GLP-1 Agonism Stimulates Browning of Subcutaneous White Adipose Tissue in Obesity Men
Status:
Completed
Trial end date:
2015-07-01
Target enrollment:
Participant gender:
Summary
Adipose tissues, which include white adipose tissue (WAT) and brown adipose tissue (BAT),
play an essential role in regulating whole-body energy homeostasis. Excess expansion of WAT
due to positive energy balance and defects in thermogenic gene expression in BAT are
associated with obesity and various metabolic diseases. Until 2009 the question of whether
adult humans had BAT and whether it could conceivably contribute to whole body energy usage
in a meaningful way was a matter of vigorous debate. The publication of three apppers in the
New England Journal of Medicine that demonstrated adult humans do have BAT, that it can be
activated, and that this activation appears to be defective in obesity reframed the debate,
and revived interest in BAT physiology. Recent studies also reveal the presence of a subset
of cells in WAT that could be induced by environmental or hormonal factors to become
''brown-like'' cells, and this ''beigeing'' process has been suggested to have strong
antiobesity and antidiabetic benefits.
The extrapancreatic actions of glucagon-like peptide-1 (GLP-1) on endothelial cells and the
liver have been reported. Additionally, effects of GLP-1 on adipose tissue have been
described. Studies performed in isolated adipocytes have demonstrated that GLP-1 has the
ability to induce both lipogenic and lipolytic mechanisms in white adipose tissue (WAT) .
More recent study showed that GLP-1 agonism stimulates brown adipose tissue thermogenesis and
browning through hypothalamic AMP-activated protein kinase (AMPK) in animal. However, there
is no data clearly show that GLP-1 agonism stimulates browning of subcutaneous white adipose
tissue (SWAT) in human obesity.