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Review
. 2013 Mar;14(1):69-76.
doi: 10.1007/s11154-013-9236-x.

The microcirculation in adipose tissue inflammation

Rosario Scalia  1
Affiliations
Review

The microcirculation in adipose tissue inflammation

Rosario Scalia. Rev Endocr Metab Disord. 2013 Mar.

Abstract

In most humans, obesity is associated with a chronic low-grade inflammatory reaction occurring in several organ tissues, including the adipose tissue. Infiltration of bone marrow derived leukocytes (granulocytes, monocytes, lymphocytes) into expanding adipose depots appears to be an integral component of inflammation in obesity. Circulating leukocytes invade organ tissues mainly through post-capillary venules in the microcirculation. The endothelium of the post-capillary venules acts as a gatekeeper to leukocyte adhesion and extravasation by displacing on its luminal surface adhesion molecules that bind the adhesive receptors expressed on circulating leukocytes. Several studies investigating the impact of obesity on the microcirculation have demonstrated the occurrence of microvascular dysfunction in experimental animal model of obesity, as well as in obese humans. To date though, working hypotheses and study designs have favored the view that microvascular alterations are secondary to adipose tissue dysfunction. Indeed, a significant amount of data exists in the scientific literature to support the concept that microvascular dysfunction may precede and cause adipose tissue inflammation in obesity. Through review of key published data, this article prospectively presents the concept that in response to nutrients overload the vascular endothelium of the microcirculation acutely activates inflammatory pathways that initiate infiltration of leukocytes in visceral adipose tissue, well before weight gain and overt obesity. The anatomical and physiological heterogeneity of different microcirculations is also discussed toward the understanding of how obesity induces different inflammatory phenotypes in visceral and subcutaneous fat depots.

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Figures

Figure 1.
Figure 1.
The obese organism experiences and abnormal infiltration of leukocytes in the adipose tissue, a process that results in adipose tissue inflammation and dysfunction. An integrated, maladaptive response involving the endothelium of the adipose tissue microcirculation may be the initiating factor in this phenomenon. Following consumption of high-fat meals, excessive levels of FFA acutely upregulate P-selectin (P-sel) in post-capillary venules of the visceral fat microcirculation by reducing AMPK/eNO signaling. P-sel initiates rolling of circulating leukocytes, especially neutrophils. Rolling leukocytes are primed for enhanced secretion and degranulation, thus releasing, among other inflammatory factors, the powerful oxidant myeloperoxidase (MPO). MPO quickly initiates adipocyte damage leading to impaired adiponectin function (early adipocyte dysfunction). With repeated high-fat meals, loss of adiponectin function further exacerbates infiltration of leukocytes via reduced AMPK/eNOS signaling in the vascular endothelium (metainflammation).
Figure 2.
Figure 2.
Potential signaling targets of MPO chlorination in adipocytes, which can impair adiponectin function in adipose depots experiencing leukocyte infiltration through inflamed microvascular networks.
See this image and copyright information in PMC

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