Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. STKE, 24 February 2004
Vol. 2004, Issue 221, p. tw75
[DOI: 10.1126/stke.2212004TW75]

EDITORS' CHOICE

METABOLIC REGULATION Resistin' a Knockout

Obesity is one of the most potent risk factors for insulin resistance and type 2 diabetes, but the molecular mechanisms underlying this link are poorly understood. The fat-derived hormone resistin has been postulated to be part of that mechanism, but its role in glucose homeostasis has been controversial. Banerjee et al. now show that mice lacking resistin have low fasted blood glucose levels caused by reduced glucose production in the liver. Resistin-null mice fed a high-fat diet were less prone to exhibit the elevated glucose levels seen in wild-type mice on a similar diet, which supports the idea that resistin mediates the hyperglycemia associated with obesity. These results will likely stimulate further research exploring whether resistin has a comparable role in humans.

R. R. Banerjee, S. M. Rangwala, J. S. Shapiro, A. S. Rich, B. Rhoades, Y. Qi, J. Wang, M. W. Rajala, A. Pocai, P. E. Scherer, C. M. Steppan, R. S. Ahima, S. Obici, L. Rossetti, M. A. Lazar, Regulation of fasted blood glucose by resistin. Science 303, 1195-1198 (2004). [Abstract] [Full Text]

Citation: Resistin' a Knockout. Sci. STKE 2004, tw75 (2004).


To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882