Scientists at the Karolinska Institutet in Sweden have identified a gene that affects the development of fat tissue in humans and the corresponding risk factor of that gene to promote insulin resistance and type 2 diabetes. The research published in the journal Cell Metabolism is based on the concept that fat tissue can expand in two ways: 1. by increasing the size and/or number of actual fat cells. Prior research has revealed that people with few fat cells that are large in size have an increased risk of developing type 2 diabetes.
The newly identified gene is called EBF1, which drives the development of unhealthy adipose tissue by encoding a protein which controls a series of other genes responsible for regulating the formation of new fat cells as well as their metabolic function.
People with low expression in EBF1 in their fat tissue revealed changed lipid mobilization and their cells were insulin resistant. Insulin resistance leads to increased circulating levels of glucose and lipids in the blood and is a condition characterized by reduced cellular response to the hormone insulin that is released when the blood glucose levels rise after a meal.
“Our findings represent an important step forward in the understanding of how adipose tissue links to the development of metabolic disease,” comments Professor Peter Arner, one of the principal investigators at Karolinska Institutet along with Hui Gao, Niklas Mejhert and Mikael Rydén. “This is the first time someone has identified a gene which may cause malfunctioning adipose tissue in (hu)man. In the future, it might be possible to develop drugs that improve EBF1 function in adipose tissue, which could be used to treat type 2-diabetes.”
In another study UCLA researchers analyzed mice models and gave more than 100 genetic strains of mice a normal diet for eight weeks, followed by a high-fat, high-sugar diet for another eight weeks.
Even though the mice were eating the exact same diets, their weight gain varied greatly. The high-fat diet caused no change in body-fat percentage for some mice while others’ body fat percentages increased by a whopping 600 percent.
The researchers attributed those differences to genetics and compared 11 genetic regions associated with obesity and fat gain in the mice, several of which overlap with genes linked to obesity in humans. The affected genes were involved in metabolic activity with some mice being naturally more active and some being more effective at generating heat, thereby burning calories.
The scientists recommended a healthy diet and exercise to combat the genetic predisposition to obesity.
Hui Gao, Niklas Mejhert, Jackie A. Fretz, Erik Arner, Silvia Lorente-Cebrián, Anna Ehrlund, Karin Dahlman-Wright, Xiaowei Gong, Staffan Strömblad, Iyadh Douagi, Jurga Laurencikiene, Ingrid Dahlman, Carsten O. Daub, Mikael Rydén, Mark C. Horowitz, Peter Arner. Early B Cell Factor 1 Regulates Adipocyte Morphology and Lipolysis in White Adipose Tissue. Cell Metabolism, 2014; DOI: 10.1016/j.cmet.2014.03.032
Brian W. Parksemail, Elizabeth Nam, Elin Org, Emrah Kostem, Frode Norheim, Simon T. Hui, Calvin Pan, Mete Civelek, Christoph D. Rau, Brian J. Bennett, Margarete Mehrabian, Luke K. Ursell, Aiqing He, Lawrence W. Castellani, Bradley Zinker, Mark Kirby, Thomas A. Drake, Christian A. Drevon, Rob Knight, Peter Gargalovic, Todd Kirchgessner, Eleazar Eskin, Aldons J. Lusisemail. Genetic Control of Obesity and Gut Microbiota Composition in Response to High-Fat, High-Sucrose Diet in Mice. Cell Metabolism Volume 17, Issue 1, p141–152, 8 January 2013