Remodeling of White Adipose Tissue after Retinoic Acid Administration in Mice

Mercader, Josep M.; Ribot, Joan; Murano, Incoronata; Felipe, Francisco; Cinti, Saverio; Bonet, M. Luisa; Palou, Andreu

doi:10.1210/en.2006-0760

Cited by 220 publications

(220 citation statements)

References 41 publications

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“…It has been shown that retinoic acid in vivo induces a recruitment of multilocular cells in mouse WAT, but stimulates more the expression of the oxidative enzymes than that of UCP1. 36 Altogether, the different modulation patterns of BAT B and WAT B adipocytes confirm a different nature of the two cell types. They are in agreement with the results of Coulter et al 16 showing that fundamentally different regulatory mechanisms exist to control the thermogenic capacities of these tissues.…”

Section: Discussionmentioning

confidence: 86%

Differentiation and characterization in primary culture of white adipose tissue brown adipocyte-like cells

Lehr¹,

Canola²,

Léger

et al. 2009

Int J Obes

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Background: Rodent brown adipose tissue (BAT) is considered the main effector of adaptative thermogenesis as it contains a unique mitochondrial uncoupling protein, termed as uncoupling protein-1 (UCP1). The emergence of ectopic brown adipocytes in the white adipose tissue (WAT), called recruitment, might play an important role in the prevention of obesity. The recruitment phenomenon has until now been investigated mostly in vivo. Objectives: This study is an attempt to mimic in vitro the recruitment phenomenon. It consisted in culturing the stroma vascular fractions of mouse BAT and WAT in a brown adipocyte differentiation medium. The multilocular cells obtained, referred to as BAT B and WAT B adipocytes, respectively, were compared. Results: The BAT B and WAT B adipocytes were morphologically different. The expressions of UCP1, peroxisome proliferatoractivated receptor-g coactivator-1a (PGC-1a), leptin and resistin mRNAs were low in WAT B adipocytes as compared with those in BAT B adipocytes. The expressions of UCP1 and PGC-1a proteins were, however, much higher in WAT B adipocytes, amounting 51% and 36% of those in BAT B adipocytes. The patterns of expression of UCP1, PGC-1a and leptin in the BAT B and in WAT B adipocytes were different with a higher relative expression of PGC-1a in the latter. Rosiglitazone increased UCP1 mRNA expression 4.5-fold in the BAT B and significantly more, 7.9-fold, in the WAT B adipocytes. Retinoic acid and triiodothyronine increased UCP1 mRNA expression in the BAT B adipocytes 1.6-and 2-fold, respectively but, surprisingly, slightly decreased UCP1 mRNA expression in the WAT B adipocytes. Conclusions: The study suggests that the nature and possibly the origin of WAT brown adipocytes is different from that of BAT brown adipocytes. It proposes an in vitro approach that could prove very useful to better characterize the WAT brown adipocyte-like cells.

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Section: Discussionmentioning

confidence: 86%

Differentiation and characterization in primary culture of white adipose tissue brown adipocyte-like cells

Lehr¹,

Canola²,

Léger

et al. 2009

Int J Obes

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“…To the best of our knowledge, only studies dealing with all-trans RA have been published. These studies showed that both in in vivo (in treated mice) and mature 3T3-L1 adipocytes, all-trans RA triggered remodelling to reduce lipogenesis and increased oxidative metabolism, as shown by gene expression changes, histological changes and in the case of cultured cells, increases in lipolysis and fatty acid oxidation [50,51].…”

Section: Lipid Metabolismmentioning

confidence: 99%

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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“…9,10 Retinoic acid (RA), its acid form, potently blocks adipogenesis of cultured preadipose cells when introduced at early stages of the differentiation process, 11 although other reports indicate that RA at low doses may in fact promote adipogenesis. [12][13][14] Studies in adult rodents treated with RA [15][16][17][18][19][20][21][22][23] or retinaldehyde 24 sustain an antiadiposity action of vitamin A derivatives in vivo. Furthermore, results from animal studies 16,[25][26][27][28] and human observational studies 29,30 point to an inverse relationship between vitamin A status and body fat content.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, results from animal studies 16,[25][26][27][28] and human observational studies 29,30 point to an inverse relationship between vitamin A status and body fat content. The antiadiposity action of RA has been traced to increased fatty acid oxidation and energy expenditure in adipose tissues, 15,19,21,31 skeletal muscle 20,32 and the liver, 33 and to reduced peroxisome proliferator-activated receptor g (PPARg) levels and activity in white fat. 16,34,35 PPARg is a nuclear receptor transcription factor key for adipogenesis and also required for lipogenesis and survival in mature adipocytes.…”

Section: Introductionmentioning

confidence: 99%

Vitamin A supplementation in early life affects later response to an obesogenic diet in rats

et al. 2012

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OBJECTIVE:To assess the influence of supplementation with a moderate dose of vitamin A in early life on adipose tissue development and the response to an obesogenic diet later in life. METHODS: During the suckling period, rat pups received a daily oral dose of retinyl palmitate corresponding to three times the vitamin A ingested daily from maternal milk. Control rats received the vehicle (olive oil). Short-term effects of treatment on gene expression and morphology of white adipose tissue (WAT) were analyzed in animals on the day after weaning (day 21). To study long-term effects, control and vitamin A-treated rats were fed, after weaning, a normal fat or a high-fat (HF) diet for 16 weeks. RESULTS: WAT of vitamin A-treated young rats (day 21) was enriched in small adipocytes with a reduced expression of adipogenic markers (peroxisome proliferator-activated receptor g and lipoprotein lipase) and an increased cell proliferation potential as indicated by increased expression of proliferating cell nuclear antigen. Increased retinoic acid (RA)-induced transcriptional responses were present in the tissues of vitamin A-treated young rats (day 21) including WAT. Vitamin A-treated rats developed higher adiposity than control rats on a HF diet as indicated by body composition analysis and increased WAT depot mass, adipocyte diameter, WAT DNA content, leptinemia and adipose leptin gene expression. Excess adiposity gain in vitamin A-treated rats developed in the absence of changes in body weight and was attributable to excess adipocyte hyperplasia. No differences in adiposity were observed between vitamin A-treated rats and control rats on a normal fat diet. Total retinol levels in WAT of vitamin A-treated rats were elevated at weaning (day 21) and normalized by day 135 of age. CONCLUSION: Vitamin A intake in the early stages of postnatal life favors subsequent HF diet-induced adiposity gain through mechanisms that may relate to changes in adipose tissue development, likely mediated by RA.

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Remodeling of White Adipose Tissue after Retinoic Acid Administration in Mice

Cited by 220 publications

References 41 publications

Differentiation and characterization in primary culture of white adipose tissue brown adipocyte-like cells

Differentiation and characterization in primary culture of white adipose tissue brown adipocyte-like cells

β-Carotene conversion products and their effects on adipose tissue

Vitamin A supplementation in early life affects later response to an obesogenic diet in rats

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