Journal
BIOMEDICINES
Volume 9, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/biomedicines9050449
Keywords
macrophages; insulin; prostaglandin E-2; interleukin-8; inflammation
Categories
Funding
- Deutsche Forschungsgemeinschaft
- Open Access Publishing Fund of University of Potsdam
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The study found that a mix of palmitate, insulin, and PGE(2) in dysfunctional adipose tissue can induce the production of the pro-inflammatory cytokine IL-8. Insulin and PGE(2) amplify the effect of palmitate on IL-8 induction, exacerbating inflammation and insulin resistance.
Macrophages in pathologically expanded dysfunctional white adipose tissue are exposed to a mix of potential modulators of inflammatory response, including fatty acids released from insulin-resistant adipocytes, increased levels of insulin produced to compensate insulin resistance, and prostaglandin E-2 (PGE(2)) released from activated macrophages. The current study addressed the question of how palmitate might interact with insulin or PGE(2) to induce the formation of the chemotactic pro-inflammatory cytokine interleukin-8 (IL-8). Human THP-1 cells were differentiated into macrophages. In these macrophages, palmitate induced IL-8 formation. Insulin enhanced the induction of IL-8 formation by palmitate as well as the palmitate-dependent stimulation of PGE(2) synthesis. PGE(2) in turn elicited IL-8 formation on its own and enhanced the induction of IL-8 release by palmitate, most likely by activating the EP4 receptor. Since IL-8 causes insulin resistance and fosters inflammation, the increase in palmitate-induced IL-8 formation that is caused by hyperinsulinemia and locally produced PGE(2) in chronically inflamed adipose tissue might favor disease progression in a vicious feed-forward cycle.
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