Talk:Adipose Tissue Development - Revision history

Z8600021 at 05:11, 13 August 2018

2018-08-13T05:11:02Z

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	PMID 17507398		PMID 17507398

			==1966==

			===Brown adipose tissue and heat production in the newborn infant===

			J Pathol Bacteriol. 1966 Jan;91(1):223-34.

			Aherne W, Hull D.

			PMID: 5941392 DOI: 10.1002/path.1700910126


			==1963==

			===THE DIFFERENTIATION OF WHITE ADIPOSE CELLS. AN ELECTRON MICROSCOPE STUDY===

			J Cell Biol. 1963 Sep;18:663-79.

			NAPOLITANO L.

			Abstract

			Differentiating white adipose tissue from presumptive and developing fat pads of newborn and young rats was fixed in buffered osmium tetroxide, embedded in Vestopal W, and examined in an electron microscope. Pre-adipose cells were found to be fibroblasts characterized by their spindle shape, long tenuous cytoplasmic extensions, and profuse endoplasmic reticulum. The developmental stages traced from fibroblast to mature adipose cell show a gradual change in cell shape, an accumulation of cytoplasm and non-membrane-bounded lipid, a decrease in the endoplasmic reticulum, and a change in shape of mitochondria. Transitory glycogen appears at mid-differentiation. Numerous smooth-membraned vesicles occur in the cytoplasm throughout differentiation. Pinocytosis is constantly evident. Cells of the multilocular stage are shown to differ from brown fat cells, particularly with respect to cytoplasmic membrane systems and mitochondria. No transport of particulate lipid from the lumen of the capillary to, or within, the adipose cell was detected, nor could any cell organelle be demonstrated to be visibly related to lipid synthesis and/or deposition.
			PMID: 14064115 PMCID: PMC2106313
			[Indexed for MEDLINE] Free PMC Article

Z8600021 at 00:52, 13 August 2018

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	PMID 27869309 DOI: 10.1002/jcp.25697		PMID 27869309 DOI: 10.1002/jcp.25697

			==2015==

			===Role of developmental transcription factors in white, brown and beige adipose tissues===

			Biochim Biophys Acta. 2015 May;1851(5):686-96. doi: 10.1016/j.bbalip.2015.02.003. Epub 2015 Feb 8.

			Hilton C1, Karpe F2, Pinnick KE3.
			Author information
			Abstract
			In this review we discuss the role of developmental transcription factors in adipose tissue biology with a focus on how these developmental genes may contribute to regional variation in adipose tissue distribution and function. Regional, depot-specific, differences in lipid handling and signalling (lipolysis, lipid storage and adipokine/lipokine signalling) are important determinants of metabolic health. At a cellular level, preadipocytes removed from their original depot and cultured in vitro retain depot-specific functional properties, implying that these are intrinsic to the cells and not a function of their environment in situ. High throughput screening has identified a number of developmental transcription factors involved in embryological development, including members of the Homeobox and T-Box gene families, that are strongly differentially expressed between regional white adipose tissue depots and also between brown and white adipose tissue. However, the significance of depot-specific developmental signatures remains unclear. Developmental transcription factors determine body patterning during embryogenesis. The divergent developmental origins of regional adipose tissue depots may explain their differing functional characteristics. There is evidence from human genetics that developmental genes determine adipose tissue distribution: in GWAS studies a number of developmental genes have been identified as being correlated with anthropometric measures of adiposity and fat distribution. Additionally, compelling functional studies have recently implicated developmental genes in both white adipogenesis and the so-called 'browning' of white adipose tissue. Understanding the genetic and developmental pathways in adipose tissue may help uncover novel ways to intervene with the function of adipose tissue in order to promote health.
			KEYWORDS:
			Adipose tissue; Body fat distribution; Development; Transcription factor
			PMID: 25668679 DOI: 10.1016/j.bbalip.2015.02.003

	==2013==		==2013==

Z8600021 at 05:52, 30 July 2018

2018-07-30T05:52:34Z

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	<pubmed limit=5>Adipose Tissue Development</pubmed>		<pubmed limit=5>Adipose Tissue Development</pubmed>

			==2018==

			===A mesodermal fate map for adipose tissue===

			Development. 2018 Jul 25. pii: dev.166801. doi: 10.1242/dev.166801. [Epub ahead of print]

			Sebo ZL1, Jeffery E2, Holtrup B1, Rodeheffer MS3,4,5,6.

			Abstract

			The embryonic origin of distinct fat depots and the role for ontogeny in specifying the functional differences among adipocyte lineages between and within depots is unclear. Using a Cre/Lox-based strategy to track the fate of major mesodermal subcompartments in mice we present evidence that fewer than 50% of interscapular brown adipocytes are derived from progenitors of the central dermomyotome. Furthermore, we demonstrate that depot-specific adipocyte lineages spatially diverge as early as gastrulation and that perigonadal adipocytes arise from separate mesodermal subcompartments in males and females. Last, we show adipocyte precursors (APs) of distinct lineages within the same depot exhibit indistinguishable responses to a high fat diet, indicating ontogenetic differences between APs do not necessarily correspond to functional differences in this context. Altogether, these findings shed light on adipose tissue patterning and suggest the behavior of adipocyte lineage cells is not strictly determined by developmental history.
			KEYWORDS:
			Adipocyte; Adipose; Development; Fate map; Lineage tracing; Mesoderm
			PMID: 30045918 DOI: 10.1242/dev.166801

	==2017==		==2017==

Z8600021 at 06:59, 12 April 2017

2017-04-12T06:59:13Z

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	<pubmed limit=5>Adipose Tissue Development</pubmed>		<pubmed limit=5>Adipose Tissue Development</pubmed>

			==2017==
			===Roles of Notch Signaling in Adipocyte Progenitor Cells and Mature Adipocytes===
			J Cell Physiol. 2017 Jun;232(6):1258-1261. doi: 10.1002/jcp.25697. Epub 2017 Jan 5.

			Shan T1, Liu J1, Wu W1, Xu Z1, Wang Y

			Abstract

			Adipose tissues, composed with mature adipocytes and preadipocytic stromal/stem cells, play crucial roles in whole body energy metabolism and regenerative medicine. Mature adipocytes are derived and differentiated from mesenchymal stem cells (MSCs) or preadipocytes. This differentiation process, also called adipogenesis, is regulated by several signaling pathways and transcription factors. Notch1 signaling is a highly conserved pathway that is indispensable for stem cell hemostasis and tissue development. In adipocyte progenitor cells, Notch1 signaling regulates the adipogenesis process including proliferation and differentiation of the adipocyte progenitor cells in vitro. Notably, the roles of Notch1 signaling in beige adipocytes formation, adipose development, and function, and the whole body energy metabolism have been recently reported. Here, we mainly review and discuss the roles of Notch1 signaling in adipogenesis in vitro as well as in beige adipocytes formation, adipocytes dedifferentiation, and function in vivo. J. Cell. Physiol. 232: 1258-1261, 2017. © 2016 Wiley Periodicals, Inc.
			© 2016 Wiley Periodicals, Inc.

			PMID 27869309 DOI: 10.1002/jcp.25697

	==2013==		==2013==

Z8600021 at 05:12, 15 March 2013

2013-03-15T05:12:54Z

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	==2013==		==2013==

			===Leptin signaling and circuits in puberty and fertility===

			Cell Mol Life Sci. 2013 Mar;70(5):841-62. doi: 10.1007/s00018-012-1095-1. Epub 2012 Aug 2.

			Elias CF, Purohit D.
			Source
			Division of Hypothalamic Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Y6-220B, Dallas, TX, 75390-9077, USA, carol.elias@utsouthwestern.edu.

			Abstract

			Leptin is an adipocyte-derived hormone involved in a myriad of physiological process, including the control of energy balance and several neuroendocrine axes. Leptin-deficient mice and humans are obese, diabetic, and display a series of neuroendocrine and autonomic abnormalities. These individuals are infertile due to a lack of appropriate pubertal development and inadequate synthesis and secretion of gonadotropins and gonadal steroids. Leptin receptors are expressed in many organs and tissues, including those related to the control of reproductive physiology (e.g., the hypothalamus, pituitary gland, and gonads). In the last decade, it has become clear that leptin receptors located in the brain are major players in most leptin actions, including reproduction. Moreover, the recent development of molecular techniques for brain mapping and the use of genetically modified mouse models have generated crucial new findings for understanding leptin physiology and the metabolic influences on reproductive health. In the present review, we will highlight the new advances in the field, discuss the apparent contradictions, and underline the relevance of this complex physiological system to human health. We will focus our review on the hypothalamic circuitry and potential signaling pathways relevant to leptin's effects in reproductive control, which have been identified with the use of cutting-edge technologies of molecular mapping and conditional knockouts.

			PMID 22851226


	==2012==		==2012==

Z8600021 at 09:44, 18 February 2013

2013-02-18T09:44:03Z

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	{{Talk Page}}		{{Talk Page}}

	[http://www.ncbi.nlm.nih.gov/pmc/?term=adipocyte+differentiation&report=imagesdocsum ~~Search for~~ adipocyte differentiation ~~images~~]		==PubMed Central Images==

			* [http://www.ncbi.nlm.nih.gov/pmc/?term=adipocyte+differentiation&report=imagesdocsum adipocyte differentiation]

	==10 Most Recent==		==10 Most Recent==

Z8600021 at 09:41, 18 February 2013

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	{{Talk Page}}		{{Talk Page}}

			[http://www.ncbi.nlm.nih.gov/pmc/?term=adipocyte+differentiation&report=imagesdocsum Search for adipocyte differentiation images]

	==10 Most Recent==		==10 Most Recent==

Z8600021: /* 2013 */

2013-02-18T09:23:02Z

2013

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	==2013==		==2013==

			==2012==


			===The fat controller: adipocyte development===
			PLoS Biol. 2012 Nov;10(11):e1001436. doi: 10.1371/journal.pbio.1001436. Epub 2012 Nov 27.

			Stephens JM.
			Source
			Adipocyte Biology Laboratory, Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana, United States of America. jsteph1@lsu.edu

			Abstract

			Obesity is a condition characterized by excess adipose tissue that results from positive energy balance and is the most common metabolic disorder in the industrialized world. The obesity epidemic shows no sign of slowing, and it is increasingly a global problem. Serious clinical problems associated with obesity include an increased risk for type 2 diabetes, atherosclerosis, and cancer. Hence, understanding the origin and development of adipocytes and adipose tissue will be critical to the analysis and treatment of metabolic diseases. Historically, albeit incorrectly, adipocytes were thought to be inert cells whose singular function was lipid storage. It is now known that adipocytes have other critical functions; the most important include sensitivity to insulin and the ability to produce and secrete adipocyte-specific endocrine hormones that regulate energy homeostasis in other tissues. Today, adipocytes are recognized as critical regulators of whole-body metabolism and known to be involved in the pathogenesis of a variety of metabolic diseases. All cells come from other cells and many cells arise from precursor cells. Adipocytes are not created from other adipocytes, but they arise from precursor cells. In the last two decades, scientists have discovered the function of many proteins that influence the ability of precursor cells to become adipocytes. If the expansion of the adipose tissue is the problem, it seems logical that adipocyte development inhibitors could be a viable anti-obesity therapeutic. However, factors that block adipocyte development and limit adipocyte expansion also impair metabolic health. This notion may be counterintuitive, but several lines of evidence support the idea that blocking adipocyte development is unhealthy. For this reason it is clear that we need a better understanding of adipocyte development.

			PMID 23209380

	==2011==		==2011==

Z8600021 at 09:19, 18 February 2013

2013-02-18T09:19:38Z

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	===Adipose Embryology===		===Adipose Embryology===

	<pubmed limit=5>Adipose Embryology/pubmed>		<pubmed limit=5>Adipose Embryology</pubmed>

	===Adipose Tissue Development===		===Adipose Tissue Development===

Z8600021 at 09:16, 18 February 2013

2013-02-18T09:16:38Z

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	{{Talk Page}}		{{Talk Page}}

			==10 Most Recent==
			{{10 Most Recent}}

			===Adipose Embryology===

			<pubmed limit=5>Adipose Embryology/pubmed>

			===Adipose Tissue Development===

			<pubmed limit=5>Adipose Tissue Development</pubmed>

			==2013==

	==2011==		==2011==