Article ID Journal Published Year Pages File Type
1998214 Molecular Genetics and Metabolism 2014 6 Pages PDF
Abstract

•Angiogenesis is closely linked to adipogenesis and adipose tissue expansion.•Angiogenesis might be involved in the metabolic outcome in obesity.•ID3 regulates transcription of many genes and is involved in angiogenesis.•We review the literature of ID3 in relation to angiogenesis and adipogenesis.•ID3 plays a potential role in the regulation of metabolic health in human obesity.

Metabolic health in obesity is known to differ among individuals, and the distribution of visceral (VAT) and subcutaneous adipose tissue (SAT) plays an important role in this regard. Adipose tissue expansion is dependent on new blood vessel formation in order to prevent hypoxia and inflammation in the tissue. Regulation of angiogenesis in SAT and VAT in response to diet is therefore crucial for the metabolic outcome in obesity.Knowledge about the underlying genetic mechanisms determining metabolic health in obesity is very limited.We aimed to review the literature of the inhibitor of differentiation-3 (ID3) gene in relation to adipose tissue and angiogenesis in humans in order to determine whether ID3 could be involved in the regulation of adipose tissue expansion and metabolic health in human obesity.We find evidence that ID3 is involved in regulatory mechanisms in adipose tissue and regulates angiogenesis in many tissues including adipose tissue. We discuss how this might influence obesity and metabolic health in obesity and further discuss some potential mechanisms by which ID3 might regulate visceral and subcutaneous adipose tissue expansion.The combined results from the reviewed literature suggest ID3 to play a potential role in the underlying regulatory mechanisms of metabolic health in human obesity. The literature is still sparse and further studies focusing on human ID3 in relation to the nature of obesity are warranted.

Related Topics
Life Sciences Biochemistry, Genetics and Molecular Biology Biochemistry
Authors
, ,