Elsevier

Surgery

Volume 145, Issue 3, March 2009, Pages 255-259
Surgery

Surgical Research Review
Inflammation in obesity-related diseases

https://doi.org/10.1016/j.surg.2008.08.038Get rights and content

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Obesity and systemic inflammation

One of the most important realizations in the field of metabolic disease over the last decade is that obesity is associated with a state of chronic, low-grade, systemic inflammation. Evidence from obese animals and humans demonstrates a clear association between weight regulation and inflammation, with abnormalities of numerous in vitro and in vivo measures of innate and adaptive immune function, including serum levels of inflammatory cytokines, peripheral blood lymphocyte subpopulation

Adipose tissue—a primary in vivo site of inflammation in obesity

Adipose tissue comprises not only adipocytes but also a stromovascular cell fraction. This stromovascular cell fraction consists of a diverse population of lymphocytes, fibroblasts, endothelial and stromal cells, and preadipocytes, which along with adipocytes, serve as a rich source of cytokines and adipokines. Adipocytes themselves are related closely to fibroblasts and macrophages, and in fact, evidence supports their ability to transdifferentiate into macrophages in vivo. Adipose tissue

Adipocytokines

Aberrant expression of a wide range of cytokines and adipokines is a central feature of the inflammatory process within adipose tissue in obesity. Although the term “adipokine” in the strictest sense refers to proteins expressed solely by adipocytes such as leptin, lymphocytes comprise up to half of the non-adipocyte cell fraction of adipose tissue and are the source of many classic cytokines, such as TNF-α and IL-1, as well as mediators described originally as having a primary role in weight

Cellular mediators of inflammation within adipose tissue

The disorders in adipocytokine expression within adipose tissue are not accompanied surprisingly by aberrations in the frequency and function of immune and inflammatory effector cells. Among them, macrophages stand out as prime candidates for cellular mediators of inflammation. The frequency of adipose tissue-associated macrophages (ATMs) is increased in obese humans and correlates directly with body mass index. Emphasizing the unique role of VAT in obesity-related inflammation, macrophage

Adipose tissue inflammation and systemic metabolic disease

Although adipose tissue is a central site of inflammation in obesity, the resultant metabolic sequelae are systemic. What are the mechanisms by which inflammation within adipose tissue influences other organ systems? One such mechanism is the intimate, anatomic association between VAT and the liver. Increased VAT leads to increased delivery of free fatty acids, well-known inflammatory adipocytokines to the liver via the portal venous system, which are phenomena that are implicated directly in

The root cause of inflammation in obesity

The underlying events that initiate inflammation within adipose tissue remain unknown. A leading hypothesis implicates adipose tissue hypoxia in the genesis of inflammation,11 which is a finding that was confirmed in murine obesity and reversed with weight loss. What causes adipose tissue hypoxia? Adipocyte enlargement is a paradigmatic histologic feature of human obesity, and adipocytes are one of the few cell types that can enlarge to sizes greater than the effective diffusion distance of

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Supported by an American Surgical Association Foundation Fellowship Award and by NIH/NIDDK Grant 1K08DK074397-01A1.

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