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Modulation of resistin expression by retinoic acid and vitamin A status
Francisco Felipe1, M Luisa Bonet, Joan Ribot
1Laboratory of Molecular Biology, Nutrition and Biotechnology, Department of Fundamental Biology and Health Sciences, University of the Balearic Islands, Palma de Mallorca, Spain.
Abstract:
This work identifies retinoic acid (RA), the acid form of vitamin A, as a signal that inhibits the expression of resistin, an adipocyte-secreted protein previously proposed to act as an inhibitor of adipocyte differentiation and as a systemic insulin resistance factor. Both 9-cis and all-trans RA reduced resistin mRNA levels in white and brown adipocyte cell model systems; the effect was time- and dose-dependent, was followed by a reduced secretion of resistin, and was reproduced by selective agonists of both RA receptors and rexinoid receptors. Association of CCAAT/enhancer-binding protein alpha (a positive regulator of the resistin gene) and its coactivators p300, cAMP response element-binding protein binding protein, and retinoblastoma protein with the resistin gene promoter was reduced in RA-treated adipocytes. RA administration to normal mice resulted in reduced resistin mRNA levels in brown and white adipose tissues, reduced circulating resistin levels, reduced body weight, and improved glucose tolerance. Resistin expression was also downregulated after dietary vitamin A supplementation in mice. The results raise the possibility that vitamin A status may contribute to modulate systemic functions through effects on the production of adipocyte-derived protein signals.
Insights
Retinoic acid (RA), a form of vitamin A, inhibits resistin, a protein linked to insulin resistance. Vitamin A supplementation reduced resistin levels, body weight, and improved glucose tolerance in mice.
Area of Science:
- Endocrinology
- Molecular Biology
- Nutritional Science
Background:
- Resistin is an adipocyte-secreted protein implicated in insulin resistance and adipocyte differentiation.
- The precise regulation of resistin expression and its systemic impact remain areas of active investigation.
Purpose of the Study:
- To investigate the role of retinoic acid (RA) in regulating resistin expression.
- To explore the potential of vitamin A as a modulator of resistin-related metabolic functions.
Main Methods:
- Utilized adipocyte cell models to assess resistin mRNA and protein levels following RA treatment.
- Examined the association of transcription factors with the resistin gene promoter using RA-treated adipocytes.
- Administered RA and vitamin A to mice to evaluate in vivo effects on resistin, body weight, and glucose tolerance.
Main Results:
- Retinoic acid (RA) significantly reduced resistin mRNA and protein levels in both white and brown adipocytes in a time- and dose-dependent manner.
- RA treatment decreased the association of CCAAT/enhancer-binding protein alpha and its coactivators with the resistin gene promoter.
- In vivo studies showed that RA administration and dietary vitamin A supplementation lowered resistin levels, reduced body weight, and improved glucose tolerance in mice.
Conclusions:
- Retinoic acid directly inhibits resistin gene expression and secretion.
- Vitamin A status may influence systemic metabolic health by modulating adipocyte-derived factors like resistin.
- These findings suggest a potential therapeutic role for vitamin A in managing metabolic disorders associated with resistin.
