The effect of leptin on Na+-H+ antiport (NHE 1) activity of obese and normal subjects erythrocytes

Konstantinou-Tegou, A; Kaloyianni, Martha; Bourikas, Dimitris; Koliakos, George

doi:10.1016/s0303-7207(01)00639-6

Cited by 31 publications

(25 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In a previous study, we had shown that leptin could activate NHE1 in human erythrocytes as represented by an increase in pHi (Konstantinou-Tegou et al 2001). We observed the same effect in human monocytes derived from healthy subjects.…”

Section: Discussionsupporting

confidence: 83%

The ambiguous role of the Na+–H+ exchanger isoform 1 (NHE1) in leptin-induced oxidative stress in human monocytes

Konstantinidis

Paletas

Koliakos

et al. 2009

Cell Stress and Chaperones

View full text Add to dashboard Cite

Leptin, a 16-kDa cytokine produced mainly by the adipose tissue, is known to increase energy expenditure while at the same time lowering food intake by acting directly on the hypothalamus. ObRb, the leptin receptor mostly involved in intracellular signaling, is expressed in a wide range of tissues, thus allowing leptin to affect a much broader diversity of biological processes. High concentrations of leptin are encountered in patients with hyperleptinemia, a condition which very often accompanies obesity and which is a direct result of leptin resistance. In the present study, moderate and high concentrations of leptin (16 and 160 ng/ml) were mostly utilized in order to investigate the role of this cytokine in oxidative stress levels in human monocytes. Leptin was found to increase oxidative species production as measured with 2',7'-dichlorodihydrofluorescein diacetate (general marker of oxidative species, but not O2-*) and dihydroethidium (marker of O2-*). Surprisingly, it also augmented superoxide dismutase activity. Inhibition of the Na+-H+ exchanger isoform 1 (NHE1) also inhibited leptin-induced superoxide anion production but at the same time amplified leptin-induced production of other oxidative species. Signaling proteins such as phosphoinositide 3 kinase and conventional isoforms of protein kinase C (alpha-, beta(i)-, beta(ii)-), as well as NADPH oxidase, also participated in leptin signaling. Finally, leptin was found to increase glutathionylation levels of NHE1-bound heat shock protein 70 kDa (Hsp70) but not Hsp70 binding to NHE1.

show abstract

Section: Discussionsupporting

confidence: 83%

The ambiguous role of the Na+–H+ exchanger isoform 1 (NHE1) in leptin-induced oxidative stress in human monocytes

Konstantinidis

Paletas

Koliakos

et al. 2009

Cell Stress and Chaperones

View full text Add to dashboard Cite

show abstract

“…It has been previously reported that insulin as well as various other ligants stimulate NHE1 by activation of PKC [15,16,20,21]. Therefore, the possible involvement of PKC in the signal transduction pathway, which stimulates NHE1 in monocytes under the influence of high glucose concentration (20 mM), was investigated by two types of experiments:…”

Section: Resultsmentioning

confidence: 99%

High glucose concentrations stimulate human monocyte sodium/hydrogen exchanger activity and modulate atherosclerosis-related functions

Koliakos

Zolota

Paletas

et al. 2004

Pflugers Arch - Eur J Physiol

View full text Add to dashboard Cite

In the present study, the effect of high (20 mM) glucose concentrations on human monocyte sodium/hydrogen exchanger (NHE1) activity, scavenger receptor CD36 expression, cell adhesion, and cell migration have been investigated. Incubation with high glucose concentrations caused an increase in NHE1 activity, as estimated by internal pH and sodium-uptake measurements. This effect was specific for glucose, since it was not observed when monocytes were incubated in the presence of 20 mM of galactose, fructose, or mannitol. In addition, the activation of sodium uptake was inhibited by ethylisopropyl amiloride (EIPA), phloretine and cytochalasine B, and calphostin C. High glucose concentrations also increased the expression of CD36 receptors on the surface of monocytes and positively influenced monocyte migration and adhesion to laminin. EIPA added together with glucose counteracted these effects. The data of the present study suggest that a high glucose concentration can influence atherosclerosis-related monocyte functions via NHE1 activation.

show abstract

“…80 These results are in line with a report by Tajima et al, who demonstrated that atrial natriuretic peptide inhibits NHE-1 activity. 84 Leptin, a protein encoded by the obesity gene, has been reported to activate NHE-1 through a PKC-dependent pathway, 85 and emerging evidence indicates that this hormone is linked to cardiac hypertrophy. 86 -88 It has been reported that leptin elevates ET-1 and ROS levels, which results in hypertrophy of neonatal rat cardiac myocytes.…”

Section: The Nhe-1 In Myocardial Hypertrophymentioning

confidence: 99%

Sodium-Hydrogen Exchanger, Cardiac Overload, and Myocardial Hypertrophy

2007

View full text Add to dashboard Cite

The effect of leptin on Na+-H+ antiport (NHE 1) activity of obese and normal subjects erythrocytes

Cited by 31 publications

References 50 publications

The ambiguous role of the Na+–H+ exchanger isoform 1 (NHE1) in leptin-induced oxidative stress in human monocytes

The ambiguous role of the Na+–H+ exchanger isoform 1 (NHE1) in leptin-induced oxidative stress in human monocytes

High glucose concentrations stimulate human monocyte sodium/hydrogen exchanger activity and modulate atherosclerosis-related functions

Sodium-Hydrogen Exchanger, Cardiac Overload, and Myocardial Hypertrophy

Contact Info

Product

Resources

About