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The biology of white adipocyte proliferation
Author(s) -
Hausman D. B.,
DiGirolamo M.,
Bartness T. J.,
Hausman G. J.,
Martin R. J.
Publication year - 2001
Publication title -
obesity reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.845
H-Index - 162
eISSN - 1467-789X
pISSN - 1467-7881
DOI - 10.1046/j.1467-789x.2001.00042.x
Subject(s) - paracrine signalling , adipose tissue , autocrine signalling , adipocyte , endocrinology , biology , medicine , white adipose tissue , growth factor , angiotensin ii , cancer research , microbiology and biotechnology , receptor , blood pressure
Summary Expanded adipose tissue mass increases the risk for many clinical conditions including diabetes, hypertension, coronary atherosclerotic heart disease, and some forms of cancer. Therefore, it is imperative that we understand the mechanisms by which fat pads expand. The enlargement of fat cells during the development of obesity has been previously hypothesized to be a triggering factor for the proliferation of new fat cells. There is now a preponderance of evidence that adipose tissue is a source of growth factors such as IGF‐I, IGF binding proteins, TNFα, angiotensin II, and MCSF that are capable of stimulating proliferation. The relative importance of these autocrine/paracrine factors in the normal control of preadipocyte proliferation is unknown. In addition, the proliferative response of preadipocytes to the paracrine milieu is undoubtedly modulated by neural inputs to fat tissue and/or serum factors. Together, these multiple regulatory controls orchestrate overall and region‐specific adipose tissue cellularity responses associated with the development of hyperplastic obesity. Both in vivo and in vitro studies are needed to understand the complex, interacting physiological mechanisms by which growth of this important organ is regulated.