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J Biol Chem, Vol. 274, Issue 25, 17541-17544, June 18, 1999
From the Gifford Laboratories, Center for Diabetes Research and the
Department of Internal Medicine, University of Texas Southwestern
Medical Center, Dallas, Texas 75235 and the Veterans Administration
Medical Center, Dallas, Texas 75216
Hyperleptinemia causes disappearance of body fat
without a rise in free fatty acids (FFA) or ketones, suggesting that
leptin can deplete adipocytes of fat without releasing FFA. To test
this, we measured FFA and glycerol released from adipocytes obtained from normal lean Zucker diabetic fatty rats (+/+) and
incubated for 0, 3, 6, or 24 h in either 20 ng/ml recombinant
leptin or 100 nM norepinephrine (NE). Whereas NE increased
both FFA and glycerol release from adipocytes of +/+ rats,
leptin increased glycerol release in +/+ adipocytes without
a parallel increase in FFA release. In adipocytes of obese Zucker
diabetic fatty rats (fa/fa) with defective leptin
receptors, NE increased both FFA and glycerol release, but leptin had
no effect on either. Leptin significantly lowered the mRNA of
leptin and fatty acid synthase of adipocytes (FAS) (p < 0.05), and up-regulated the mRNA of peroxisome proliferator-activated receptor (PPAR)-
, carnitine palmitoyl transferase-1, (CPT-1), and acyl CoA oxidase (ACO) (p < 0.05). NE (100 nM) also lowered leptin mRNA
(p < 0.05) but did not affect FAS, PPAR, ACO, or
CPT-1 expression. We conclude that in normal adipocytes leptin directly
decreases FAS expression, increases PPAR and the enzymes of FFA
oxidation, and stimulates a novel form of lipolysis in which glycerol
is released without a proportional release of FFA.
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