Talk:Connective Tissue Development

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Cite this page: Hill, M.A. (2019, June 24) Embryology Connective Tissue Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Connective_Tissue_Development

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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)


Connective Tissue Development

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

2013

2011

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.

Source

Metabolic Signaling and Disease Program, Diabetes and Obesity Research Center, Sanford-Burnham Medical Research Institute, 6400 Sanger Road, Orlando, FL 32827, USA.

Abstract

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.

PMID 21982708

2007

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. billon@unice.fr

Abstract

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.

PMID 17507398