Genetic deletion of mast cell serotonin synthesis prevents the development of obesity and insulin resistance

Julian M. Yabut, Eric M. Desjardins, Eric J. Chan, Emily A. Day, Julie M. Leroux, Bo Wang, Elizabeth D. Crane, Wesley Wong, Katherine M. Morrison, Justin D. Crane, Waliul I. Khan and Gregory R. Steinberg ()
Additional contact information
Julian M. Yabut: McMaster University
Eric M. Desjardins: McMaster University
Eric J. Chan: McMaster University
Emily A. Day: McMaster University
Julie M. Leroux: McMaster University
Bo Wang: McMaster University
Elizabeth D. Crane: Northeastern University
Wesley Wong: Northeastern University
Katherine M. Morrison: McMaster University
Justin D. Crane: Northeastern University
Waliul I. Khan: McMaster University
Gregory R. Steinberg: McMaster University

Nature Communications, 2020, vol. 11, issue 1, 1-11

Abstract: Abstract Obesity is linked with insulin resistance and is characterized by excessive accumulation of adipose tissue due to chronic energy imbalance. Increasing thermogenic brown and beige adipose tissue futile cycling may be an important strategy to increase energy expenditure in obesity, however, brown adipose tissue metabolic activity is lower with obesity. Herein, we report that the exposure of mice to thermoneutrality promotes the infiltration of white adipose tissue with mast cells that are highly enriched with tryptophan hydroxylase 1 (Tph1), the rate limiting enzyme regulating peripheral serotonin synthesis. Engraftment of mast cell-deficient mice with Tph1−/− mast cells or selective mast cell deletion of Tph1 enhances uncoupling protein 1 (Ucp1) expression in white adipose tissue and protects mice from developing obesity and insulin resistance. These data suggest that therapies aimed at inhibiting mast cell Tph1 may represent a therapeutic approach for the treatment of obesity and type 2 diabetes.

Date: 2020
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DOI: 10.1038/s41467-019-14080-7

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