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The biology of white adipocyte proliferation.

Authors
  • Hausman, D B
  • DiGirolamo, M
  • Bartness, T J
  • Hausman, G J
  • Martin, R J
Type
Published Article
Journal
Obesity reviews : an official journal of the International Association for the Study of Obesity
Publication Date
Nov 01, 2001
Volume
2
Issue
4
Pages
239–254
Identifiers
PMID: 12119995
Source
Medline
License
Unknown

Abstract

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, TNF alpha, 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.

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