Stimulation of uncoupling protein 1 expression in brown adipocytes by naturally occurring carotenoids

Serra, Francisca; Bonet, M. Luisa; Puigserver, Pere; Oliver, Jordi; Palou, Andreu

doi:10.1038/sj.ijo.0800897

Cited by 58 publications

(32 citation statements)

References 24 publications

(29 reference statements)

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“…Provitamin A carotenoids also induced UCP1 expression in primary brown adipocytes differentiated in culture [61]. This induction is explained by the existence of RA and PPAR response elements in the UCP1 gene promoter.…”

Section: Adipocyte Differentiationmentioning

confidence: 82%

β-Carotene conversion products and their effects on adipose tissue

et al. 2009

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Recent epidemiological data suggest that b-carotene may be protective against metabolic diseases in which adipose tissue plays a key role. Adipose tissue constitutes the major b-carotene storage tissue and its functions have been shown to be modulated in response to b-carotene breakdown products, especially retinal produced after cleavage by b-carotene 15,15 0 -monooxygenase (BCMO1), and retinoic acid arising from oxidation of retinal. However, the possibility exists that b-carotene in its intact form can also affect adipocyte function. Development of a knock out model and identification of a loss-offunction mutation have pointed out BCMO1 as being probably the sole enzyme responsible for provitamin A conversion into retinal in mammals. The utilisation of BCMO1 -/-mice should provide insights on b-carotene effect on its own in the future. In humans, intervention studies have highlighted the huge interindividual variation of b-carotene conversion efficiency, possibly due to genetic polymorphisms, which might impact on response to b-carotene. This brief review discusses the processes involved in b-carotene conversion and the effect of cleavage products on body fat and adipose tissue function.

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Section: Adipocyte Differentiationmentioning

confidence: 82%

β-Carotene conversion products and their effects on adipose tissue

et al. 2009

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“…b-carotene and other naturally occurring carotenoids also stimulate UCP1 expression in cultured brown adipocytes, an effect that could be due, at least in part, to their local conversion into RA [47]. In confluent brown adipocytes in primary culture, alltrans RA and 9-cis RA displayed a similar effectiveness as UCP1 inducers that was comparable to that of noradrenaline, dose-dependent and dependent on the stage of cell differentiation, the effect being restricted to differentiated cells [43,44].…”

Section: Vitamin a And Ucp1 Expressionmentioning

confidence: 97%

Vitamin A and the regulation of fat reserves

Bonet

Ribot

Felipe

et al. 2003

Cellular and Molecular Life Sciences (CMLS)

161

125

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Beyond their classical nutritional roles, nutrients modify gene expression and function in target cells and, by so doing, affect many fundamental biological processes. An emerging example, which is the focus of this review, is the involvement of vitamin A in the regulation of the level and functioning of body fat reserves. Retinoic acid, the carboxylic acid form of vitamin A, is a transcriptional activator of the genes encoding uncoupling proteins, and results in animals indicate that whole body thermogenic capacity is related to the vitamin A status. Retinoic acid also influences adipocyte differentiation and survival, with high doses inhibiting and low doses promoting adipogenesis of preadipose cells in culture. Moreover, vitamin A status can influence the development and function of adipose tissues in whole animals, with a low vitamin A status favouring increased fat deposition.

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“…20 On the other hand, retinoic acid (RA), the carboxylic acid form of vitamin A and a well-known modulator of gene transcription, has been shown to up-regulate the expression of the UCPs in cell model systems, 21 -25 an effect that, in the case of UCP1, has also been demonstrated for certain pro-vitamin A carotenoids. 26 Up-regulation of BAT UCP1 22,27,28 and UCP2 28 expression was also reported after acute RA-treatment in intact rodents, where it correlated with a significant reduction of body weight and body adiposity. 22,28,29 Moreover, mice fed a vitamin A-deficient diet had reduced levels of expression of UCP1 and UCP2 in BAT, increased levels of expression of adipogenic transcription factors in white fat depots, and a higher adiposity and body weight than control mice, 28,29 suggesting that the vitamin A status can affect both the thermogenic and the adipogenic capacity of rodents.…”

Section: Introductionmentioning

confidence: 93%

Up-regulation of muscle uncoupling protein 3 gene expression in mice following high fat diet, dietary vitamin A supplementation and acute retinoic acid-treatment

et al. 2003

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OBJECTIVE:To analyse the impact of vitamin A supplementation of both a normal fat (NF) diet and a high fat (HF) diet and of acute retinoic acid (RA)-treatment on the expression of uncoupling protein 3 (UCP3) in mice. DESIGN: C57BL=6J mice were fed for 18 weeks a NF or a HF diet (10 and 45 energy% as fat, respectively), both with the normal vitamin A content or an excess vitamin A (8 mg and 320 mg retinyl palmitate=kg diet, respectively). Body weight and energy intake were recorded periodically. UCP3 mRNA and UCP3 protein levels in skeletal muscle (soleus=gastrocnemius) were analysed, as well as UCP1, UCP2 and UCP3 mRNA levels in interscapular brown adipose tissue (BAT), and UCP2 mRNA, UCP2 protein and leptin mRNA levels in white adipose tissue (WAT) depots. The effect of acute RA-treatment (100 mg=kg=day, 4 days) on UCP3 mRNA levels in skeletal muscle and BAT of NMRI mice was also assessed. RESULTS: Vitamin A supplementation of a NF diet led to increased levels of UCP3 mRNA and UCP3 protein in muscle, UCP1 mRNA in BAT, and UCP2 mRNA in inguinal WAT, but had no impact on body weight or adiposity of B6 mice. HF diet promoted obesity and increased levels of UCP3 mRNA and UCP3 protein in skeletal muscle, and of the mRNAs for all three UCPs in BAT. Supplementing the HF diet with vitamin A had little effect on the final obesity reached and did not lead to further increases of muscle UCP3 mRNA nor BAT UCP1 mRNA over the levels achieved with the non-supplemented HF diet. Adipose leptin mRNA levels were down regulated after vitamin A supplementation, independently of the fat content of the diet. Up-regulation of muscle, but not BAT, UCP3 mRNA levels was also found after acute RA-treatment in NMRI mice. CONCLUSION:The results provide evidence of a stimulatory effect of retinoids on muscle UCP3 expression in vivo, and a differential retinoid-regulation of the UCP3 gene in muscle and BAT.

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Stimulation of uncoupling protein 1 expression in brown adipocytes by naturally occurring carotenoids

Cited by 58 publications

References 24 publications

β-Carotene conversion products and their effects on adipose tissue

β-Carotene conversion products and their effects on adipose tissue

Vitamin A and the regulation of fat reserves

Up-regulation of muscle uncoupling protein 3 gene expression in mice following high fat diet, dietary vitamin A supplementation and acute retinoic acid-treatment

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