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20th World Congress on Heart Disease



Guo-Ping Shi, SC.D., D.SC.
, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA


Mast cells contribute to the pathogenesis of obesity and diabetes. Deficiency or pharmacological inactivation of mast cells protects mice from these metabolic diseases. This study demonstrates that leptin deficiency slants otherwise pro-inflammatory mast cells toward anti-inflammatory functions. Mast cells in the white adipose tissues of lean humans and mice are leptin-deficient. Adoptive transfer of leptin-deficient mast cells expanded ex vivo mitigates diet-induced and pre-established obesity and diabetes in diet-induced and genetic obese mice. Mechanistic studies show that leptin-deficient mast cells polarize macrophages from M1 to M2 functions because of an altered balance between pro- and anti-inflammatory cytokines, but do not affect T-cell differentiation. Rampant body weight gain in ob/ob mice, a strain that lacks leptin, associates with reduced mast cell content in the white adipose tissues. In ob/ob mice, genetic depletion of mast cells exacerbates obesity and diabetes, and repopulation of bone marrow in vitro differentiated mast cells ameliorates obesity and diabetes.



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