Format

Send to

Choose Destination
See comment in PubMed Commons below
Adipocyte. 2012 Apr 1;1(2):80-88.

Quantitative dynamics of adipose cells.

Author information

  • 1Laboratory of Biological Modeling; National Institute of Diabetes and Digestive and Kidney Diseases; National Institutes of Health; Bethesda, MD USA.

Abstract

Adipose cells are unique in the dynamism of their sizes, a requisite for their main function of storing and releasing lipid. Lipid metabolism is crucial for energy homeostasis. However, the regulation of lipid storage capacity in conditions of energy excess and scarcity is still not clear. It is not technically feasible to monitor every process affecting storage capacity such as recruitment, growth/shrinkage and death of individual adipose cells in real time for a sufficiently long period. However, recent computational approaches have allowed an examination of the detailed dynamics of adipose cells using statistical information in the form of precise measurements of adipose cell-size probability distributions. One interesting finding is that the growth/shrinkage of adipose cells (> 50 μm diameter) under positive/negative energy balance is proportional to the surface area of cells, limiting efficient lipid absorption/release from larger adipose cells. In addition to the physical characteristics of adipose cells, quantitative modeling integrates dynamics of adipose cells, providing the mechanism of cell turnover under normal and drug-treated conditions. Thus, further use of mathematical modeling applied to experimental measurements of adipose cell-size probability distributions in conjunction with physiological measurements of metabolic state may help unravel the intricate network of interactions underlying metabolic syndromes in obesity.

KEYWORDS:

adipogenesis; apoptosis; cell size distribution; lipid droplet; lipogenesis; lipolysis; mathematical modeling; size-dependent growth; turnover

PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis Icon for PubMed Central
    Loading ...
    Write to the Help Desk