4.7 Article

Adipose and Liver Expression of Interleukin (IL)-1 Family Members in Morbid Obesity and Effects of Weight Loss

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MOLECULAR MEDICINE
卷 17, 期 7-8, 页码 840-845

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FEINSTEIN INST MED RES
DOI: 10.2119/molmed.2010.00108

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  1. Christian Doppler Research Society

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Morbid obesity is associated with a state of chronic inflammation. Interleukin-1 family (IL-1F) cytokine members are produced by human adipose tissue in obesity. Whereas certain IL-1F members such as IL-1 beta or IL-18 are potently proinflammatory, others such as IL-1 receptor antagonist (IL-1Ra) or IL-37 (formerly IL-1F7) are antiinflammatory. The NLRP3 inflammasome plays a key role in the processing of bioactive IL-1 beta and IL-18. We investigated the effect of excessive weight loss on subcutaneous adipose tissue and liver expression of IL-1 alpha, IL-1 beta, IL-18, IL-1Ra, IL-37 and NLRP3. Twenty-one severely obese patients undergoing laparoscopic adjustable gastric banding were studied. Tissue samples were collected before and 6 months after laparoscopic adjustable gastric banding surgery. mRNA expression of all studied IL-1F members, but especially of IL-37, was much higher in subcutaneous/visceral adipose tissue compared with their liver expression. Subcutaneous adipose tissue mRNA expression of IL-1 beta decreased significantly after extensive weight loss; expression of IL-18 and IL-1Ra did not change, whereas IL-37 expression increased. Weight loss led to a significant reduction in liver IL-1 beta, IL-18 and IL-1Ra expression, whereas hepatic IL-37 mRNA expression remained stable. Adipose/liver NLRP3 inflammasome and IL-l alpha expression were not affected by weight loss. Tissue expression of IL-1 beta, IL-18 and IL-37 were significantly higher in subcutaneous/visceral adipose tissue compared with the liver. In conclusion, expression of IL-1F members is more pronounced in adipose compared with liver tissue in patients with severe obesity. Excessive weight loss changes the adipose and liver expression profile of IL-1F members toward a more antiinflammatory direction. (C) 2011 The Feinstein Institute for Medical Research, www.feinsteininstitute.org

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