Endothelial effects of leptin: Implications in health and diseases

被引：45

作者：

Rahmouni K. ^{[1
]}

Haynes W.G. ^{[1
]}

机构：

[1] Department of Internal Medicine, General Clinical Research Center, University of Iowa College of Medicine, Iowa City, IA 52242

来源：

Current Diabetes Reports | 2005年 / 5卷 / 4期

关键词：

Nitric Oxide; Vascular Endothelial Growth Factor; Human Umbilical Vein Endothelial Cell; Vascular Endothelial Growth Factor mRNA; Vascular Endothelial Growth Factor Gene;

D O I：

10.1007/s11892-005-0020-5

中图分类号：

学科分类号：

摘要：

Leptin is an adipocyte-clerived hormone that plays a major role in the regulation of energy homeostasis through its action in the central nervous system. Leptin also acts on several peripheral tissues, including the vascular endothelium. The leptin receptor has been identified in endothelial cells. Leptin action on the endothelium modulates several physiologic processes, with potential implications in pathophysiologic diseases associated with obesity. Leptin stimulation of angiogenesis has attracted attention because of its potential involvement in retinopathy and atherosclerosis. Leptin activation of endothelial oxidative stress also has implications in atherosclerosis and inflammation. However, data on the impact of the endothelial effect of leptin on arterial pressure are contrasting. Although some investigators have shown that leptin action on the endothelial nitric oxide system tends to decrease arterial pressure, others have shown no contribution from the endothelial effect of leptin to the control of arterial pressure. Further characterization of the endothelial effects of leptin will, it is hoped, help in the understanding of the different pathophysiologic diseases associated with obesity. Copyright © 2005 by Current Science Inc.

引用

页码：260 / 266

页数：6

共 49 条

[31]

Wolf G., Hamann A., Han D.C., Et al., Leptin stimulates proliferation and TGF-beta expression in renal glomerular endothelial cells: Potential role in glomerulosclerosis, Kidney Int., 56, pp. 860-872, (1999)

[32]

Beltowski J., Wojcicka G., Jamroz A., Leptin decreases plasma paraoxonase 1 (PON1) activity and induces oxidative stress: The possible novel mechanism for proatherogenic effect of chronic hyperleptinemia, Atherosclerosis, 170, pp. 21-29, (2003)

[33]

Nakazono K., Watanabe N., Matsuno K., Et al., Does superoxide underlie the pathogenesis of hypertension?, Proc. Natl. Acad. Sci. USA, 88, pp. 10045-10048, (1991)

[34]

Beltowski J., Wojcicka G., Marciniak A., Jamroz A., Oxidative stress, nitric oxide production, and renal sodium handling in leptin-induced hypertension, Life Sci., 74, pp. 2987-3000, (2004)

[35]

Contreras F., Rivera M., Vasquez J., Et al., Endothelial dysfunction in arterial hypertension, J. Hum. Hypertens., 14, (2000)

[36]

Lembo G., Vecchione C., Fratta L., Et al., Leptin induces direct vasodilation through distinct endothelial mechanisms, Diabetes, 49, pp. 293-297, (2000)

[37]

Kimura K., Tsuda K., Baba A., Et al., Involvement of nitric oxide in endothelium-dependent arterial relaxation by leptin, Biochem. Biophys. Res. Commun., 273, pp. 745-749, (2000)

[38]

Winters B., Mo Z., Brooks-Asplund E., Reduction of obesity, as induced by leptin, reverses endothelial dysfunction in obese (Lep(ob)) mice, J. Appl. Physiol., 89, pp. 2382-2390, (2000)

[39]

Pannirselvam M., Verma S., Anderson T.J., Triggle C.R., Cellular basis of endothelial dysfunction in small mesenteric arteries from spontaneously diabetic (db/db -/-) mice: Role of decreased tetrahydrobiopterin bioavailability, Br. J. Pharmacol., 136, pp. 255-263, (2002)

[40]

Nakagawa K., Higashi Y., Sasaki S., Et al., Leptin causes vasodilation in humans, Hypertens. Res., 25, pp. 161-165, (2002)

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