Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 Mar;1842(3):463-72.
doi: 10.1016/j.bbadis.2013.06.003. Epub 2013 Jun 12.

Adipose tissue angiogenesis: impact on obesity and type-2 diabetes

Silvia Corvera  1 , Olga Gealekman  2
Affiliations
Review

Adipose tissue angiogenesis: impact on obesity and type-2 diabetes

Silvia Corvera et al. Biochim Biophys Acta. 2014 Mar.

Abstract

The growth and function of tissues are critically dependent on their vascularization. Adipose tissue is capable of expanding many-fold during adulthood, therefore requiring the formation of new vasculature to supply growing and proliferating adipocytes. The expansion of the vasculature in adipose tissue occurs through angiogenesis, where new blood vessels develop from those pre-existing within the tissue. Inappropriate angiogenesis may underlie adipose tissue dysfunction in obesity, which in turn increases type-2 diabetes risk. In addition, genetic and developmental factors involved in vascular patterning may define the size and expandability of diverse adipose tissue depots, which are also associated with type-2 diabetes risk. Moreover, the adipose tissue vasculature appears to be the niche for pre-adipocyte precursors, and factors that affect angiogenesis may directly impact the generation of new adipocytes. Here we review recent advances on the basic mechanisms of angiogenesis, and on the role of angiogenesis in adipose tissue development and obesity. A substantial amount of data points to a deficit in adipose tissue angiogenesis as a contributing factor to insulin resistance and metabolic disease in obesity. These emerging findings support the concept of the adipose tissue vasculature as a source of new targets for metabolic disease therapies. This article is part of a Special Issue entitled: Modulation of Adipose Tissue in Health and Disease.

Keywords: Adipocyte; Blood vessel; Capillary; Endothelial; Fat; Vascular.

PubMed Disclaimer

Figures

Figure 1
Figure 1. Two possible models for the stimulation of angiogenesis during adipose tissue growth
A. Increased caloie consumption results in adipocyte hypertrophy and hyperplasis, generating areas of tissue hypoxia. Hypoxia, and/or other factors released from the tissue stimulate angiogenesis. Angiogenesis results in mitigation of hypoxia and appropriate tissue architecture and function. B. Increased calorie consumption results in systemic changes in trophic factors such as insulin, which directly stimulate angiogenesis within adipose tissue. Increased angiogenesis facilitates lipid storage in adipocytes and adipocyte hyperplasia. The simultaneous expansion of adipocytes and vasculature prevents development of hypoxia and metabolic stress.
Figure 2
Figure 2. Different consequences of HIF expression in tumors and adipose tissue
A. Rapid cell proliferation during tumor growth elicits hypoxia, which activates HIF1 signaling, VEGF production and angiogenesis. Increased vascularization allows the tumor to grow. B. HIF1 expression in adipose tissue does not elicit VEGF production, but rather to a pro-fibrotic program, which is followed by inflammation, macrophage infiltration and cell death.
Figure 3
Figure 3. Hypothetical model for coordination of angiogenesis and adipocyte proliferation
A. Quiescent multi-potent progenitors reside within the adipose tissue vasculature. B. Endothelial cells are stimulated to proliferate by VEGF, resulting in the formation of tip cells (green) expressing Dll4, which suppresses VEGF signaling in adjacent cells via activation of Notch, forming new capillary sprouts. This is accompanied by proliferation of progenitors. C. Progenitors differentiate into adipocytes and/or other cell types such as endothelial or mural cells.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Nakagami T, Qiao Q, Carstensen B, Nhr-Hansen C, Hu G, Tuomilehto J, Balkau B, Borch-Johnsen K. Age, body mass index and Type 2 diabetes-associations modified by ethnicity. Diabetologia. 2003;46:1063–1070. - PubMed
    1. Preis SR, Massaro JM, Robins SJ, Hoffmann U, Vasan RS, Irlbeck T, Meigs JB, Sutherland P, D’Agostino RB, Sr, O’Donnell CJ, Fox CS. Abdominal subcutaneous and visceral adipose tissue and insulin resistance in the Framingham heart study. Obesity (Silver Spring) 2010;18:2191–2198. - PMC - PubMed
    1. McLaughlin T, Lamendola C, Liu A, Abbasi F. Preferential fat deposition in subcutaneous versus visceral depots is associated with insulin sensitivity. J Clin Endocrinol Metab. 2011;96:E1756–1760. - PMC - PubMed
    1. Virtue S, Vidal-Puig A. Adipose tissue expandability, lipotoxicity and the Metabolic Syndrome--an allostatic perspective. Biochim Biophys Acta. 2010;1801:338–349. - PubMed
    1. Hardy OT, Czech MP, Corvera S. What causes the insulin resistance underlying obesity? Curr Opin Endocrinol Diabetes Obes. 2012;19:81–87. - PMC - PubMed

Publication types

MeSH terms