Arachidonic acid inhibits lipogenic gene expression in 3T3-L1 adipocytes through a prostanoid pathway

J Lipid Res. 1998 Jul;39(7):1327-34.

Abstract

This report examines the effect of polyunsaturated fatty acids (PUFA) on lipogenic gene expression in cultured 3T3-L1 adipocytes. Arachidonic acid (20:4, n-6) and eicosapentaenoic acid (20:5, n-3) suppressed mRNAs encoding fatty acid synthase (FAS) and S14, but had no effect on beta-actin. Using a clonal adipocyte cell line containing a stably integrated S14CAT fusion gene, oleic acid (18:1, n-9), arachidonic acid (20:4, n-6) and eicosapentaenoic acid (20:5, n-3) inhibited chloramphenicol acetyltransferase (CAT) activity with an ED50 of 800, 50, and 400 microM, respectively. Given the high potency of 20:4, n-6, its effect on adipocyte gene expression was characterized. Arachidonic acid suppressed basal CAT activity, but did not affect glucocorticoid-mediated induction of S14CAT expression. The effect of 20:4, n-6 on S14CAT expression was blocked by an inhibitor of cyclooxygenase implicating involvement of prostanoids. Prostaglandins (PGE2 and PGF2alpha at 10 microM) inhibited CAT activity through a pertussis toxin-sensitive Gi/Go-coupled signalling cascade. Our results suggest that 20:4, n-6 inhibits lipogenic gene expression in 3T3-L1 adipocytes through a prostanoid pathway. This mechanism of control differs from the polyunsaturated fatty acid-mediated suppression of hepatic lipogenic gene expression.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 3T3 Cells
  • Actins / genetics
  • Adipocytes / drug effects
  • Adipocytes / metabolism*
  • Animals
  • Arachidonic Acid / pharmacology*
  • Chloramphenicol O-Acetyltransferase / biosynthesis
  • Chloramphenicol O-Acetyltransferase / genetics
  • Cyclooxygenase Inhibitors / pharmacology
  • Dexamethasone / pharmacology
  • Dinoprost / pharmacology
  • Dinoprostone / pharmacology
  • Eicosapentaenoic Acid / pharmacology*
  • Fatty Acids, Nonesterified / metabolism
  • Fatty Acids, Nonesterified / pharmacology
  • Fatty Acids, Unsaturated / pharmacology
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / physiology*
  • Mice
  • Oleic Acid / pharmacology*
  • Pertussis Toxin
  • Prostaglandins / physiology*
  • RNA, Messenger / metabolism
  • Signal Transduction / drug effects
  • Signal Transduction / physiology
  • Transcription, Genetic / drug effects
  • Transfection
  • Triglycerides / metabolism
  • Virulence Factors, Bordetella / pharmacology

Substances

  • Actins
  • Cyclooxygenase Inhibitors
  • Fatty Acids, Nonesterified
  • Fatty Acids, Unsaturated
  • Prostaglandins
  • RNA, Messenger
  • Triglycerides
  • Virulence Factors, Bordetella
  • Arachidonic Acid
  • Oleic Acid
  • Dexamethasone
  • Eicosapentaenoic Acid
  • Dinoprost
  • Chloramphenicol O-Acetyltransferase
  • Pertussis Toxin
  • Dinoprostone