Editor's Correspondence |

It Is Time We Ended the Myth of Insulin as an Atherogenic Hormone—Reply

Chin-Hsiao Tseng, MD, PhD
Arch Intern Med. 2007;167(8):858-859. doi:10.1001/archinte.167.8.859-a.
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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 α and interleukin 6 increase the expression of visfatin from visceral fat, and in return, visfatin increases the expression of peroxisome proliferator-activated receptors γ (PPARγ) 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 PPARγ and adiponectin.

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