Novel form of lipolysis induced by leptin

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Abstract

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 (fe/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)-α, 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, PPARα, ACO, or CPT-1 expression. We conclude that in normal adipocytes leptin directly decreases FAS expression, increases PPARα and the enzymes of FFA oxidation, and stimulates a novel form of lipolysis in which glycerol is released without a proportional release of FFA.

Original languageEnglish (US)
Pages (from-to)17541-17544
Number of pages4
JournalJournal of Biological Chemistry
Volume274
Issue number25
DOIs
StatePublished - Jun 18 1999

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Lipolysis
Leptin
Nonesterified Fatty Acids
Adipocytes
Glycerol
Fatty Acid Synthases
Peroxisome Proliferator-Activated Receptors
Norepinephrine
Acyl-CoA Oxidase
Rats
Carnitine
Transferases
Messenger RNA
Fats
Leptin Receptors
Ketones
Adipose Tissue
Oxidation
Enzymes

ASJC Scopus subject areas

  • Biochemistry

Cite this

Novel form of lipolysis induced by leptin. / Wang, May-Yun; Lee, Young H; Unger, Roger H.

In: Journal of Biological Chemistry, Vol. 274, No. 25, 18.06.1999, p. 17541-17544.

Research output: Contribution to journalArticle

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