Differential effects of flavonoids on 3T3-L1 adipogenesis and lipolysis

Am J Physiol Cell Physiol. 2001 Apr;280(4):C807-13. doi: 10.1152/ajpcell.2001.280.4.C807.

Abstract

Flavonoids, polyphenolic compounds that exist widely in plants, inhibit cell proliferation and increase cell differentiation in many cancerous and noncancerous cell lines. Because terminal differentiation of preadipocytes to adipocytes depends on proliferation of both pre- and postconfluent preadipocytes, we predicted that flavonoids would inhibit adipogenesis in the 3T3-L1 preadipocyte cell line. The flavonoids genistein and naringenin inhibited proliferation of preconfluent preadipocytes in a time- and dose-dependent manner. When added to 2-day postconfluent preadipocytes at the induction of differentiation, genistein inhibited mitotic clonal expansion, triglyceride accumulation, and peroxisome proliferator-activated receptor-gamma expression, but naringenin had no effect. The antiadipogenic effect of genistein was not due to inhibition of insulin receptor subtrate-1 tyrosine phosphorylation. When added 3 days after induction of differentiation, neither flavonoid inhibited differentiation. In fully differentiated adipocytes, genistein increased basal and epinephrine-induced lipolysis, but naringenin had no significant effects. These data demonstrate that genistein and naringenin, despite structural similarity, have differential effects on adipogenesis and adipocyte lipid metabolism.

Publication types

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

MeSH terms

  • 3T3 Cells
  • Adipocytes / cytology*
  • Adipocytes / drug effects
  • Adipocytes / metabolism
  • Animals
  • Antineoplastic Agents / pharmacology*
  • Cell Differentiation / drug effects
  • Dose-Response Relationship, Drug
  • Estrogen Antagonists / pharmacology
  • Flavanones*
  • Flavonoids / pharmacology*
  • Genistein / pharmacology*
  • Insulin Receptor Substrate Proteins
  • Lipolysis / drug effects*
  • Mice
  • Mitosis / drug effects
  • Phosphoproteins / metabolism
  • Receptors, Cytoplasmic and Nuclear / metabolism
  • Transcription Factors / metabolism

Substances

  • Antineoplastic Agents
  • Estrogen Antagonists
  • Flavanones
  • Flavonoids
  • Insulin Receptor Substrate Proteins
  • Irs1 protein, mouse
  • Phosphoproteins
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors
  • Genistein
  • naringenin