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Am J Physiol Endocrinol Metab (May 20, 2003). doi:10.1152/ajpendo.00119.2003
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Submitted on March 20, 2003
Accepted on May 11, 2003

TNF{alpha} Acutely Inhibits Vascular Effects of Physiologic but not High Insulin or Contraction

Lei Zhang1, Catherine M Wheatley1, Stephen M Richards1, Eugene J Barrett2, Michael G Clark1, and Stephen Rattigan1*

1 Department of Biochemistry, University of Tasmania, Hobart, Tasmania, Australia
2 Health Sciences Center, University of Virginia, Charlottesville, Virginia, USA

* To whom correspondence should be addressed. E-mail: S.Rattigan{at}utas.edu.au.

TNF{alpha} is elevated in many states of insulin resistance and acutely administered TNF{alpha} in vivo inhibits insulin-mediated hemodynamic effects and glucose uptake in muscle. In this study we assess whether the inhibitory effects of TNF{alpha} are affected by insulin dose or muscle contraction. Whole body glucose infusion (GIR), femoral blood flow (FBF), hindleg vascular resistance (VR), hindleg glucose uptake (HGU), 2-deoxyglucose uptake into muscles of the lower leg (R'g) and hindleg metabolism of infused 1-methylxanthine (1-MX) a measure of capillary recruitment were determined. Three groups were studied with and without infusion of TNF{alpha}: euglycemic insulin-clamped, one-leg field stimulated (2 Hz, 0.1 ms at 30V) and saline-infused control anesthetized rats. Insulin infusions were 3, 10 or 30 mU. kg-1.min-1 x 2h. 1-MX metabolism was maximally increased by all three doses of insulin. GIR, HGU and R'g were maximal at 10 mU and FBF at 30 mU insulin. Contraction increased FBF, HGU and 1-MX. TNF{alpha} (0.5 µg.kg-1.h-1) totally blocked the 3 and 10mU insulin-mediated increases in FBF and 1-MX, and partly blocked GIR, HGU and R'g. None of the increases due to twitch contraction was affected by TNF{alpha} and only the increase in FBF due to 30 mU insulin was partly affected. We conclude that muscle capillary recruitment and glucose uptake due to high levels of insulin or muscle contraction under twitch stimuli at 2Hz are resistant to TNF{alpha}. The findings may have implications for ameliorating muscle insulin resistance resulting from increased plasma TNF{alpha} and for the differing mechanisms by which contraction and insulin recruit capillary flow in muscle.




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