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1 Department of Applied Physiology & Kinesiology, University of Florida, Gainesville, Florida, USA; Malcom Randall VA Medical Center, Gainesville, Florida, USA
2 Department of Applied Physiology & Kinesiology, University of Florida, Gainesville, Florida, USA
3 Malcom Randall VA Medical Center, Gainesville, Florida, USA
4 Department of Physiology, Louisiana State University Health Science Center, New Orleans, Louisiana, USA
* To whom correspondence should be addressed. E-mail: seborst{at}ufl.edu.
We examined the possible role of tumor necrosis factor-
(TNF-) as a mediator of insulin
resistance in aged, male Sprague-Dawley rats. Rats were treated either with goat anti-murine
TNF- IgG (anti-TNF-) or goat non-immune IgG (NI) for 7 days. Vascular catheters were
implanted and rats were fasted overnight before performing hyperinsulinemic, euglycemic clamp
(HUC) studies. TNF- neutralization increased the rate of glucose infusion required to maintain
euglycemia by 68%. Insulin-stimulated glucose transport into individual tissues was measured
following bolus administration of [14C]2-deoxyglucose during HUC. Anti-TNF- administration
increased glucose transport in muscles composed predominantly of fast-twitch fibers: white
gastrocnemius muscle (68% increase) and tibialis anterior muscle (64% increase). There were
non-significant trends for increased glucose transport in the slow-twitch soleus muscle and in the
mixed-fiber red gastrocnemius muscle. Glucose transport was unchanged in visceral and
subcutaneous fat. Anti-TNF treatment did not alter body weight, muscle mass or fat mass. Anti-
TNF- did not alter the distribution of the 17 kDa and 26 kDa forms of TNF- in either muscle
or fat. However, anti-TNF- treatment caused an approximately 50% reduction in the secretion
of TNF- bioactivity in vitro by explants of visceral and subcutaneous fat. We conclude that
TNF- neutralization reversed insulin resistance substantially in fast-twitch muscle and may
have done so in other muscles, while having little effect in fat. TNF- neutralization was
accompanied by reduced TNF- bioactivity without tissue depletion of TNF- protein.
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