATPase activity suggesting that the two renal ouabain-sensitive ATPases are separately regulated.
Źródło:
Acta Biochimica Polonica; 2002, 49, 2; 515-527
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Time-dependent effect of leptin on renal Na+,K+-ATPase activity
Autorzy:
Marciniak, Andrzej
Jamroz-Wiśniewska, Anna
Borkowska, Ewelina
Bełtowski, Jerzy
Powiązania:
https://bibliotekanauki.pl/articles/1041321.pdf
Data publikacji:
2005
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
mitogen-activated protein kinases
leptin
obesity
arterial hypertension
hydrogen peroxide
Na+,K+-ATPase
Opis:
Leptin, secreted by adipose tissue, is involved in the pathogenesis of arterial hypertension, however, the mechanisms through which leptin increases blood pressure are incompletely elucidated. We investigated the effect of leptin, administered for different time periods, on renal Na+,K+-ATPase activity in the rat. Leptin was infused under anesthesia into the abdominal aorta proximally to the renal arteries for 0.5-3 h. Leptin administered at doses of 1 and 10 µg/min per kg for 30 min decreased the Na+,K+-ATPase activity in the renal medulla. This effect disappeared when the hormone was infused for ≥1 h. Leptin infused for 3 h increased the Na+,K+-ATPase activity in the renal cortex and medulla. The stimulatory effect was abolished by a specific inhibitor of Janus kinases (JAKs), tyrphostin AG490, as well as by an NAD(P)H oxidase inhibitor, apocynin. Leptin increased urinary excretion of hydrogen peroxide (H2O2) between 2 and 3 h of infusion. The effect of leptin on renal Na+,K+-ATPase and urinary H2O2 was augmented by a superoxide dismutase mimetic, tempol, and was abolished by catalase. In addition, infusion of H2O2 for 30 min increased the Na+,K+-ATPase activity. Inhibitors of extracellular signal regulated kinases (ERKs), PD98059 or U0126, prevented Na+,K+-ATPase stimulation by leptin and H2O2. These data indicate that leptin, by acting directly within the kidney, has a delayed stimulatory effect on Na+,K+-ATPase, mediated by JAKs, H2O2 and ERKs. This mechanism may contribute to the abnormal renal Na+ handling in diseases associated with chronic hyperleptinemia such as diabetes and obesity.
Źródło:
Acta Biochimica Polonica; 2005, 52, 4; 803-809
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-3 z 3

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