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Chin-Hsiao Tseng, MD, PhD

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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]

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RELATED LETTER

It Is Time We Ended the Myth of Insulin as an Atherogenic Hormone
Shirwan A. Mirza
Arch Intern Med. 2007;167(8):858-859.
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