This Article  • Full text  • PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Topic Collections  • Nutritional and Metabolic Disorders  • Nutritional and Metabolic Disorders, Other  • Cardiovascular System  • Cardiovascular Disease/ Myocardial Infarction  • Endocrine Diseases  • Diabetes Mellitus  • Hypertension  • Alert me on articles by topic  Social Bookmarking   What's this?

Chin-Hsiao Tseng, MD, PhD

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

In reply

The proposed linkage between visfatin and insulin-induced hypertension by Oh et al may explain the linkage between exogenous insulin use and hypertension as observed in the article.¹ Proinflammatory cytokines such as tumor necrosis factor and interleukin 6 increase the expression of visfatin from visceral fat, and in return, visfatin increases the expression of peroxisome proliferator-activated receptors (PPAR) and adiponectin, both of which have been shown to exert a blood pressure–lowering effect.^2-3 Because Haider et al⁴ demonstrated that glucose-induced visfatin secretion is opposed by coinfusion of exogenous insulin in humans, it is possible that prolonged use of exogenous insulin decreases visfatin secretion and induces hypertension via a mechanism involving hyposecretion of PPAR and adiponectin.

Mirza criticized the finding of the possible induction of hypertension by exogenous insulin injection in patients with type 2 diabetes based on the following points: (1) insulin might have vasodilatory, . . . [Full Text of this Article]

AUTHOR INFORMATION


CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?