Guardian of corpulence : a hypothesis on p53 signaling in the fat cell
(2009) In Clinical lipidology 4(2). p.231-243- Abstract
Adipocytes provide an organism with fuel in times of caloric deficit, and are an important type of endocrine cell in the maintenance of metabolic homeostasis. In addition, as a lipid-sink, adipocytes serve an equally important role in the protection of organs from the damaging effects of ectopic lipid deposition. For the organism, it is of vital importance to maintain adipocyte viability, yet the fat depot is a demanding extracellular environment with high levels of interstitial free fatty acids and associated lipotoxic effects. These surroundings are less than beneficial for the overall health of any resident cell, adipocyte and preadipocyte alike. In this review, we discuss the process of adipogenesis and the potential involvement of... (More)
Adipocytes provide an organism with fuel in times of caloric deficit, and are an important type of endocrine cell in the maintenance of metabolic homeostasis. In addition, as a lipid-sink, adipocytes serve an equally important role in the protection of organs from the damaging effects of ectopic lipid deposition. For the organism, it is of vital importance to maintain adipocyte viability, yet the fat depot is a demanding extracellular environment with high levels of interstitial free fatty acids and associated lipotoxic effects. These surroundings are less than beneficial for the overall health of any resident cell, adipocyte and preadipocyte alike. In this review, we discuss the process of adipogenesis and the potential involvement of the p53 tumor-suppressor protein in alleviating some of the cellular stress experienced by these cells. In particular, we discuss p53-mediated mechanisms that prevent damage caused by reactive oxygen species and the effects of lipotoxicity. We also suggest the potential for two p53 target genes, START domain-containing protein 4 (StARD4) and oxysterol-binding protein (OSBP), with the concomitant synthesis of the signaling molecule oxysterol, to participate in adipogenesis.
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- author
- Bazuine, Merlijn ; Stenkula, Karin G LU ; Cam, Maggie ; Arroyo, Mathilde and Cushman, Samuel W
- publishing date
- 2009-04-01
- type
- Contribution to journal
- publication status
- published
- in
- Clinical lipidology
- volume
- 4
- issue
- 2
- pages
- 231 - 243
- publisher
- Taylor & Francis
- external identifiers
-
- pmid:20126301
- ISSN
- 1758-4299
- language
- English
- LU publication?
- no
- id
- 92910ad9-8b25-42d8-acbd-05b916cdb376
- alternative location
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746679/
- date added to LUP
- 2021-05-20 14:38:00
- date last changed
- 2021-05-20 16:17:46
@article{92910ad9-8b25-42d8-acbd-05b916cdb376,
abstract = {{<p>Adipocytes provide an organism with fuel in times of caloric deficit, and are an important type of endocrine cell in the maintenance of metabolic homeostasis. In addition, as a lipid-sink, adipocytes serve an equally important role in the protection of organs from the damaging effects of ectopic lipid deposition. For the organism, it is of vital importance to maintain adipocyte viability, yet the fat depot is a demanding extracellular environment with high levels of interstitial free fatty acids and associated lipotoxic effects. These surroundings are less than beneficial for the overall health of any resident cell, adipocyte and preadipocyte alike. In this review, we discuss the process of adipogenesis and the potential involvement of the p53 tumor-suppressor protein in alleviating some of the cellular stress experienced by these cells. In particular, we discuss p53-mediated mechanisms that prevent damage caused by reactive oxygen species and the effects of lipotoxicity. We also suggest the potential for two p53 target genes, START domain-containing protein 4 (StARD4) and oxysterol-binding protein (OSBP), with the concomitant synthesis of the signaling molecule oxysterol, to participate in adipogenesis.</p>}},
author = {{Bazuine, Merlijn and Stenkula, Karin G and Cam, Maggie and Arroyo, Mathilde and Cushman, Samuel W}},
issn = {{1758-4299}},
language = {{eng}},
month = {{04}},
number = {{2}},
pages = {{231--243}},
publisher = {{Taylor & Francis}},
series = {{Clinical lipidology}},
title = {{Guardian of corpulence : a hypothesis on p53 signaling in the fat cell}},
url = {{https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746679/}},
volume = {{4}},
year = {{2009}},
}