J Genomics 2013; 1:1-4. doi:10.7150/jgen.3276
Adipogenesis: It Is Not Just Lipid That Comprises Adipose Tissue
1. Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA
2. USDA-ARS, Richard B. Russell Agricultural Research Station, Athens, GA 30604, USA
Dodson MV, Jiang Z, Du M, Hausman GJ. Adipogenesis: It Is Not Just Lipid That Comprises Adipose Tissue. J Genomics 2013; 1:1-4. doi:10.7150/jgen.3276. Available from http://www.jgenomics.com/v01p0001.htm
Adipogenesis is the initial component of forming cells (adipocytes) capable of assimilating lipid. Lipid metabolism is a metabolic process whereby lipid is stored for use when energy is required. Both processes involve cellular and molecular components. The gene regulations of each are different and (yet) confusingly, markers for both are used interchangeably. The focus of this paper is to provide elementary information regarding both processes and to introduce this issue of Journal of Genomics, whereby important aspects of adipogenesis and lipid metabolism involving gene expression are provided.
Keywords: Adipogenesis, Lipid Metabolism, Gene Regulation
The total amount of adipose tissue, or fat, that a person or animal possesses tells a story about their lives [1-3]. Species, gender, age and health condition are clearly correlated with total adipose load of the body [4-7]. In general, a high body fat load suggests that a person over eats, or consumes a disproportionate level of energy, without a compensating level of exercise [8,9]. In animals, especially meat animals, a high percentage of body fat commonly means that the overall content of lean meat will be reduced [8,10-14]. The physiology and end-effects of whole body adipose load is important and has been recently reviewed [1-3,7,8,10-14]. While one might think that adipose tissue is the same regardless of anatomical locale, it is not [8,11,12,15]. Different adipose tissue depots exist in humans and in animals, and the regulation of these fat deposits appear to be different [8,11,15-27]. Moreover, some adipose tissue depots possess ability to synthesize and release into the systemic circulation whole-body regulators possessing numerous physiology changing signals [11,28]. Due to this, attention has been given to elucidating adipose-depot-specific capability to regulate other aspects of body physiology [10,11]. Differences and influences of different adipose tissue depots have been introduced by papers within this issue. Moreover, if one were to look closely at the structural make-up of a small portion of any adipose tissue depot it would be readily apparent that the tissue is composed of important structures that might play a role in the regulation of the depot [11,29-30]. Blood supply, extracellular components and proportion of different cells all contribute to the overall physiology of any adipose tissue. Histology of adipose tissue has been recently reviewed [29-31].
A wide variety of cells exist in association with adipose tissue [8,11,14,17,29-30]. Lipid-containing cells called adipocytes may be white or brown [11,14,29,32]. Cells committed to the adipose lineage, but not filled with lipid termed preadipocytes/adipofibroblasts also exist and are reported to be capable of providing new cells to the adipose tissue depot if needed for energy storage [11,17,29,33]. Other cell types such as a variety of blood-type cells exist in adipose tissue [11,29-30]. The mechanism(s) through which all cells of the adipose tissue work together to make the tissue function remain unknown. Moreover, the regulation exerted on individual cells to other cells is also unknown.
Adipogenesis is the process of forming lipid-assimilating adipocytes from cells committed to doing so, whereas lipid metabolism is the process of accepting lipid, storing it, and releasing it from an adipocyte [1-3,11,12,34-39]. Usually, one thinks of adipogenesis occurring during late fetal development, and into early adolescence. However, it may occur at any time throughout the lifetime of the person/animal [1,7,8,11]. Lipid metabolism occurs continuously, but has been highlighted in humans as something that leads to obesity and the adverse health effects of possessing too much lipid metabolism that leads to excess lipid stores [1,7,8,11]. A variety of protein markers have been identified that are associated with both adipogenesis and lipid metabolism [12,13,40]. These markers have been discerned through the use of both cell lines and primary cultures of cells derived from different animals [11,14,29]. Blood tests and associated metabolic panels have been devised utilizing some of these markers to inform humans about potential problems associated with variables of lipid health . Usefulness of cell line identified markers to other (specific) animal model systems is being explored [3,12,13].
Traditional cell biology principals suggest that once a cell has been committed to a specific lineage and begins to express the lineage-specific markers of differentiation that the cell is terminally differentiated--possessing no further capabilities to exhibit primordial phenotypes [34-37,40,42-46]. In the case of adipocytes, traditional thought is that once any cell begins to assimilate lipid into vesicles (undergoes lipid metabolism) that the cell no longer possesses the ability to proliferate (undergo adipogenesis). Recent reports suggest that this just does not hold true for (even) mature adipocytes [8,11,17,34-37,40,42-46]. As such, cells provided by the dedifferentiation of mature adipocytes to form proliferative-competent progeny cells needs to be explored as potential mechanisms of additional adipogenesis/lipid metabolism [8,11,12,17,19,23,34-39,42-45]. Moreover, such cells may actually provide for a relatively new source of cells for tissue regenerative/reconstruction measures/procedures and other uses of potential stem cells [42,43].
The physical presence of genes and the expression of genes are two different processes that need to be explored in the realm of adipogenesis and lipid metabolism [3,11,12,24-26,32,38,47-48]. Are there specific gene products that can be exploited to help regulate adipogenesis and/or lipid metabolism? Are these easily expressed as detectable markers, whereby one might use them as diagnostic tools? Are all animals genetically regulated similarly in terms of adipogenesis/lipid metabolism? The contributions of this issue of the Journal of Genomics add to our knowledge of important aspects of adipogenesis and lipid metabolism.
Conflict of Interest
The authors have declared that no conflict of interest exists.
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Dr. Michael V. Dodson is a Professor in the Animal Sciences Department at Washington State University (WSU), and affiliate faculty of the Center for Integrated Biotechnology (WSU) and Washington Center for Muscle Biology (collective effort between WSU and the University of Washington). For nearly three decades Dr. Dodson has studied skeletal muscle-derived stem cells. This work has resulted in nearly 150 papers on new methods for satellite cell- and adipocyte-derived stem cell isolation, culture, analysis and interpretation. Dr. Dodson has supported team research for his entire career, including a variety of efforts related to the USDA-sponsored research projects: NC1131 Molecular mechanisms regulating skeletal muscle growth and differentiation and NCCC201 Regulation of adipose tissue accretion in meat-producing animals (NCR97).
Dr. Zhihua Jiang is an Associate Professor in the Animal Sciences Department at Washington State University. Since the early 1990's, Dr. Jiang's research has focused on comparative genome biology with aims at understanding how orthologous genes have evolved and shuffled during evolution. The overall objective of his research program is to develop comparative genomic tools and reagents for determining gene sequence, location, expression and function, thus advancing genome sciences and their applications in agriculture and biomedicine. Dr. Jiang has published more than 110 publications that were well cited in the field. He was editor of the book "Reproductive Genomics in Domestic Animals" Published by Wiley-Blackwell in 2010. Dr. Jiang has received eight US patent awards.
Dr. Min Du was an associate professor in the Department of Animal Science at University of Wyoming and has recently moved to the Animal Sciences Department at Washington State University as a Professor and Funded Chair in Animal Sciences. His research focuses on the physiological conditions regulating skeletal muscle growth and development, and mechanisms governing differentiation of mesenchymal stem cells into myocytes, adipocytes and fibroblasts during fetal development. He has been publishing actively and currently serving as reviewers for a number of funding agencies and journals.
Dr. Gary J. Hausman has authored or co-authored nearly 200 scientific articles published in refereed journals, and have given a multitude of invited presentations at national and international scientific meetings. Dr. Hausman's research reputation is reflected in invitations to present and discuss research data and requests to consult with colleagues in academia, in industry, and in other governmental institutions throughout the world. In addition, he has conceived, planned and organized major symposia for the national American Society of Animal Science and the Experimental Biology Meetings. Dr. Hausman has also served on an NIH grant review panel and several committees that impact Agency, Departmental and Congressional policy makers.
Corresponding author: Dr. M.V. Dodson, Department of Animal Sciences, Washington State University, Pullman, WA 99164; Tel: +1 509-335-9644; FAX: +1 509 335 1082; E-mail: dodsonedu