β-Carotene accumulation in 3T3-L1 adipocytes inhibits the elevation of reactive oxygen species and the suppression of genes related to insulin sensitivity induced by tumor necrosis factor-α

Abstract Objective β-Carotene is an abundant carotenoid with potent antioxidative activities and accumulates in adipose tissue. However, its physiologic functions are poorly understood. In this study, we examined whether accumulation of β-carotene for 4 d in insulin-resistant 3T3-L1 adipocytes alter...

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Published inNutrition (Burbank, Los Angeles County, Calif.) Vol. 26; no. 11; pp. 1151 - 1156
Main Authors Kameji, Hiroyuki, M.S, Mochizuki, Kazuki, Ph.D, Miyoshi, Noriyuki, Ph.D, Goda, Toshinao, Ph.D
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.11.2010
[New York]: Elsevier Science Inc
Elsevier
Elsevier Limited
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Summary:Abstract Objective β-Carotene is an abundant carotenoid with potent antioxidative activities and accumulates in adipose tissue. However, its physiologic functions are poorly understood. In this study, we examined whether accumulation of β-carotene for 4 d in insulin-resistant 3T3-L1 adipocytes alters the expression of genes related to insulin sensitivity. Methods The 3T3-L1 adipocytes were treated with/without 10 or 20 μM β-carotene during differentiation for 4 d. The cells treated with 10 μM β-carotene for 4 d were subsequently incubated with/without 5 ng/mL of tumor necrosis factor-α for 48 h in the medium without β-carotene. The mRNA levels of genes in the cells and adiponectin protein levels in the medium were determined by real-time reverse transcription–polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Reactive oxygen species levels in the cells were assessed by oxidation of 2′,7′-dichlorodihydrofluorescein diacetate. Result β-Carotene treatment at a concentration of 20 μM, but not 10 μM, in 3T3-L1 adipocytes during differentiation for 4 d enhanced the expression of genes related to insulin sensitivity, including adiponectin, adipocyte lipid-binding protein, glucose transporter-4, peroxisome proliferator-activated receptor-γ2, and adiponectin protein in the medium. Tumor necrosis factor-α treatment repressed the expression of these genes and adiponectin protein in the medium and induced reactive oxygen species levels. In contrast, cells that accumulated β-carotene at a concentration of 10 μM did not show these alterations. Conclusion The accumulation of the β-carotene in 3T3-L1 adipocytes restores the expression of genes related to insulin sensitivity and reactive oxygen species levels in insulin-resistant adipocytes.
Bibliography:http://dx.doi.org/10.1016/j.nut.2009.09.006
ObjectType-Article-1
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ISSN:0899-9007
1873-1244
DOI:10.1016/j.nut.2009.09.006