Brown adipose tissue hyperplasia: a fundamental mechanism of adaptation to cold and hyperphagia

Bukowiecki, L. J.; Collet, André; Follea, N.; Guay, G.; Jahjah, Liliane

doi:10.1152/ajpendo.1982.242.6.e353

Cited by 133 publications

(132 citation statements)

References 17 publications

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“…11,32 Precursor cells in BAT are known to undergo proliferation during the first week of cold exposure and give rise to new mature brown adipocytes between 4 and 16 days after the beginning of cold stimulation. 31,39,40 In similar conditions, the decrease in BUG transcript level implies that this RNA is not located in precursor cells induced to proliferate under this stimulus. Moreover, the observed variation is progressive compared to the UCP-1 one.…”

Section: Discussionmentioning

confidence: 98%

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Cloning of BUG demonstrates the existence of a brown preadipocyte distinct from a white one

et al. 2001

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BACKGROUND: Several indirect arguments agree with the existence of a brown preadipocyte distinct from a white one. Nevertheless, to date, no molecular marker has been available to directly in vivo demonstrate this hypothesis. OBJECTIVE: The aim of this study was to find a gene expressed in brown preadipocyte but not in white and to use it as a molecular marker to analyse brown preadipocyte recruitment in different physiological and physiopathological situations. METHOD: Differential display was performed on stromal-vascular and adipocyte fractions of white and brown adipose tissues in rat. RESULTS: We identified a new gene, BUG, preferentially expressed in the stromal-vascular fraction of brown fat vs other adipose tissues fractions in adult rat. This RNA is also highly expressed in heart and, to a lesser extent, in other tissues such as kidney and brain. The BUG transcript is detected by in situ hybridization in putative preadipocytes within brown adipose tissue. Its level is transiently and specifically up-regulated during early stages of brown preadipocyte differentiation in a primary culture system, before the acquisition of late brown adipocyte phenotype. During development, BUG can be detected before the emergence of UCP-1 expression. In adult rats, BUG expression is inversely associated to brown adipose tissue (BAT) activation during cold exposure as well as in obese animals. CONCLUSIONS: The pattern of BUG expression agrees with an early divergence between brown and white adipocyte lineages. It also reveals the existence of a pool of committed brown preadipocytes within BAT that are recruited during cold exposure. BUG expression is increased in obese animals, suggesting that an early defect in brown preadipocyte differentiation could account for impaired BAT function in genetically obese rats.

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Section: Discussionmentioning

confidence: 98%

“…31 Rats were exposed to a temperature of 4 C for 5 days. A 4-fold induction of UCP-1 mRNA occurred in the interscapular BAT after only 10 h of cold exposure, then the level fell and remained around 2-fold higher than in the control ( Figure 5A, upper panel).…”

Section: Cloning Of Bug a Marker Of Brown Preadipocyte K Moulin Et Almentioning

confidence: 99%

Cloning of BUG demonstrates the existence of a brown preadipocyte distinct from a white one

et al. 2001

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“…3). Prolonged cold exposure also stimulates the proliferation and differentiation of brown precursor cells to expand BAT mass and increase thermogenic capacity 70 . Conversely, at warmer housing temperatures or in surgically denervated BAT, the expression of Ucp1 and other thermogenic factors are substantially reduced in mice 71,72 .…”

Section: Sympathetic Nerve Control Of Brown and Beige Fatmentioning

confidence: 99%

“…Cold also stimulates sympathetic nerve branching and recruitment during the browning response of WAT 81 . In addition, cold exposure induces the sprouting and growth of blood vessels in adipose to facilitate oxygen delivery and heat exchange 70,72,88 . This angiogenic effect is regulated through increased production of vascular endothelial growth factor (Vegf) by a mechanism that does not involve hypoxia [89][90][91] .…”

Section: Sympathetic Nerve Control Of Brown and Beige Fatmentioning

confidence: 99%

Brown and beige fat: development, function and therapeutic potential

Harms

Seale

2013

Nat Med

1,903

2,054

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Adipose tissue, best known for its role in fat storage, can also suppress weight gain and metabolic disease through the action of specialized, heat-producing adipocytes. Brown adipocytes are located in dedicated depots and express constitutively high levels of thermogenic genes, whereas inducible 'brown-like' adipocytes, also known as beige cells, develop in white fat in response to various activators. The activities of brown and beige fat cells reduce metabolic disease, including obesity, in mice and correlate with leanness in humans. Many genes and pathways that regulate brown and beige adipocyte biology have now been identified, providing a variety of promising therapeutic targets for metabolic disease.npg

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“…Long-term thermogenic induction ultimately leads to the enlargement of BAT mass through promotion of tissue hypertrophy and hyperplasia. 3 Persistent thermogenic stimulation leads not only to the enlargement of BAT at its anatomical locations but also promotes the appearance of brown adipocytes in anatomical sites of white adipose tissue (WAT). 4 This latter process is commonly called 'browning' of WAT, and the brown adipocytes that appear in WAT depots are termed 'brite' (from brown-in-white) 5 or beige 6 adipocytes.…”

Section: Introductionmentioning

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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Brown adipose tissue hyperplasia: a fundamental mechanism of adaptation to cold and hyperphagia

Cited by 133 publications

References 17 publications

Cloning of BUG demonstrates the existence of a brown preadipocyte distinct from a white one

Cloning of BUG demonstrates the existence of a brown preadipocyte distinct from a white one

Brown and beige fat: development, function and therapeutic potential

Non-sympathetic control of brown adipose tissue

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