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Gifford Laboratories, Touchstone Center for Diabetes Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75235; and Veterans Affairs North Texas Healthcare System, Dallas, Texas 75216
Address all correspondence and requests for reprints to: Roger H. Unger, M.D., Center for Diabetes Research, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235-8854. E-mail: runger{at}mednet.swmed.edu
Peroxisome proliferator-activated receptor-
coactivator-1 (PGC-1), a
cold-induced protein expressed in brown adipose tissue (BAT), plays a
role in adaptive thermogenesis by up-regulating uncoupling proteins
(UCP). Here, we explore its relationship to the thermogenic actions of
leptin, which also up-regulates UCPs. We find that PGC-1 messenger RNA
(mRNA) is markedly reduced in BAT of obese leptin-deficient
(ob/ob mice) and leptin-unresponsive
(db/db mice and Zucker diabetic fatty
fa/fa rats) rodents. Whereas, after cold exposure (6 C
for 7 h), PGC-1 mRNA increases 2.6-fold in BAT of lean +/+ rats,
it rises only 30% in fa/fa rats. Four days after
induction of hyperleptinemia (>30 ng/ml) in Wistar rats, by adenovirus
gene transfer, PGC-1 mRNA in BAT was 2.3-fold and UCP-1, 4-fold above
controls. In isolated white adipocytes, PGC-1 mRNA increased 4.4-fold
within 6 h of incubation with 20 ng/ml of leptin. We conclude that
leptin action is required for normal basal and cold-stimulated PGC-1
expression in BAT in rodents and that hyperleptinemia rapidly
up-regulates its expression, at least in part, by direct action.
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