| Chapter title |
Adipocyte-Macrophage Cross-Talk in Obesity
|
|---|---|
| Chapter number | 14 |
| Book title |
Obesity and Lipotoxicity
|
| Published in |
Advances in experimental medicine and biology, June 2017
|
| DOI | 10.1007/978-3-319-48382-5_14 |
| Pubmed ID | |
| Book ISBNs |
978-3-31-948380-1, 978-3-31-948382-5
|
| Authors |
Ayse Basak Engin Ph.D., Ph.D., Engin, Ayse Basak, Ayse Basak Engin |
| Editors |
Ayse Basak Engin, Atilla Engin |
| Abstract |
Obesity is characterized by the chronic low-grade activation of the innate immune system. In this respect, macrophage-elicited metabolic inflammation and adipocyte-macrophage interaction has a primary importance in obesity. Large amounts of macrophages are accumulated by different mechanisms in obese adipose tissue. Hypertrophic adipocyte-derived chemotactic monocyte chemoattractant protein-1 (MCP-1)/C-C chemokine receptor 2 (CCR2) pathway also promotes more macrophage accumulation into the obese adipose tissue. However, increased local extracellular lipid concentrations is a final mechanism for adipose tissue macrophage accumulation. A paracrine loop involving free fatty acids and tumor necrosis factor-alpha (TNF-alpha) between adipocytes and macrophages establishes a vicious cycle that aggravates inflammatory changes in the adipose tissue. Adipocyte-specific caspase-1 and production of interleukin-1beta (IL-1beta) by macrophages; both adipocyte and macrophage induction by toll like receptor-4 (TLR4) through nuclear factor-kappaB (NF-kappaB) activation; free fatty acid-induced and TLR-mediated activation of c-Jun N-terminal kinase (JNK)-related pro-inflammatory pathways in CD11c+ immune cells; are effective in macrophage accumulation and in the development of adipose tissue inflammation. Old adipocytes are removed by macrophages through trogocytosis or sending an "eat me" signal. The obesity-induced changes in adipose tissue macrophage numbers are mainly due to increases in the triple-positive CD11b+ F4/80+ CD11c+ adipose tissue macrophage subpopulation. The ratio of M1-to-M2 macrophages is increased in obesity. Furthermore, hypoxia along with higher concentrations of free fatty acids exacerbates macrophage-mediated inflammation in obesity. The metabolic status of adipocytes is a major determinant of macrophage inflammatory output. Macrophage/adipocyte fatty-acid-binding proteins act at the interface of metabolic and inflammatory pathways. Both macrophages and adipocytes are the sites for active lipid metabolism and signaling. |
X Demographics
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 3 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 3 | 100% |
Mendeley readers
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 142 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Master | 15 | 11% |
| Student > Doctoral Student | 14 | 10% |
| Student > Bachelor | 14 | 10% |
| Researcher | 12 | 8% |
| Student > Postgraduate | 9 | 6% |
| Other | 22 | 15% |
| Unknown | 56 | 39% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 23 | 16% |
| Biochemistry, Genetics and Molecular Biology | 22 | 15% |
| Agricultural and Biological Sciences | 6 | 4% |
| Nursing and Health Professions | 4 | 3% |
| Immunology and Microbiology | 4 | 3% |
| Other | 14 | 10% |
| Unknown | 69 | 49% |