Talk:Adipose Tissue Development
|About Discussion Pages|
Cite this page: Hill, M.A. (2021, April 18) Embryology Adipose Tissue Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Adipose_Tissue_Development
PubMed Central Images
10 Most Recent
Note - This sub-heading shows an automated computer PubMed search using the listed sub-heading term. References appear in this list based upon the date of the actual page viewing. Therefore the list of references do not reflect any editorial selection of material based on content or relevance. In comparison, references listed on the content page and discussion page (under the publication year sub-headings) do include editorial selection based upon relevance and availability. (More? Pubmed Most Recent)
<pubmed limit=5>Adipose Embryology</pubmed>
Adipose Tissue Development
<pubmed limit=5>Adipose Tissue Development</pubmed>
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.
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
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
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
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
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, email@example.com.
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.
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. firstname.lastname@example.org
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.
Orexin is required for brown adipose tissue development, differentiation, and function
Cell Metab. 2011 Oct 5;14(4):478-90.
Sellayah D, Bharaj P, Sikder D.
Metabolic Signaling and Disease Program, Diabetes and Obesity Research Center, Sanford-Burnham Medical Research Institute, 6400 Sanger Road, Orlando, FL 32827, USA.
Orexin (OX) neuropeptides stimulate feeding and arousal. Deficiency of orexin is implicated in narcolepsy, a disease associated with obesity, paradoxically in the face of reduced food intake. Here, we show that obesity in orexin-null mice is associated with impaired brown adipose tissue (BAT) thermogenesis. Failure of thermogenesis in OX-null mice is due to inability of brown preadipocytes to differentiate. The differentiation defect in OX-null neonates is circumvented by OX injections to OX-null dams. In vitro, OX, triggers the full differentiation program in mesenchymal progenitor stem cells, embryonic fibroblasts and brown preadipocytes via p38 mitogen activated protein (MAP) kinase and bone morphogenetic protein receptor-1a (BMPR1A)-dependent Smad1/5 signaling. Our study suggests that obesity associated with OX depletion is linked to brown-fat hypoactivity, which leads to dampening of energy expenditure. Thus, orexin plays an integral role in adaptive thermogenesis and body weight regulation via effects on BAT differentiation and function.
Copyright © 2011 Elsevier Inc. All rights reserved.
The generation of adipocytes by the neural crest
Development. 2007 Jun;134(12):2283-92. Epub 2007 May 16.
Billon N, Iannarelli P, Monteiro MC, Glavieux-Pardanaud C, Richardson WD, Kessaris N, Dani C, Dupin E. Source Institut de Recherche, Signalisation, Biologie du Développement et Cancer, CNRS UMR 6543, Centre de Biochimie, Faculté des Sciences, Université Nice Sophia-Antipolis, Nice, France. email@example.com
Fat cells (adipocytes) develop from adipocyte precursor cells (preadipocytes) that themselves derive from mesenchymal progenitors. Although the events controlling preadipocyte differentiation into mature adipocytes have been largely explored, the mechanisms that direct mesenchymal progenitors down the adipocyte pathway remain unknown. Similarly, although adipocytes are generally thought to derive from mesoderm, key information is lacking regarding the origin and the development of the adipose tissue during embryogenesis. The aim of this study was to gain insight into the ontogeny of fat cells, both in mouse embryonic stem (mES) cell-derived cultures and during normal development. We first used genetically engineered mES cells to produce and select ES cell-derived neuroepithelial progenitors and showed that neuroectoderm, rather than mesoderm, may be a source of adipocytes in mES cell-derived cultures. We then used primary and secondary cultures of developing quail neural crest (NC) cells to demonstrate that NC cells are able, upon stimulation with defined factors, to differentiate into adipocytes, thus providing a powerful system to study the earliest stages of adipocyte differentiation. Finally, we mapped NC derivatives in vivo using Cre-mediated recombination in transgenic mice and demonstrated that a subset of adipocytes originates from the NC during normal development.
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
THE DIFFERENTIATION OF WHITE ADIPOSE CELLS. AN ELECTRON MICROSCOPE STUDY
J Cell Biol. 1963 Sep;18:663-79.
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