Cellular Retinol-Binding Protein Type I (CRBP-I) Regulates Adipogenesis

ABSTRACT Adipogenesis is governed by a well-documented cascade of transcription factors. However, less is known about non-transcription factors that govern early stages of adipogenesis. Here we show that cellular retinol-binding protein type I (CRBP-I), a small cytosolic binding protein for retinol and retinaldehyde, is specifically restricted to preadipocytes in white adipose tissue. The absence of CRBP-I in mice (CRBP-I-KO mice) leads to increased adiposity. Despite increased adiposity, CRBP-I-KO mice remain more glucose tolerant and insulin sensitive during high-fat-diet feeding. 3T3-L1 cells deficient in CRBP-I or mouse embryonic fibroblasts derived from CRBP-I-KO mice had increased adipocyte differentiation and triglyceride (TG) accumulation. This was due to increased expression and activity of PPARγ, while other transcription factor pathways in early and late differentiation remained unchanged. Conversely, the overexpression of CRBP-I in 3T3-L1 cells results in decreased TG accumulation. In conclusion, CRBP-I is a cytosolic protein specifically expressed in preadipocytes that regulates adipocyte differentiation in part by affecting PPARγ activity.

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Effect of endurance training on retinol-binding protein 4 gene expression and its protein level in adipose tissue and the liver in diabetic rats induced by a high-fat diet and streptozotocin

Journal of Diabetes Investigation ◽

10.1111/jdi.12186 ◽

2014 ◽

Vol 5 (5) ◽

pp. 484-491 ◽

Cited By ~ 11

Author(s):

Masoume Mansouri ◽

Rohollah Nikooie ◽

Abasali Keshtkar ◽

Bagher Larijani ◽

Kobra Omidfar

Keyword(s):

Gene Expression ◽

Adipose Tissue ◽

Endurance Training ◽

Protein Level ◽

High Fat Diet ◽

Binding Protein ◽

Diabetic Rats ◽

Retinol Binding Protein ◽

High Fat ◽

Retinol Binding Protein 4

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Cellular retinol-binding protein type I is prominently and differentially expressed in the sensory epithelium of the rat cochlea and vestibular organs

The Journal of Comparative Neurology ◽

10.1002/cne.903490407 ◽

1994 ◽

Vol 349 (4) ◽

pp. 596-602 ◽

Cited By ~ 19

Author(s):

Jukka Ylikoski ◽

Ulla Pirvola ◽

Ulf Eriksson

Keyword(s):

Binding Protein ◽

Sensory Epithelium ◽

Differentially Expressed ◽

Retinol Binding Protein ◽

Type I ◽

Rat Cochlea ◽

Vestibular Organs ◽

Cellular Retinol Binding Protein

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Mass spectrometry techniques for detection of ligand-dependent changes in the conformational flexibility of cellular retinol-binding protein type I localized by hydrogen/deuterium exchange

Rapid Communications in Mass Spectrometry ◽

10.1002/rcm.2547 ◽

2006 ◽

Vol 20 (13) ◽

pp. 1973-1980 ◽

Cited By ~ 7

Author(s):

M. Careri ◽

L. Elviri ◽

A. Mangia ◽

I. Zagnoni ◽

F. Torta ◽

...

Keyword(s):

Mass Spectrometry ◽

Binding Protein ◽

Conformational Flexibility ◽

Deuterium Exchange ◽

Retinol Binding Protein ◽

Type I ◽

Hydrogen Deuterium Exchange ◽

Hydrogen Deuterium ◽

Cellular Retinol Binding Protein

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Antiobesity activity of Acer tegmentosum Maxim on 3T3-L1 preadipocyte and high-fat diet-induced obese rats

10.21203/rs.2.24283/v1 ◽

2020 ◽

Author(s):

Hang-Hee Cho ◽

Soo-Jung Lee ◽

Sung-Ho Kim ◽

Sun-Hee Jang ◽

Chungkil Won ◽

...

Keyword(s):

Adipose Tissue ◽

Fatty Acid ◽

Lipid Accumulation ◽

High Fat Diet ◽

Adipocyte Differentiation ◽

Binding Protein ◽

High Fat ◽

Tissue Mass ◽

Fatty Acid Binding ◽

Obese Rats

Abstract Background: The aim of this study was to investigate the effect of Acer tegmentosum Maxim (ATM) on adipocyte differentiation in 3T3-L1 adipocyte-derived cells and anti-obesity properties in high fat diet (HFD)-induced obese rats. Methods: 3T3-L1 adipocytes and HFD-induced obese rats were treated with ATM, and its effect on gene expression was analyzed using RT-PCR and Western blotting experiments. Results: Cellular lipid contents in DMI (dexamethasone, 3-isobutyl-1-methylxanthine, and insulin mixture)-treated cells increased, while ATM treatment caused a significant reduction in lipid accumulation in differentiated 3T3-L1 cells. ATM caused inhibition of adipogenesis via down-regulation of the CCAAT/enhancer binding protein β (C/EBPβ), C/EBPα, and peroxisome proliferator-activated receptor γ (PPARγ) expressions in 3T3-L1 cells. Moreover, treatment with ATM caused a decrease in the expressions of adipocyte-specific genes, such as adipocyte fatty acid-binding protein-2 (aP2), fatty acid synthase (FAS), and lipoprotein lipase (LPL), compared with DMI-stimulated adipocytes. In addition, phosphorylation levels of protein kinase B (Akt) and its downstream substrate, glycogen synthase kinase 3β (GSK3β), were significantly decreased by ATM treatment of 3T3-L1 adipocytes. Together, these results indicated that ATM caused inhibition of both adipocyte differentiation via suppression of the C/EBP family and PPARγ expressions and the Akt signaling pathway in 3T3-L1 adipocytes. In the present study, we further investigated anti-obesity effects of ATM on HFD-induced obese rats. Rats fed with HFD demonstrated elevations in body weight gain, while the administration of ATM significantly reversed BW gains and adipose tissue weights in rats fed HFD. ATM supplementation also caused a decrease in the circulating triglyceride levels and total cholesterol levels and led to inhibition of lipid accumulation in the adipose tissues in HFD-induced obesity in rats. Furthermore, epididymal fat exhibited larger adipocytes in the HFD group, whereas the ATM-treated group was significantly smaller than that of HFD group. These results strongly demonstrate that ATM administration caused a reduction in adiposity via attenuation in adipose tissue mass and adipocyte size. Conclusion: These finding demonstrated that ATM exerted anti-obesity effects through inhibition of adipocyte differentiation and adipogenesis, leading to a decrease in BW and fat tissue mass in HFD-induced obesity in rats.

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