Inflammation in fat tissue helps prevent metabolic disease
DALLAS – June 18, 2014 – Chronic tissue inflammation is typically associated with obesity and metabolic disease, but new research from UT Southwestern Medical Center now finds that a level of “healthy” inflammation is necessary to prevent metabolic diseases, such as fatty liver.
“There is such a thing as ‘healthy’ inflammation, meaning inflammation that allows the tissue to grow and has overall benefits to the tissue itself and the whole body,” said Dr. Philipp Scherer, Director of the Touchstone Center for Diabetes Research and Professor of Internal Medicine and Cell Biology at UT Southwestern. “The same principle also applies in muscle: Exercise induces some inflammation in the tissue, but also leads to better and stronger muscles and, consequently, a healthier organism.”
Using animal models, Dr. Scherer and his team, with first author, Dr. Ingrid Wernstedt Asterholm, former Assistant Instructor at UT Southwestern and current Assistant Professor at the University of Gothenburg in Sweden, found that suppressing inflammation in fat tissue results in reduced fat expansion and thus leaner mice, even when the animals are fed a high-fat diet. The findings were first published online June 12 in Cell Metabolism.
What Dr. Scherer, holder of the Gifford O. Touchstone, Jr. and Randolph G. Touchstone Distinguished Chair in Diabetes Research, and his team expected to find that the reduced body fat content would lead to improvements in metabolism and a lower incidence of metabolic disease. Unexpectedly, the team found that the lean mice showed symptoms of metabolic disease, such as glucose intolerance.
This result might be because when fat tissue expands, it absorbs excess lipids, preventing them from being deposited in other tissues, such as the liver. Indeed, the animal models showed signs of fatty liver, caused by buildup of fat in liver cells, and a “leaky gut,” caused by disruption of the gut wall.
“What our research shows is that we need some localized inflammation to remodel our fat tissue and to prevent metabolic diseases such as fatty liver,” said Dr. Asterholm. “This finding may explain in part why anti-inflammatory medicines have so far not been successful as anti-diabetic treatments. The effects of interventions that promote local low-level inflammation in fat tissue remain to be determined.”
Additional study contributors at UT Southwestern include graduate students Caroline Tao and Thomas Morley; Dr. Qiong Annabel Wang, postdoctoral research fellow in Internal Medicine; and Dr. Zhao Wang, Instructor of Internal Medicine.
The research was supported by the National Institutes of Health, the Throne-Holst Foundation, the Swedish Research Council, VINNOVA, the NovoNordisk Excellence Project Award, the American Heart Association, and the American Diabetes Association.
About UT Southwestern Medical Center
UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty includes many distinguished members, including six who have been awarded Nobel Prizes since 1985. Numbering more than 2,700, the faculty is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide medical care in 40 specialties to nearly 91,000 hospitalized patients and oversee more than 2 million outpatient visits a year.
Media Contact: Lisa Warshaw
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