Promoting brown and beige adipocyte biogenesis through the PRDM16 pathway

Kajimura, Shingo

doi:10.1038/ijosup.2015.4

Cited by 38 publications

(33 citation statements)

References 41 publications

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“…BAT-specific deletion of Mettl3 decreases iBAT-specific mRNA m 6 A modification and expression, including Prdm16, Pparg, and Ucp1 transcripts. One target of METTL3 is Prdm16, which has been shown to drive the differentiation of brow fat cells and browning of WAT by activating the expression of BAT-selective genes including Ucp1 and Pgc-1α 11,45,46 . Similarly, BAT-specific deletion of Mettl3 impaired BAT development and also impaired the development of beige adipocytes in iWAT.…”

Section: Discussionmentioning

confidence: 99%

METTL3 is essential for postnatal development of brown adipose tissue and energy expenditure in mice

et al. 2020

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Brown adipose tissue (BAT) undergoes rapid postnatal development and then protects against cold and obesity into adulthood. However, the molecular mechanism that determines postnatal development and maturation of BAT is largely unknown. Here we show that METTL3 (a key RNA methyltransferase) expression increases significantly in interscapular brown adipose tissue (iBAT) after birth and plays an essential role in the postnatal development and maturation of iBAT. BAT-specific deletion of Mettl3 severely impairs maturation of BAT in vivo by decreasing m 6 A modification and expression of Prdm16, Pparg, and Ucp1 transcripts, which leads to a marked reduction in BAT-mediated adaptive thermogenesis and promotes high-fat diet (HFD)-induced obesity and systemic insulin resistance. These data demonstrate that METTL3 is an essential regulator that controls iBAT postnatal development and energy homeostasis.

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Section: Discussionmentioning

confidence: 99%

METTL3 is essential for postnatal development of brown adipose tissue and energy expenditure in mice

et al. 2020

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“…Thus, UCP1 expression has been indicated as a therapeutic target to increase energy expenditure. In response to physiological stimuli, such as exposure to cold temperatures, some adipocytes in WAT are differentiated into brown like-adipocytes, known as beige or brite adipocytes, that acquire UCP1 expression [8]. This process requires the same major transcriptional factors and indicators as those used to develop brown adipocytes, and they include PR domaincontaining 16 (PRDM16), peroxisome proliferator-activated receptor gamma coactivator 1α (PGC1α), and cell death-inducing DFFA-like effector (CIDEA) [9].…”

Section: Introductionmentioning

confidence: 99%

Quercetin, a functional compound of onion peel, remodels white adipocytes to brown-like adipocytes

Lee

Parks

Kang

2017

The Journal of Nutritional Biochemistry

113

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Adipocyte browning is a promising strategy for obesity prevention. Using onion-peel-derived extracts and their bioactive compounds, we demonstrate that onion peel, a by-product of onion, can change the characteristics of white adipocytes to those of brown-like adipocytes in the white adipose tissue of mice and 3T3-L1 cells. The expression of the following brown adipose tissue-specific genes was increased in the retroperitoneal and subcutaneous adipose tissues of 0.5% onion-peel-extract-fed mice: PR domain-containing 16, peroxisome proliferator-activated receptor gamma coactivator 1α, uncoupling protein 1, fibroblast growth factor 21 and cell death-inducing DFFA-like effector. In 3T3-L1 adipocytes, onion peel extract induced the expression of brown adipose tissue-specific genes and increased the expression of carnitine palmitoyltransferase 1α. This effect was supported by decreased lipid levels and multiple small-sized lipid droplets. The ethyl acetate fraction of the onion peel extract that contained the highest proportion of hydrophobic molecules showed the same browning effect in 3T3-L1 adipocytes. A high-performance liquid chromatography analysis further identified quercetin as a functional compound in the browning effect of onion peel. The quercetin-associated browning effect was mediated in part by the activation of AMP-activated protein kinase. In summary, our study provides the first demonstration of the browning effects of onion peel and quercetin using both animal and cell models. This result indicates that onion peel has the potential to remodel the characteristics of white adipocytes to those of brown-like adipocytes.

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“…PRDM16 is a well-characterized transcriptional co-regulator that plays a pivotal role in both brown and beige adipocyte development and function [50,51]. PRDM16 can repress WAT-specific genes and activate BAT-specific genes [50].…”

Section: Browning/beiging Of White Adipose Tissuementioning

confidence: 99%

Latest advances in STAT signaling and function in adipocytes

2020

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Adipocytes and adipose tissue are not inert and make substantial contributions to systemic metabolism by influencing energy homeostasis, insulin sensitivity, and lipid storage. In addition to well-studied hormones such as insulin, there are numerous hormones, cytokines, and growth factors that modulate adipose tissue function. Many endocrine mediators utilize the JAK-STAT pathway to mediate dozens of biological processes, including inflammation and immune responses. JAKs and STATs can modulate both adipocyte development and mature adipocyte function. Of the seven STAT family members, four STATs are expressed in adipocytes and regulated during adipogenesis (STATs 1, 3, 5A, and 5B).

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Promoting brown and beige adipocyte biogenesis through the PRDM16 pathway

Cited by 38 publications

References 41 publications

METTL3 is essential for postnatal development of brown adipose tissue and energy expenditure in mice

METTL3 is essential for postnatal development of brown adipose tissue and energy expenditure in mice

Quercetin, a functional compound of onion peel, remodels white adipocytes to brown-like adipocytes

Latest advances in STAT signaling and function in adipocytes

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