Mitochondrial Biogenesis and Thyroid Status Maturation in Brown Fat Require CCAAT/Enhancer-binding Protein α

Carmona, Mamen; Iglesias, Roser; Obregón, Marı́a-Jesús; Darlington, Gretchen J.; Villarroya, Francesc; Giralt, Marta

doi:10.1074/jbc.m201710200

Cited by 51 publications

(38 citation statements)

References 56 publications

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“…Morever, different C/EBPs (C/EBPa, C/EBPb, and C/EBPd) appeared able to transactivate the D2 rat promoter. Interestingly, knocking out C/EBPa leads to a decrease in D2 expression in brown adipose tissue (Carmona et al 2002). Further directed mutagenesis experiments might allow us to confirm the implication of the C/EBP-binding site in the rat dio2 promoter.…”

Section: Discussionmentioning

confidence: 99%

Bacterial lipopolysaccharide induces type 2 deiodinase in cultured rat astrocytes

Lamirand¹,

Ramaugé²,

Martineau³

et al. 2010

Journal of Endocrinology

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In the brain, 3,5,3 0 -triiodothyronine, which binds to the thyroid hormone receptor with high affinity, is locally generated from thyroxine by type 2 iodothyronine deiodinase (D2) expressed mainly in astrocytes and tanycytes. We have investigated the effects of bacterial lipopolysaccharide (LPS) on D2 in cultured rat astrocytes. LPS induced D2 activity with a lag-time of 4-8 h and a maximum at 24 h. LPS also promoted D2 mRNA accumulation. Glucocorticoids enhanced both the basal and LPS-stimulated D2 activity and mRNA accumulation. These glucocorticoid effects were blocked by the glucocorticoid receptor antagonist RU486. Our results obtained with different specific signaling pathway inhibitors indicated that D2 induction by LPS required ERK and p38-MAPK signaling pathways. NF-kB inhibitor sulfasalazine blocked the effects of LPS on both D2 activity and mRNA accumulation. Hence, D2 induction by LPS appeared to implicate NF-kB pathway in astrocytes. NF-kB responsiveness of the rat dio2 gene was studied in astrocytes with dio2 5 0 -flanking region promoter assays. The long form of the dio2 promoter was transactivated by NF-kB. CCAAT/enhancer-binding protein b, which is upregulated by LPS in astrocytes, increased the transcriptional activity of the dio2 promoter in its long or truncated forms containing CCAATs. Our observations, which demonstrate D2 induction by LPS in astrocytes and specify some characteristics of D2 induction mechanism, support the possible implication of brain D2 in adaptative responses to an infectious stress.

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Section: Discussionmentioning

confidence: 99%

Bacterial lipopolysaccharide induces type 2 deiodinase in cultured rat astrocytes

Lamirand¹,

Ramaugé²,

Martineau³

et al. 2010

Journal of Endocrinology

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“…Furthermore, the absence of C/EBP-α in mice impairs the development of WAT, but interestingly, it has no effect on BAT. Thus, some researchers have speculated that the lack of C/EBP-α can be compensated for in brown fat development by C/EBP-β [35] .…”

Section: Differentiation Of Adipocytesmentioning

confidence: 99%

Distinction of white, beige and brown adipocytes derived from mesenchymal stem cells

Park

Kim

Bae

2014

WJSC

209

177

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pattern distinct from that of either white or brown fat cells. The current epidemic of obesity has increased the interest in studying adipocyte formation (adipogenesis), especially in beige/brite cells. This review summarizes the developmental process of adipose tissues that originate from the mesenchymal stem cells and the features of these three different types of adipocytes.© 2014 Baishideng Publishing Group Co., Limited. All rights reserved.Key words: White adipocytes; Brown adipocytes; Beige/ brite adipocytes; Mesenchymal stem cells; Adipogenesis; Thermogenesis; Browning Core tip: Here, we summarize the characteristic differences of the white, brown and beige adipocytes derived from mesenchymal stem cells, including their anatomical location. In particular, we focus on the newly discovered brown-like adipocytes called beige/brite adipocytes. A deeper understanding of the molecular mechanism of these adipocytes may provide clues for overcoming obesity and its associated metabolic diseases. AbstractAdipose tissue is a major metabolic organ, and it has been traditionally classified as either white adipose tissue (WAT) or brown adipose tissue (BAT). WAT and BAT are characterized by different anatomical locations, morphological structures, functions, and regulations. WAT and BAT are both involved in energy balance. WAT is mainly involved in the storage and mobilization of energy in the form of triglycerides, whereas BAT specializes in dissipating energy as heat during cold-or diet-induced thermogenesis. Recently, brownlike adipocytes were discovered in WAT. These brownlike adipocytes that appear in WAT are called beige or brite adipocytes. Interestingly, these beige/brite cells resemble white fat cells in the basal state, but they respond to thermogenic stimuli with increased levels of thermogenic genes and increased respiration rates. In addition, beige/brite cells have a gene expression

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“…Control experiments were performed using purified rabbit IgG. Adipocyte size and distribution were determined by the vertical sections method (44,45). Fatty acid oxidation in liver.…”

Section: S 26948 a New Antidiabetes Drugmentioning

confidence: 99%

S 26948

et al. 2007

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OBJECTIVE-Rosiglitazone displays powerful antidiabetes benefits but is associated with increased body weight and adipogenesis. Keeping in mind the concept of selective peroxisome proliferator-activated receptor (PPAR)␥ modulator, the aim of this study was to characterize the properties of a new PPAR␥ ligand, S 26948, with special attention in body-weight gain.RESEARCH DESIGN AND METHODS-We used transient transfection and binding assays to characterized the binding characteristics of S 26948 and GST pull-down experiments to investigate its pattern of coactivator recruitment compared with rosiglitazone. We also assessed its adipogenic capacity in vitro using the 3T3-F442A cell line and its in vivo effects in ob/ob mice (for antidiabetes and antiobesity properties), as well as the homozygous human apolipoprotein E2 knockin mice (E2-KI) (for antiatherogenic capacity).RESULTS-S 26948 displayed pharmacological features of a high selective ligand for PPAR␥ with low potency in promoting adipocyte differentiation. It also displayed a different coactivator recruitment profile compared with rosiglitazone, being unable to recruit DRIP205 or PPAR␥ coactivator-1␣. In vivo experiments showed that S 26948 was as efficient in ameliorating glucose and lipid homeostasis as rosiglitazone, but it did not increase body and white adipose tissue weights and improved lipid oxidation in liver. In addition, S 26948 represented one of the few molecules of the PPAR␥ ligand class able to decrease atherosclerotic lesions.CONCLUSIONS-These findings establish S 26948 as a selective PPAR␥ ligand with distinctive coactivator recruitment and gene expression profile, reduced adipogenic effect, and improved biological responses in vivo.

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Mitochondrial Biogenesis and Thyroid Status Maturation in Brown Fat Require CCAAT/Enhancer-binding Protein α

Cited by 51 publications

References 56 publications

Bacterial lipopolysaccharide induces type 2 deiodinase in cultured rat astrocytes

Bacterial lipopolysaccharide induces type 2 deiodinase in cultured rat astrocytes

Distinction of white, beige and brown adipocytes derived from mesenchymal stem cells

S 26948

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