Opposite regulation of PPAR-α and -γ gene expression by both their ligands and retinoic acid in brown adipocytes

Valmaseda, Angel; Carmona, Mamen; Barberà, Maria José; Viñas, Octavi; Mampel, Teresa; Iglesias, Roser; Villarroya, Francesc; Giralt, Marta

doi:10.1016/s0303-7207(99)00081-7

Cited by 59 publications

(71 citation statements)

References 45 publications

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“…In standard diet-fed animals, reduction of adiposity and body weight after tRA treatment correlated with a general down-regulation of the expression of PPAR␥2 in all the adipose depots examined. This is in agreement with previous results obtained in in vitro systems (3T3-L1 cells and brown adipocytes differentiated in primary culture), showing RA-induced down-regulation of PPAR␥ expression (21,35), and is consistent with the proposed mechanism of action of RA on preadipose cells. Thus, through binding to RAR, RA is believed to block the C/EBP␤-mediated induction of downstream genes, notably PPAR␥, at early stages of the adipogenic process (22).…”

Section: Effects Of Tra Treatmentsupporting

confidence: 93%

Changes of Adiposity in Response to Vitamin A Status Correlate with Changes of PPARγ2 Expression

et al. 2001

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RIBOT, JOAN, FRANCISCO FELIPE, M. LUISA BONET, AND ANDREU PALOU. Changes of adiposity in response to vitamin A status correlate with changes of PPAR␥2 expression. Obes Res. 2001;9:500 -509. Objective: To gain insight into the in vivo modulation of the expression of the adipogenic transcription factors PPAR␥2, C/EBP␣, and ADD1/SREBP1c by retinoids and its relationship with whole-body adiposity. Research Methods and Procedures: Three-week-old mice were fed with standard chow or a vitamin A-deficient diet for 10 weeks. During the 4 days immediately before they were killed, the animals were treated either with all-trans retinoic acid (tRA; 100 mg/kg per day, subcutaneously) or vehicle. The specific levels of the mRNAs for the three transcription factors were analyzed in epididymal white adipose tissue (eWAT) and inguinal white adipose tissue and in brown adipose tissue (BAT). Other parameters determined were leptin and UCP2 levels in white adipose tissue depots, total cholesterol and triglyceride serum levels, energy intake, body weight, and adiposity. Results: Vitamin A-deficient diet feeding led to a marked increase of adiposity and to a small increase of body weight. Hypertrophy of white adipose tissue depots correlated with enhanced PPAR␥2 expression. Hypertrophy of BAT, in contrast, correlated with a decrease of PPAR␥2 expression that may contribute to the known reduced thermogenic potential of BAT under conditions of vitamin A restriction. Treatment with tRA triggered a reduction of adiposity and body weight that correlated with a down-regulation of PPAR␥2 expression in all adipose tissues. The effects of tRA were more pronounced in eWAT, where C/EBP␣ and ADD1/SREBP1c levels were also reduced. The response to tRA was impaired in the eWAT and BAT of animals fed the vitamin A-deficient diet. Discussion: The results emphasize the importance of retinoids as physiological regulators of adipose tissue development and function in intact animals.

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Section: Effects Of Tra Treatmentsupporting

confidence: 93%

Changes of Adiposity in Response to Vitamin A Status Correlate with Changes of PPARγ2 Expression

et al. 2001

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“…In contrast to PPAR and PPAR expression however, which is attained early (while cells do not show signs of adipocyte conversion) PPAR mRNA becomes detectable and increases during terminal differentiation co-incident with UCP1 expression [80].…”

Section: Pparmentioning

confidence: 88%

“…On the other hand, whilst not detected in HIB-1B clonal adipocytes (irrespective of whether they are exposed to norepinephrine) PPAR mRNA is expressed in differentiated primary murine brown adipocytes [80]. In contrast to PPAR and PPAR expression however, which is attained early (while cells do not show signs of adipocyte conversion) PPAR mRNA becomes detectable and increases during terminal differentiation co-incident with UCP1 expression [80].…”

Section: Pparmentioning

confidence: 99%

“…PPAR may serve to stimulate adipogenesis (perhaps in response to activation by long chain FFA) by inducing PPAR expression and promoting mitotic clonal expansion [77][78][79]. PPAR gene expression likewise increases during early brown adipogenesis [80]. While PPAR -deficient brown fat cells differentiate normally in vitro they display dramatically decreased expression of UCP1 and mitochondrial metabolic genes (in the context of normal PPAR , PPAR , and PGC-1 expression).…”

Section: Ppar and Insulin Resistancementioning

confidence: 99%

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PPARs and adipocyte function

Christodoulides

Vidal-Puig

2010

Molecular and Cellular Endocrinology

115

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Abstract:For long viewed as passive lipid storage depots, adipocytes are now recognised as key players in the pathogenesis of insulin resistance and metabolic disease. In parallel, the last two decades of research have seen the emergence of transcription factors of the peroxisome proliferator-activated receptor (PPAR) family as central regulators of lipid and glucose homeostasis and molecular targets for drugs to treat hyper-lipidaemia and type 2 diabetes mellitus. In this review we discuss the characteristics of PPARs and the role of the different isotypes in adipocyte biology.

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“…30 Thiazolidinedione treatment in vivo recruits BAT depots and promotes the browning of WAT, but there are indications that parallel noradrenergic activation is required for thiazolidinediones to produce effective thermogenic induction. 31 In contrast to PPARγ, which is expressed in and regulates adipogenesis in both white and brown adipocytes, PPARα is preferentially expressed in BAT, 32 and genetic data point to PPARα as an essential component of the BAT-specific phenotype. 33 Ligand-dependent activation of PPARα induces UCP1 expression and some other aspects of thermogenic activation in brown adipocytes.…”

Section: Hormones Vitamins and Metabolites That Act Through Nuclear mentioning

confidence: 99%

Non-sympathetic control of brown adipose tissue

Cereijo

Villarroya

2015

Int J Obes Supp

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The thermogenic activity of brown adipose tissue (BAT) in the organism is tightly regulated through different processes, from short-term induction of uncoupling protein-1-mediated mitochondrial proton conductance to complex processes of BAT recruitment, and appearance of the beige/brite adipocytes in white adipose tissue (WAT), the so-called browning process. The sympathetic nervous system is classically recognized as the main mediator of BAT activation. However, novel factors capable of activating BAT through non-sympathetic mechanisms have been recently identified. Among them are members of the bone morphogenetic protein family, with likely autocrine actions, and activators of nuclear hormone receptors, especially vitamin A derivatives. Multiple endocrine factors released by peripheral tissues that act on BAT have also been identified. Some are natriuretic peptides of cardiac origin, whereas others include irisin, originating in skeletal muscle, and fibroblast growth factor-21, mainly produced in the liver. These factors have cell-autonomous effects in brown adipocytes, but indirect effects in vivo that modulate sympathetic activity toward BAT cannot be excluded. Moreover, these factors can affect to different extents such as the activation of existing BAT, the induction of browning in WAT or both. The identification of non-sympathetic controllers of BAT activity is of special biomedical interest as a prerequisite for developing pharmacological tools that influence BAT activity without the side effects of sympathomimetics.

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Opposite regulation of PPAR-α and -γ gene expression by both their ligands and retinoic acid in brown adipocytes

Cited by 59 publications

References 45 publications

Changes of Adiposity in Response to Vitamin A Status Correlate with Changes of PPARγ2 Expression

Changes of Adiposity in Response to Vitamin A Status Correlate with Changes of PPARγ2 Expression

PPARs and adipocyte function

Non-sympathetic control of brown adipose tissue

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