PRDM16: the interconvertible adipo-myocyte switch

Frühbeck, Gema; Sesma, P.; Burrell, Marı́a A.

doi:10.1016/j.tcb.2009.01.007

Cited by 55 publications

(55 citation statements)

References 29 publications

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“…These cells when treated with a β-adrenoreceptor agonist express UCP1, which is a hallmark of brown adipocytes (Inokuma et al, 2005;Kozak et al, 1992). Myf5 lineage tracing studies suggest that brown adipocytes are derived from precursor cells capable of differentiating into myoblasts (Fruhbeck et al, 2009). DNA microarray experiments conducted by Timmons et al support the notion of similarity between skeletal muscle and BAT origin, as the precursors of the two tissue possess many genes and micro-RNA in common (Timmons et al, 2007;Walden et al, 2009).…”

Section: Origin Of White and Brown Adipocytesmentioning

confidence: 99%

Adipocyte transdifferentiation and its molecular targets

et al. 2014

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Section: Origin Of White and Brown Adipocytesmentioning

confidence: 99%

Adipocyte transdifferentiation and its molecular targets

et al. 2014

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“…Brown adipocytes are smaller than white adipocytes, are usually multi-locular (in comparison with white adipocytes with a single lipid droplet) and contain relatively large numbers of mitochondria. Brown adipocytes may be characterized by the expression of uncoupling protein-1 in the inner mitochondrial membrane, which allows energy expenditure through thermogenesis (Vernon, 1986;Cannon and Nedergaard, 2004) as well as by the expression of proteins involved in mitochondrial biogenesis and oxidative activity (Fruhbeck et al, 2009). Growth of BAT and WAT results from increases in adipocyte number (hyperplasia) and/or volume (hypertrophy).…”

Section: Dynamics Of At Growthmentioning

confidence: 99%

Ontogenesis of muscle and adipose tissues and their interactions in ruminants and other species

Bonnet

Cassar-Malek

Chilliard

et al. 2010

Animal

107

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The lean-to-fat ratio, that is, the relative masses of muscle and adipose tissue, is a criterion for the yield and quality of bovine carcasses and meat. This review describes the interactions between muscle and adipose tissue (AT) that may regulate the dynamic balance between the number and size of muscle v. adipose cells. Muscle and adipose tissue in cattle grow by an increase in the number of cells (hyperplasia), mainly during foetal life. The total number of muscle fibres is set by the end of the second trimester of gestation. By contrast, the number of adipocytes is never set. Number of adipocytes increases mainly before birth until 1 year of age, depending on the anatomical location of the adipose tissue. Hyperplasia concerns brown pre-adipocytes during foetal life and white pre-adipocytes from a few weeks after birth. A decrease in the number of secondary myofibres and an increase in adiposity in lambs born from mothers severely underfed during early pregnancy suggest a balance in the commitment of a common progenitor into the myogenic or adipogenic lineages, or a reciprocal regulation of the commitment of two distinct progenitors. The developmental origin of white adipocytes is a subject of debate. Molecular and histological data suggested a possible transdifferentiation of brown into white adipocytes, but this hypothesis has now been challenged by the characterization of distinct precursor cells for brown and white adipocytes in mice. Increased nutrient storage in fully differentiated muscle fibres and adipocytes, resulting in cell enlargement (hypertrophy), is thought to be the main mechanism, whereby muscle and fat masses increase in growing cattle. Competition or prioritization between adipose and muscle cells for the uptake and metabolism of nutrients is suggested, besides the successive waves of growth of muscle v. adipose tissue, by the inhibited or delayed adipose tissue growth in bovine genotypes exhibiting strong muscular development. This competition or prioritization occurs through cellular signalling pathways and the secretion of proteins by adipose tissue (adipokines) and muscle (myokines), putatively regulating their hypertrophy in a reciprocal manner. Further work on the mechanisms underlying cross-talk between brown or white adipocytes and muscle fibres will help to achieve better understanding as a prerequisite to improving the control of body growth and composition in cattle.

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“…The formation of the mature brown adipocytes is achieved upon the expression of the specific markers for brown fat cells including Uncoupling-Protein-1 (UCP-1), PPARg Coactivator-1a (PGC-1a), Elongation of Very Long chain fatty acids gene 3 (Elovl3) and Cell Death-Inducing DNA Fragmentation Factor-like Effector A (Cidea). 12 p53, the well known tumor suppressor, that is central for the regulation of cell proliferation and apoptosis was also found to be involved in numerous other process. [13][14][15][16][17] Notably, p53 has been demonstrated as an important regulator of development and differentiation programs, either via its control of cell proliferation or by regulating the expression of specific genes involved in these specific programs.…”

mentioning

confidence: 99%

p53 is required for brown adipogenic differentiation and has a protective role against diet-induced obesity

et al. 2013

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Proper regulation of white and brown adipogenic differentiation is important for maintaining an organism's metabolic profile in a homeostatic state. The recent observations showing that the p53 tumor suppressor plays a role in metabolism raise the question of whether it is involved in the regulation of white and brown adipocyte differentiation. By using several in vitro models, representing various stages of white adipocyte differentiation, we found that p53 exerts a suppressive effect on white adipocyte differentiation in both mouse and human cells. Moreover, our in vivo analysis indicated that p53 is implicated in protection against diet-induced obesity. In striking contrast, our data shows that p53 exerts a positive regulatory effect on brown adipocyte differentiation. Abrogation of p53 function in skeletal muscle committed cells reduced their capacity to differentiate into brown adipocytes and histological analysis of brown adipose tissue revealed an impaired morphology in both embryonic and adult p53-null mice. Thus, depending on the specific adipogenic differentiation program, p53 may exert a positive or a negative effect. This cell type dependent regulation reflects an additional modality of p53 in maintaining a homeostatic state, not only in the cell, but also in the organism at large.

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PRDM16: the interconvertible adipo-myocyte switch

Cited by 55 publications

References 29 publications

Adipocyte transdifferentiation and its molecular targets

Adipocyte transdifferentiation and its molecular targets

Ontogenesis of muscle and adipose tissues and their interactions in ruminants and other species

p53 is required for brown adipogenic differentiation and has a protective role against diet-induced obesity

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