Aging in adipocytes: potential impact of inherent, depot-specific mechanisms |
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Authors: | Cartwright Mark J Tchkonia Tamara Kirkland James L |
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Affiliation: | Department of Medicine, Section of Geriatrics, Boston University Medical Center, 650 Albany St., Boston, MA 02118, USA. |
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Abstract: | Fat mass and tissue distribution change dramatically throughout life. Fat depot sizes reach a peak by middle or early old age, followed by a substantial decline, together with fat tissue dysfunction and redistribution in advanced old age. These changes are associated with health complications, including type 2 diabetes, atherosclerosis, dyslipidemia, thermal dysregulation, and skin ulcers, particularly in advanced old age. Fat tissue growth occurs through increases in size and number of fat cells. Fat cells turn over throughout the lifespan, with new fat cells developing from preadipocytes, which are of mesenchymal origin. The pool of preadipocytes comprises 15-50% of the cells in fat tissue. Since fat tissue turns over throughout life, characteristics of these cells very likely have a significant impact on fat tissue growth, plasticity, function, and distribution. The aims of this review are to highlight recent findings regarding changes in preadipocyte cell dynamics and function with aging, and to consider how inherent characteristics of these cells potentially contribute to age- and depot-dependent changes in fat tissue development and function. |
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Keywords: | C/EBP, CCAAT enhancer binding protein PPAR, peroxisome proliferator activated receptor RXRα, retinoid X receptor α LIP, liver inhibitory protein LAP, liver activating protein CHOP, C/EBP homologous protein CUGBP, GUG triplet binding protein aP2, adipocyte fatty acid binding protein PGC1, PPARγ coactivator-1 CPT1, carnitine palmitoyl transferase-1 |
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