It is now well recognised that infiltration of adipose tissue with pro-inflammatory macrophages (white blood cells) is an important factor in the development of the metabolic complications of obesity.
In a paper we published in HYPERTENSION in 2005, we examined the relationship between markers of macrophage activitation (DC11b) on circulating monocytes and expression of pro-inflammatory genes in adipose tissue biopsies. We also used in-vivo microdialysis to examine glucose metabolism in adipose tissue.
We found that participants with higher CD11b expression on monocytes also had increased expression of the macrophage marker CD68 in adipose tissue.
Although we found no differences in systemic insulin sensitivity, subjects with higher peripheral CD11b expression also showed a markedly augmented increase in dialysate glucose in adipose tissue during oral glucose tolerance testing as well as increased adipose tissue lipolysis.
Thus, out data showed that human monocyte activation is associated with tissue-specific changes in glucose and lipid metabolism, which may in part be explained by monocyte/macrophage infiltration of adipose tissue.
Since then, the concept of adipose tissue inflammation and its relation to metabolic complications of obesity have been well characterized and this continues to be a hot area of research.
Indeed, there is now much data to support the notion that it may well be that the presence or absence of adipose tissue inflammatory response is the key defining difference between those who are considered metabolically ‘healthy’ obese and those who develop metabolic complications.
AMS
Edmonton, Alberta
In The News
September 15th, 2012 at 8:40 am
Chronic inflammation again.
On points of information for a curious 26.5 BMI bystander with HsCRP of 0.7:
i) Were all the biopsies on WAT, or did some originate in VAT?
(if so)
ii) Was there any difference between WAT and VAT?
Slainte