Preadipocytes possess cellular retinoid binding proteins and their differentiation is inhibited by retinoids

https://doi.org/10.1016/S0006-291X(80)80113-6Get rights and content

Summary

ST 13 preadipocytes can be induced to differentiate into mature adipocytes by maintaining them as a confluent monolayer in a medium containing insulin. The differentiated cells synthesize and accumulate a large amount of triglyceride in their cytoplasm as multiple lipid droplets, and at the same time, their insulin binding activity increased 50 fold over that of the undifferentiated cells. Vitamin A, an essential nutrient for animals, inhibited the preadipocyte differentiation reversibly at a non-toxic dose. Retinol- and retinoic acid binding proteins were detected in the cytoplasm of preadipocytes suggesting the inhibition of differentiation might be mediated by these proteins.

References (20)

  • StricklandS. et al.

    Cell

    (1978)
  • PennypackerJ.P. et al.

    Arch. Biochem. Biophys.

    (1978)
  • SpelsbergT.C. et al.

    Biochim. Biophys. Acta

    (1973)
  • GreenH. et al.

    Cell

    (1974)
  • RubinC.S. et al.

    J. Biol. Chem.

    (1978)
  • FletcherM.J.

    Clin. Chim. Acta.

    (1968)
  • LowryO.H. et al.

    J. Biol. Chem.

    (1951)
  • KohnoK. et al.

    Biochem. Biophys. Res. Commun.

    (1980)
  • OngD.E. et al.

    J. Biol. Chem.

    (1975)
  • LotanR.

    Biochim. Biophysic. Acta.

    (1980)
There are more references available in the full text version of this article.

Cited by (72)

  • SIRT1 induces the adipogenic differentiation of mouse embryonic stem cells by regulating RA-induced RAR expression via NCOR1 acetylation

    2020, Stem Cell Research
    Citation Excerpt :

    RA has diverse regulatory roles in adipogenesis. In particular, it inhibits the formation of mature adipose tissue from pre-adipocytes (Kuri-Harcuch, 1982; Murray and Russell, 1980; Sato et al., 1980), and thus, may have a suppressive role during late stage adipogenesis. RA treatment also suppresses fat accumulation in diet-induced models of obesity.

  • RARγ-C-Fos-PPARγ2 signaling rather than ROS generation is critical for all-trans retinoic acid-inhibited adipocyte differentiation

    2014, Biochimie
    Citation Excerpt :

    Low concentration of RA (1 pM–10 nM range) was shown to promote adipocyte differentiation [44]. In contrast, supraphysiological (0.1–10 μM range) of RA inhibited the differentiation of preadipocytes to adipocytes [18,45]. However, the mechanism of the inhibitory effect of RA on adipocyte differentiation is still largely unknown.

  • All-trans retinoic acid modulates bone morphogenic protein 9-induced osteogenesis and adipogenesis of preadipocytes through BMP/Smad and Wnt/β-catenin signaling pathways

    2014, International Journal of Biochemistry and Cell Biology
    Citation Excerpt :

    We have previously demonstrated the synergism between RA and BMP9 in inducing osteogenic differentiation of MSCs (Zhang et al., 2010). Moreover, RA was shown to be able to inhibit adipogenic differentiation and cooperate with BMP2 to induce osteogenic differentiation in preadipocytes (Sato et al., 1980; Skillington et al., 2002). These observations suggest the potential of RA to cooperate with BMP9 to promote osteogenesis and reverse BMP9-induced adipogenesis in preadipocytes.

  • Retinoic acid signaling pathways in development and diseases

    2014, Bioorganic and Medicinal Chemistry
    Citation Excerpt :

    Major metabolic disorders that are linked with retinoids are obesity, diabetes, and the metabolic syndrome. Multiple studies have documented that RA regulates adipogenesis.63–66 RA acts as a high affinity ligand for the nuclear receptor peroxisome proliferation-activated receptor β/δ (PPARβ/δ).

View all citing articles on Scopus
View full text